StemCell Therapy

Genetics seems rather intimidating, but in its purest sense it is rather simple.The basis of genetics is fairly simple: DNA => RNA => A Protein.

DNA, or deoxyribonucleic acid, (DNA) is a long molecule that contains our unique genetic code. Nearly every cell in a persons body has the same DNA. Most DNA is located in the cell nucleus (where it is called nuclear DNA), but a small amount of DNA can also be found in the mitochondria (where it is called mitochondrial DNA or mtDNA).

The information in DNA is stored as a code made up of four chemical bases: adenine (A), guanine (G), cytosine (C), and thymine (T). Human DNA consists of about 3 billionof these bases, and more than 99 percent of those bases are the same in every person. The order, or sequence, of these bases determines the information available for building and maintaining an organism.

DNA bases pair up with each other, A with T and C with G, to form units called base pairs. Each base is also attached to a sugar molecule and a phosphate molecule. Together, a base, sugar, and phosphate are called a nucleotide. Nucleotides are arranged in two long strands that form a spiral called a double helix. The structure of the double helix is somewhat like a ladder, with the base pairs forming the ladders rungs and the sugar and phosphate molecules forming the vertical sidepieces of the ladder.

Ribonucleic acid (RNA) is very similar to DNA, but differs in a few important structural details: RNA nucleotides contain ribose sugars while DNA contains deoxyribose and RNA uses predominantly uracil instead of thymine present in DNA. RNA is transcribed (synthesized) from DNA by enzymes called RNA polymerases and further processed by other enzymes. RNA serves as the template for translation of genes into proteins, transferring amino acids to the ribosome to form proteins, and also translating the transcript into proteins.

RNAs serve as the working set of blue prints for a gene. Each gene is read, and then the messenger RNAs are sent to the molecular factories (ribosomes) that build proteins. These factories read the blueprints and use the information to make the appropriate protein. When the cell no longer needs to make any more of that protein, the RNA blueprints are destroyed. but because the master copy in the DNA remains intact, the cell can always go back to the DNA and make more RNA copies when it needs more of the encoded protein.

An example would be the suns UV light activating the genes in your skin cells to tan you. The gene is read and the RNA takes the message or blueprint to the ribosomes where melanin, the protein that tans your skin, is made.

As we discussed, each gene is made up of a series of bases and those bases provide instructions for making a single protein. Any change in the sequence of bases may be considered a mutation. Most of the mutations are naturally-occurring. For example, when a cell divides, it makes a copy of its DNA and sometimes the copy is not quite perfect. That small difference from the original DNA sequence is a mutation.

Mutations can also be caused by exposure to specific chemicals, metals, viruses, and radiation. These have the potential to modify the DNA. This is not necessarily unnatural even in the most isolated and pristine environments, DNA breaks down. Nevertheless, when the cell repairs the DNA, it might not do a perfect job of the repair. So the cell would end up with DNA slightly different than the original DNA and hence, a mutation.

Some mutations have little or no effect on the protein, while others cause the protein not to function at all. Other mutations may create a new effect that did not exist before. Many diseases are a result of mutations in certain genes. One example is the gene for sickle cell anemia. The mutation causing the blood disorder sickle cell anemia is a single nucleotide substitution (A to T) in the base number 17 out of 438 As, Ts, Cs and Gs . By changing the amino acid at that point, the impact is that the red blood cells are no longer round, but sickle in shape and carry less oxygen.

Some of these changes occur in cells of the body such as in skin cells as a result of sun exposure. Fortunately these types of changes are not passed on to our children. However, other types of errors can occur in the DNA of cells that produce the eggs and sperm. These errors are called germ line mutations and can be passed from parent to child. If a child inherits a germ line mutation from their parents, every cell in their body will have this error in their DNA. Germ line mutations are what cause diseases to run in families, and are responsible for hereditary diseases.

Sudden cardiac death (SCD) is a widespread health problem with several known inherited causes. Inherited SCD generally occurs in healthy individuals who do not have other conventional cardiac risk factors. Mutations in the genes in charge of creating the electrical activity of the heart have been found to be responsible for most arrhythmias, among them Short QT Syndrome, Long QT Syndrome, Brugada Syndrome, Familial Bundle Branch Block, Sudden Infant Death Syndrome and Sudden Unexpected Death Syndrome.

As researchers discover the role genes play in disease, there will be more genetic tests available to help doctors make diagnoses and pinpoint the cause of the disease. For example, heart disease can be caused either by a mutation in certain genes, or by environmental factors such as diet or exercise to name a few.

Physicians can easily diagnose a person with heart disease once they present symptoms. However, physicians can not easily identify the cause of the heart disease is in each person. Thus, most patients receive the same treatment regardless of underlying cause of the disease.

In the future, a panel of genetic tests for heart disease might reveal the specific genetic factors that are involved in a given person. People with a specific mutation may be able to receive treatment that is directed to that mutation, thereby treating the cause of the disease, rather than just the symptoms.

The ultimate goal of the MMRLs Molecular Genetics Program is to identify the factors that are responsible for these diseases. This knowledge will facilitate the development ofgene-specific therapies and cures for arrhythmias and identify individuals at risk for sudden cardiac deaths.

With the addition of the Molecular Biology and Molecular Genetics programs, MMRL is now integrally involved in both basic and clinical research, and is among the relatively few institutions worldwide with a consistent and concerted focus on bridging basic and clinical science. With an eye toward designing specific treatments and cures for disease, the Laboratorys research has the potential to affect us all.

See more here:
Molecular Genetics - mmrl.edu

Contact: (0191) 241 8600 - Dr David Bourn, Head of Laboratory, Molecular Genetics

The molecular laboratory service provides genetic diagnosis for those families suffering from inherited conditions caused by mutation of specific single genes.Testing is performed using a variety of DNA analysis techniques to identify causative mutations or to track defective genes through families.

The Molecular Genetics Laboratory operates within the Professional Guidelines of the Clinical Molecular Genetics Society (CMGS).

The laboratory is accredited by Clinical Pathology Accreditation

Clinical scientists and MLSO staff are State Registered with the Health Professions Council after the required period of training.

The Molecular Genetics Laboratory participates in the following external quality assurance schemes:

Northern Genetics Service Institute of Genetic Medicine Central Parkway Newcastle upon Tyne NE1 3BZ

Tel: 0191 241 8600

The laboratory operates Monday to Friday between the hours of 08.30 and 17.00.For the receipt and analysis of very urgent samples outside these hours, please make special arrangements with the laboratory.

Head of Laboratory

Dr David Bourn

telephone: 0191 241 8600

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Newcastle Hospitals - Molecular Genetics

Jeffrey M. Friedman Professor; Investigator, HHMI

The application of modern methods in genetics has led to the identification of a new hormone, leptin, that regulates body weight. Leptin is an adipose tissue hormone that interacts with receptors in the brain to regulate food intake, energy expenditure and other neuroendocrine systems. The molecular mechanisms of leptin in the brain are under investigation. These studies are being conducted in parallel with efforts to identify obesity genes in the human.

1995 Amgen Inc.

Although the physiological regulation of body weight and appetite has been strongly suggested by experimental evidence, the elucidation of the relevant molecular mechanisms has proven difficult. The possible role of a brain-gut peptide, cholecystokinin (CCK), in these processes was the initial subject of investigation in this laboratory. CCK has been extensively evaluated as a possible satiety factor. CCK is secreted as a 33 amino acid peptide from endocrine cells in the jejeunum where it is released in response to nutrient in the intestinal lumen. The same CCK precursor is posttranslationally processed to an 8 amino acid peptide in brain. The single copy CCK gene is differentially regulated in brain and intestine during development and expressed ectopically in a class of primitive neuronal tumors3-6. The physiological role of CCK in controlling appetite is unclear. In 1973 Smith and Gibbs showed that injections of CCK reduce food intake in food deprived rodents. In addition, the levels of brain CCK were reported by Straus et al to be low in genetically obese (ob) mice8. However, nonpeptide CCK antagonists developed by Squibb and other pharmaceutical companies do not affect food intake and body weight in the long term9. Moreover, overexpression of CCK in transgenic mice did not affect food intake or body weight (unpublished data). Genetic mapping of the CCK gene to mouse chromosome 9 excluded it as being etiologic in any of the inherited rodent obesity syndromes10. These data raised the question as to the molecular basis of the phenotype in genetically obese (ob) and diabetic (db) mice.

Mutations in the mouse ob and db genes result in obesity and diabetes in a syndrome resembling morbid human obesity11, 12. Coleman, using the method of parabiosis, predicted that the ob gene encoded a novel hormone and that the db gene encoded its receptor11. Recent data from this laboratory are consistent with this hypothesis. The ob gene was identified by positional cloning and found to encode a 4.5 kB RNA expressed exclusively in adipocytes13-16. The ob gene product, known as LEPTIN, circulates as a 16 kilodalton protein in mouse and human plasma but is undetectable in plasma from C57BL/6J ob/ob mice17. Plasma levels of this protein are increased in diabetic (db ) mice, a mutant thought to be resistant to the effects of ob17. The levels of protein are also increased in several other genetic and environmentally induced forms of rodent obesity including mice with lesions in the hypothalamus16. Daily intraperitoneal injections of recombinant mouse leptin reduced body weight of ob/ob mice by 30% at 2 weeks and by 40 % after four weeks but had no effect on db/db mice17. The protein reduced food intake and increased energy expenditure in ob/ob mice. Injections of wild type mice twice daily with the mouse protein resulted in a sustained 12% weight loss, decreased food intake and a reduction of body fat from 12.2 to 0.7%. Recombinant human leptin reduced body weight with equivalent potency to mouse leptin when injected into ob mice17. In human, the plasma level of leptin correlated with body mass index (BMI) and % body fat18. However at a given BMI, there was significant variability in the leptin level. In all cases analyzed weight loss in human was associated with a decrease in plasma leptin concentration18. These data suggest that leptin serves an endocrine function to regulate body fat stores. In most instances, obesity is associated with an apparent decrease in sensitivity to endogenous leptin resulting in a compensatory increase in adipocyte mass. However, in a subset of cases human obesity appears to result from subnormal leptin secretion18-20.

The complete insensitivity of db mice to leptin and the identical phenotype of ob and db mice suggested that the db locus encodes the leptin receptor 11, 17. The db gene was localized to a 300 kB interval on mouse chromosome 419-21. Exon trapping and cDNA selection identified a candidate gene in this region. This candidate was found to be identical to a receptor (ob-R) which was functionally cloned from choroid plexus21, 22. However, because this receptor was normal in db mice, the possibility was raised that the db mutation affected an alternatively spliced form. The Ob-R gene was found to encode at least five alternatively spliced forms 21. One of the splice variants is expressed at a high level in the hypothalamus and at a lower level in other tissues. This transcript is mutant in C57BL/Ks db/db mice21. The mutation is the result of abnormal splicing leading to a 106 bp insertion into the 3' end of its RNA. The mutant protein is missing the cytoplasmic region and is likely to be defective in signal transduction. A nonsense mutation in facp rats, a rat equivalent of db, leads to premature termination NH2-terminal of the transmembrane domain (unpublished data). These data suggest that the weight reducing effects of leptin are mediated by signal transduction through a receptor in the hypothalamus and elsewhere.

Further studies have revealed that the Stat3 transcription factor is activated specifically in hypothalamus within 15 minutes of a single injection of leptin in ob and wild type but not in db mice23. In situ hybridization indicates that Ob-Rb is expressed in three different hypothalamic regions: the arcuate, ventromedial and lateral hypothalamic nuclei (in preparation). Lesions of each of these nuclei are known to affect body weight regulation. Further characterization of the neurons in these brain regions and their connections will have important implications for our understanding of leptin's actions and the molecular mechanisms regulating body weight.

Advances in genetics make it possible to identify human disease genes. The implementation of a genetic approach to the study of obesity will help establish whether the human ob or db genes account for genetic forms of obesity and also lead to the identification or validation of other candidate genes. Such studies require that large numbers of families be collected in which the trait of interest is inherited.

In order to implement this approach for the study of obesity, this laboratory has developed a collaboration with the Department of Health on the island of Kosrae in Micronesia. The citizens of this island have a high incidence of obesity, the basis of which is not understood. The Kosraen population is highly admixed between Micronesian and Caucasian ancestors, a fact that facilitates genetic analysis. A study has now been completed in which the entire adult population of Kosrae over twenty years of age, ~2500 individuals, has had a complete medical workup including measurements of height, weight, blood pressure, and glucose levels. In addition, measurements of serum insulin, and eventually leptin, will be made. Measurements of serum cholesterol, and triglycerides have already been completed by Dr. Jan Breslows laboratory at Rockefeller University. In collaboration with the Stoffel laboratory, DNA has been isolated from each individual as well as information about the identity and medical status of other family members. To date, all 2500 DNA samples have been processed ad genetic analyses have begun. The availability of a complete clinical profile on an entire population, combined with modern methods in genetics should make it possible to establish the possible relationship of genetic variation at the human ob and db genes to human obesity. In addition, a highly admixed population provides an opportunity to identify additional loci that affect the control of body weight, as well as the medical problems that are often associated with obesity such as hypertension, diabetes, heart disease.

Future studies will also focus on the physiologic effects of leptin. These include studies of leptin's effects on lipid metabolism, glucose metabolism and insulin action. Available data suggest that neurons in the hypothalamus are a principle target of leptin actin. Studies to establish the neurotransmitter profile and projection of Ob-Rb positive neurons have begun. Analysis of the electrophysiologic effects of leptin on these cells will proceed simultaneously. Efforts to produce a higher activity version of leptin are also underway in studies of the structure function relationship of leptin and its receptors (collaborative with the Burley laboratory).

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The Rockefeller University Laboratory of Molecular Genetics

We use DNA analysis techniques on blood samples to carry out testing for a wide range of genetic disorders. Full details of all the tests available and the turnaround times are in ourdirectory of tests for bothinherited and acquired disorders. Pleasecontact us if the test you require is not listed in our directory.

The types of investigation include:

The laboratory offers testing for a range of core disorders plus a set of more specialist services for which samples are received on a supra-regional or national basis.

The laboratory is also a member of theUKGenetic Testing Network (UKGTN) and we can forward DNA samples to other UK genetics laboratories for testing of a large range of single gene disorders, where appropriate. ContactUKGTN or our laboratory for full details. Details of services for rare disorders not currently available in the UK are available fromOrphanet andGeneTests as well as our laboratory.

DNA can be extracted from 2ml saliva (collected using the OrageneTM DNA collection system), or using buccal swabs (collected using the IsoHelixTM system). Please note that buccal swabs may not necessarily provide sufficient DNA for all available tests. Please contact us using these sampling methods to ensure that the test required can be carried out. DNA can be extracted from fresh or frozen tissue samples, and it also possible to obtain limited results for some assays from blood spots or paraffin embedded fixed tissue samples. Please contact us before using these sampling methods to ensure that sufficient DNA of appropriate quality for the test required can be extracted. Prenatal diagnosis for single gene disorders is usually carried out on chorionic villus samples, but amniotic fluid or fetal blood samples can be used where necessary. Rapid aneuploidy (QF-PCR) testing can be carried out on DNA extracted from amniotic fluid or chorionic villus samples, as appropriate.

Please note that clotted blood samples or samples that are inadequately labelled or packaged will not be accepted by the laboratory. If samples are known to present a high risk to laboratory staff, then this should be clearly indicated on the referral card and sample tube.

We can provide advice on scientific and technical issues. Please call us on 0151 702 4228. The Trust voice mail system operates on all external lines. When diverted to voice mail, please leave a message and someone from the laboratory will get back to you as soon as possible. In addition the laboratory has the nhs.net email account dna.liverpool@nhs.net that is monitored daily. This account is suitable for receipt of patient-identifiable information sent to the laboratory providing the sender also uses an nhs.net account. Patient-identifiable information should NOT be sent to other laboratory email addresses.

Please note for advice on clinical and counselling issues, telephone theClinical Genetics Service on 0151 802 5001.

Mailing address for correspondence and samples

Merseyside and Cheshire Regional Molecular Genetics Laboratory Liverpool Womens NHS Foundation Trust Crown Street Liverpool L8 7SS

Other ways of contacting the laboratory

Tel: 0151 702 4228 Fax: 0151 702 4226 E-mail: dna.liverpool@nhs.net

Laboratory Staff

Head of Laboratory - Roger Mountford (Consultant Clinical Scientist) Tel: 0151 702 4219 E-mail: roger.mountford@lwh.nhs.uk

Duty Head Victoria Stinton (State Registered Clinical Scientist) Tel: 0151 702 4231 Email: Victoria.Stinton@lwh.nhs.uk

Other Scientific staff

Emma McCarthy - State Registered Clinical Scientist - 0151 702 4011 Diane Cairns - State Registered Clinical Scientist - 0151 702 4225 Kym Jones - State Registered Clinical Scientist - 0151 702 4225 Abi Rousseau - State Registered Clinical Scientist - 0151 702 4011 Trudie Cottrell - STP Trainee Healthcare Scientist (Genetics) 0151 702 4011 John Hall - Trainee Clinical Molecular Geneticist 0151 702 4011 Emma Brownsell - Trainee Clinical Molecular Geneticist 0151 702 4225

Laboratory working hours

Laboratory working hours are: 9am -5:30pm Monday - Friday (An out-of-hours service is not currently provided)

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Molecular Genetics - Liverpool Women's NHS Foundation Trust

Mona Batish, Ph.D. Research Focus: Exploring the gene expression regulation by single molecule RNA imaging

Vivian Bellofatto, Ph.D. Research Focus: Regulation of Gene Expression in Parasitic Protozoa

Purnima Bhanot, Ph.D. Research Focus: Biology of the Malaria Parasite, Plasmodium

Raymond Birge, Ph.D. Research Focus: Cellular actions of oncogenes and proto-oncogenes; Recognition and phagocytosis of apoptotic cells

Sylvia Christakos, Ph.D. Research Focus: Mechanisms involved in the pleitropic actions of 1,25 dihydroxyvitamin D3

Emanuel Goldman, Ph.D. Research Focus: Accuracy and Efficiency of Protein Synthesis Elongation in Escherichia coli

Laura Goldsmith, Ph.D. Research Focus: Signal transduction mechanisms involved in ovarian hormone production and function

Utz Herbig, Ph.D. Research Focus: Telomere induced Senescence in Cancer and Aging

Richard Howells, Ph.D. Research Focus: Investigation of opioids, opioids receptors, opioid tolerance and physical dependence and the therapeutic potential of these drugs as anti-cancer agents

M. Zafri Humayun, Ph.D. Research Focus: Fidelity of DNA Replication

Hieronim Jakubowski, Ph.D. Research Focus: Homocysteine in Protein Structure/Function andHuman Disease

David B. Kaback, Ph.D. Research Focus: Meiotic Pairing and Chromosome Segregation

Sergei Kotenko, Ph.D. Research Focus: Study of cytokines, their receptors and biological activities

Suriender Kumar, Ph.D. Research Focus: Proteolytic enzymes in tumor growth, inflammation and bone resorption

Deborah Lazzarino, Ph.D. Research Focus: Cellular and molecular events that regulate the growth and differentiation of mammary epithelial cells, particularly to identify, isolate and characterize mammary stem and progenitor cells in hopes of understanding the role they play in normal and disease states of the breast.

Michael Lea, Ph.D. Research Focus: Regulation of growth and differentiation of cancer cells

Hong Li, Ph.D. Research Focus: Proteomics and bioinformatics research

David Lukac, Ph.D. Research Focus: Molecular host-virus interactions that regulate lytic reactivation of Kaposi's Sarcoma-associated Herpesvirus from latency

Carol Lutz, Ph.D. Research Focus: Regulation of gene expression by post-transcriptional mechanisms

Wlodek Mandecki, Ph.D. Research Focus: Ribosome as Molecular Machine for Acquiring Sequence Information

Mukund Modak, Ph.D. Research Focus: Molecular effectors of enzymatic synthesis of DNA

Matthew B. Neiditch, Ph.D. Research Focus: Structural Biology of Bacterial Quorum Sensing Signal Transduction

Patrick O'Connor, Ph.D. Research Focus: Molecular mechanisms that regulate bone regeneration

Virendranath Pandey, Ph.D. Research Focus: HIV-1 and HCV replication; Development of antiviral/virucidal drugs

Nikhat Parveen, Ph.D. Research Focus: Virulence factors of Pseudomonas aeruginosa and Lyme disease spirochete, Borrelia burgdorferi

Melissa Rogers, Ph.D. Research Focus: Cellular and molecular biology of BMP2

Katsunori Sugimoto, Ph.D. Research Focus: Cell Cycle, DNA damage signaling, Checkpoint, Cellular signal transduction, telomere regulation, Cancer

Carolyn Suzuki, Ph.D. Research Focus: Regulation of mitochondrial genome stability and expression; Mitochondrial apoptosis

Bin Tian, Ph.D. Research Focus: Study of RNA genomics and post-transcriptional gene regulation by bioinformatics approaches

Ian P. Whitehead, Ph.D. Research Focus: Signal Transduction and Oncogenesis

Hua Zhu, Ph.D. Research Focus: Herpesviruses and Host Cell Interaction

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Laboratories - Rutgers New Jersey Medical School

OMICS International welcomes all the attendees, speakers, sponsors and other research expertise from all over the world to theInternational conferenceon Clinical and Molecular Genetics (Clinical Genetics 2016)which is going to be held duringNovember 28-30,2016inChicago, USA.We are very much honored to invite you all to exchange and share your views and experience on theCurrent Advancements and Novel Research on Genetics at Clinical and Molecular level.

Clinical and molecular geneticsare involved in the diagnosis and management ofhereditary disorderswhich determines the safety and effectiveness ofmedications,devices,diagnostic productsandtreatment regimenswhich are intended for human use and also be used for prevention, treatment, diagnosis or for relieving symptoms of a disease. There is a rapid growth in the field of Clinical and Molecular Genetics because of the increased prevalence of infectious diseases, causative mutating organisms which led to the discovery of novel clinical and genetic testing methods. TheGenetic testingmarket sale is estimated to reach $25 billion annually by 2021 with a growth rate of 10% in the United States. The genetic testing market is believed to reach approximately $60 billion by 2020 globally. US represent the largest market for genetic testing worldwide.

Track -1:Mendelian Genetics: Past and the future

For thousands of years there were lot of questions about genetics and people followed different processes to produce hybrids of different plants and animals. But most of their trails failed as the actual mechanism behind it was unknown. ThereafterMendelwas the first to explain the concept of heredity after experimenting on pea plant (Pisum sativum)through his laws. He proposed Law of Segregation where only one allele pass from parent to offspring as the allele of parents gets separated ,Law of independent Assortment where different pairs of allele passes from parents independently, Law of Dominance where some alleles are dominant the remaining are recessive. Based on this, several hypotheses were proposed later.

Currently there are vast advancements in the field of genetics where researches are focusing on the different diseases caused by variations in genes and many institutions are investing in the research. For example, US government, along with NIH funded Human Genome project based onDNA sequencingtechnologies. Due to the development of new techniques in Bioinformatics there is a huge decrease in the price of genome sequencing, from $100 million to $1000.

The involvement of genetics in heart diseases, cancer and other implications remained far from clear. There are possibilities of practicing human cloning, eugenics apart from these genetic advancements.

Related Conferences:

World congress on Human Genetics, October 31 - November 02, 2016 Valencia, Spain; International Conference on Genetics Counseling and Genomics Medicine, Aug 11-12, 2016 Birmingham, UK; International conference on Histocompatibility and Immunogenetics, November 28-30, 2016 San Antonio, USA; 6thInternational Conference on Genomics & Pharmacogenomics, September 12-14, 2016, Berlin, Germany; 5th International Conference on Cancer Genomics, Aug 8-9, 2016 Las Vegas, USA; 5thGeneticsand Genomics Conference, June 1-3, 2016, Nanjing, China; DNA Damage, Mutation & Cancer, March 13-18, 2016, Ventura, USA; Chromatin andEpigenetics, 20 March 2016, Dubrovnik, Croatia; Chromatin,Non-coding RNAsand RNAP II Regulation in Development and Disease Conference, 29 March 2016, Austin, USA; Maintenance ofGenome Stability2016, March 7-10, 2016, Panama, Central America

Track-2:Clinical Genomics

Clinical genomics is the use ofgenomic sequencingin clinical basis like for diagnosis, treatment of disease caused in patients. It is a new and rapidly changing field. The diseases like cystic fibrosis and sickle cell anaemia, which are caused by a single base pair change to DNA sequencing, these mutations can be corrected by CRISPR/ Cas technology.

Cas technologyis based on genome editing which is proposed by Editas Medicine with an investment of about $43million. Researchers adopted this technique as most of the microbes use protein and RNAs against invading viruses. The technique involves the editing of stretches in DNA and also to edit single base pairs of the human genome. It was also believed to cure untreatable diseases possibly.

Related Conferences:

World congress on Human Genetics, October 31 - November 02, 2016 Valencia, Spain; International Conference on Genetics Counseling and Genomics Medicine, Aug 11-12, 2016 Birmingham, UK; International conference on Histocompatibility and Immunogenetics, November 28-30, 2016 San Antonio, USA; 6thInternational Conference on Genomics & Pharmacogenomics, September 12-14, 2016, Berlin, Germany; 5th International Conference on Cancer Genomics, Aug 8-9, 2016 Las Vegas, USA; 5thGeneticsand Genomics Conference, June 1-3, 2016, Nanjing, China; DNA Damage, Mutation & Cancer, March 13-18, 2016, Ventura, USA; Chromatin andEpigenetics, 20 March 2016, Dubrovnik, Croatia; Chromatin,Non-coding RNAsand RNAP II Regulation in Development and Disease Conference, 29 March 2016, Austin, USA; Maintenance ofGenome Stability2016, March 7-10, 2016, Panama, Central America

Track-3:Oncogenomics and Therapeutics

Oncogenomics is the study of the relationship between cancer and the genome of an individual. Its goal is to identifyoncogenesfor the diagnosis and treatment of cancer. Cancer is a genetic disease as it is caused by genetic variation in DNA.NIH offers about $7.4 billion on research related to genetics and about $5.8 on cancer related research. The various techniques used are DNA sequencing, microarray, digital karyotyping, bacterial artificial chromosome.

The American Cancer Society reported that among 1.5 million cases half a million die from the disease mostly of breast cancer, lung cancer, bladder cancer, leukemia. The expenditure on cancer care in 2010 was $125 billion and is estimated to reach $156 billion by 2020 in US.US occupies seventh place inbreast cancerworldwide.

Related Conferences:

World congress on Human Genetics, October 31 - November 02, 2016 Valencia, Spain; International Conference on Genetics Counseling and Genomics Medicine, Aug 11-12, 2016 Birmingham, UK; International conference on Histocompatibility and Immunogenetics, November 28-30, 2016 San Antonio, USA; 6thInternational Conference on Genomics & Pharmacogenomics, September 12-14, 2016, Berlin, Germany; 5th International Conference on Cancer Genomics, Aug 8-9, 2016 Las Vegas, USA; 5thGeneticsand Genomics Conference, June 1-3, 2016, Nanjing, China; DNA Damage, Mutation & Cancer, March 13-18, 2016, Ventura, USA; Chromatin andEpigenetics, 20 March 2016, Dubrovnik, Croatia; Chromatin,Non-coding RNAsand RNAP II Regulation in Development and Disease Conference, 29 March 2016, Austin, USA; Maintenance ofGenome Stability2016, March 7-10, 2016, Panama, Central America

Track- 4:Clinical Epigenetics

Clinical epigenetics uses the techniques involved in molecular biology to detect the alterations in DNA methylation or histone modification to diagnose disorders produced by heritable defects in thegene expression. DNA methylation involves in the addition of methyl groups to adenine and guanine bases. DNA is useful for cell development and when methylation occurs on CpG dinucleotide where cytosine precedes guanine suppresses the gene regulation. The nucleosome consists of historians where the tails of histone protrude from nucleosome and therefore they can be modified. The chemical groups attract activating or suppressing complexes to chromatin, which affects its shape, making it more or less available for gene expression. Epigenetic enzyme marketing consists of DNA-modifying, RNA-modifying, Protein is modifying Enzymes which is expected to reach a high rate by 2019. Bisulfite conversion kits; ChIP- seq kits; RNA sequencing kits; whole genome amplification kits are some of the epigenetic kits among which ChIP-seq kits segment had the biggest share in 2014.The market value ofepigeneticswas $413.24 million in 2014, it is expected to reach a CAGR of 13.64% from 2014 to 2019 and it is estimated to grow $783.17 million by 2019 globally.

Related Conferences:

World congress on Human Genetics, October 31 - November 02, 2016 Valencia, Spain; International Conference on Genetics Counseling and Genomics Medicine, Aug 11-12, 2016 Birmingham, UK; International conference on Histocompatibility and Immunogenetics, November 28-30, 2016 San Antonio, USA; 6thInternational Conference on Genomics & Pharmacogenomics, September 12-14, 2016, Berlin, Germany; 5th International Conference on Cancer Genomics, Aug 8-9, 2016 Las Vegas, USA; 5thGeneticsand Genomics Conference, June 1-3, 2016, Nanjing, China; DNA Damage, Mutation & Cancer, March 13-18, 2016, Ventura, USA; Chromatin andEpigenetics, 20 March 2016, Dubrovnik, Croatia; Chromatin,Non-coding RNAsand RNAP II Regulation in Development and Disease Conference, 29 March 2016, Austin, USA; Maintenance ofGenome Stability2016, March 7-10, 2016, Panama, Central America

Track-5:Regenerative biology and Stem Cell research

Regenerative biology involves the restoration or renewal of damaged genes, cells, tissues, organisms or ecosystem that is produced by some natural fluctuations.Regenerationis mediated by gene regulation and it may be complete (same as old tissue) or incomplete (fibrosis). The market value for tissue engineering and regeneration products was $55.9 billion in 2010 and $59.8 billion in 2011, and is expected to reach $89.7 billion by 2016 at a CAGR of 8.4% globally. According to the reports, the market value of regenerative medicine was about $2.5 billion in the US.

Stem cells are undifferentiated biological cells that undergo mitosis to produce more cells, which are found in multicellular organisms. They are of two types, embryonic and adult stem cells. The stem cell treatment was found to be a lifesaving treatment for the patients with solid tumors and blood disorders.Stem cellscan be obtained from the umbilical cord after babys birth. Possibly they can also be obtained from peripheral blood and bone marrow. According to the reports, in US the availability of stem cell therapy was $15.2 million in 2007 and $16.5 million in 2008 and it is estimated to reach $11 billion by 2020.

Related Conferences:

World congress on Human Genetics, October 31 - November 02, 2016 Valencia, Spain; International Conference on Genetics Counseling and Genomics Medicine, Aug 11-12, 2016 Birmingham, UK; International conference on Histocompatibility and Immunogenetics, November 28-30, 2016 San Antonio, USA; 6thInternational Conference on Genomics & Pharmacogenomics, September 12-14, 2016, Berlin, Germany; 5th International Conference on Cancer Genomics, Aug 8-9, 2016 Las Vegas, USA; 5thGeneticsand Genomics Conference, June 1-3, 2016, Nanjing, China; DNA Damage, Mutation & Cancer, March 13-18, 2016, Ventura, USA; Chromatin andEpigenetics, 20 March 2016, Dubrovnik, Croatia; Chromatin,Non-coding RNAsand RNAP II Regulation in Development and Disease Conference, 29 March 2016, Austin, USA; Maintenance ofGenome Stability2016, March 7-10, 2016, Panama, Central America

Track-6:Microbial and Human Genetics

There are millions of microorganisms that have a rapid impact on our health. They play a vital role in maintaining the health as well as in the onset of diseases.

Genomics applies DNA sequencing methods andBioinformaticsto analyze the structure and function of genomes. It started from bacteriophage but was overtaken by bacterial genomics. Its applications were included in the fields of medicine, biotechnology and social sciences.

Proteomics is the study of the structure and functions of proteins as they are the essential components of the various metabolic pathways of cells. It is more complicated when compared to genomic studies as it varies from cell to cell.Mass spectroscopyand microarray techniques are mostly used to study proteins presently.

The global market for DNA sequencing products and services in 2012 was $3.5 billion and $4.5 billion in 2013. It is expected to reach $11.7 billion by 2018 with a CAGR of 21.2%.

Related Conferences:

World congress on Human Genetics, October 31 - November 02, 2016 Valencia, Spain; International Conference on Genetics Counseling and Genomics Medicine, Aug 11-12, 2016 Birmingham, UK; International conference on Histocompatibility and Immunogenetics, November 28-30, 2016 San Antonio, USA; 6thInternational Conference on Genomics & Pharmacogenomics, September 12-14, 2016, Berlin, Germany; 5th International Conference on Cancer Genomics, Aug 8-9, 2016 Las Vegas, USA; 5thGeneticsand Genomics Conference, June 1-3, 2016, Nanjing, China; DNA Damage, Mutation & Cancer, March 13-18, 2016, Ventura, USA; Chromatin andEpigenetics, 20 March 2016, Dubrovnik, Croatia; Chromatin,Non-coding RNAsand RNAP II Regulation in Development and Disease Conference, 29 March 2016, Austin, USA; Maintenance ofGenome Stability2016, March 7-10, 2016, Panama, Central America

Track-7:Next Generation Sequencing

Next Generation Sequencing is a novel method for sequencing DNA and RNA more rapidly, which has made the study of genomics easy. It is the most versatile tool for medical and biological research. The techniques involved are Illumina sequencing, Roche 454 sequencing, Ion torrent: proton sequencing,Solid sequencing. Illumina sequencing is based on DNA colonies or clusters that involves in the clonal amplification of DNA on a surface.454 pyro sequencing amplifies DNA in side water droplets in an oily solution. Ion torrent sequencing is based on using sequencing chemistry with semiconductor based detection system. It is based on detection of hydrogen ions used during polymerisation of DNA whereas solid sequencing involves sequencing by ligation. The NGS market reached $231.7 million in 2012 and $510.7 million in 2013 and is expected to reach $7.6 billion by 2018 with a CAGR of 71.6% globally.

Related Conferences:

World congress on Human Genetics, October 31 - November 02, 2016 Valencia, Spain; International Conference on Genetics Counseling and Genomics Medicine, Aug 11-12, 2016 Birmingham, UK; International conference on Histocompatibility and Immunogenetics, November 28-30, 2016 San Antonio, USA; 6thInternational Conference on Genomics & Pharmacogenomics, September 12-14, 2016, Berlin, Germany; 5th International Conference on Cancer Genomics, Aug 8-9, 2016 Las Vegas, USA; 5thGeneticsand Genomics Conference, June 1-3, 2016, Nanjing, China; DNA Damage, Mutation & Cancer, March 13-18, 2016, Ventura, USA; Chromatin andEpigenetics, 20 March 2016, Dubrovnik, Croatia; Chromatin,Non-coding RNAsand RNAP II Regulation in Development and Disease Conference, 29 March 2016, Austin, USA; Maintenance ofGenome Stability2016, March 7-10, 2016, Panama, Central America

Track-8:Clinical metabolics and Lipidomics

Lipids are the major components of biological membranes as well as the metabolites of organisms. Lipids play crucial role in biology. Imbalance in the lipid molecules leads to numerous diseases like atherosclerosis, obesity, diabetes, andAlzheimer's disease. Lipidomics is a system-based study of all lipids, which aims at the analysis of lipids in the biological system. Lipidomics is the main tool for potential biomarker discovery, diagnosis the disease and to understand disease pathology mainly in the fields of neurodegeneration, psychiatry, oncology, metabolic diseases, and infectious diseases. The global biomarkers market was $29.3 billion in 2013 and is expected to grow $53.6 billion in 2018 at a CAGR of 12.8%.

Clinical metabolomics is the major and the most powerful tool to screen metabolites in the biological samples. These provide predictive and prognostic biomarkers which are useful to monitor disease states and to improve therapeutic levels. Discovery of biomarkers to differentiate diseases at molecular levels is a difficult task as the metabolite profile is related to the phenotype of an organism;metabolomicsprovide a better understanding of systemic diseases. Metabolomics is also practiced in crop breeding, toxicology, plant biotechnology. The market value for metabolomics was $712 million in 2012 and is expected to reach nearly $1.4 billion in 2017 at a CAGR of 14.2% globally.

Related Conferences:

World congress on Human Genetics, October 31 - November 02, 2016 Valencia, Spain; International Conference on Genetics Counseling and Genomics Medicine, Aug 11-12, 2016 Birmingham, UK; International conference on Histocompatibility and Immunogenetics, November 28-30, 2016 San Antonio, USA; 6thInternational Conference on Genomics & Pharmacogenomics, September 12-14, 2016, Berlin, Germany; 5th International Conference on Cancer Genomics, Aug 8-9, 2016 Las Vegas, USA; 5thGeneticsand Genomics Conference, June 1-3, 2016, Nanjing, China; DNA Damage, Mutation & Cancer, March 13-18, 2016, Ventura, USA; Chromatin andEpigenetics, 20 March 2016, Dubrovnik, Croatia; Chromatin,Non-coding RNAsand RNAP II Regulation in Development and Disease Conference, 29 March 2016, Austin, USA; Maintenance ofGenome Stability2016, March 7-10, 2016, Panama, Central America

Track-9:Medical and Developmental genetics

Right from the zygote to a developed individual every process is regulated by genes. Developmental genetics is concerned with the process in which genes regulate the development. It is the study of cell fate, cell determination and embryonic development. There are many theories proposed and among them differential gene expression is the most accepted one. The ability to produce an organism from cells is called totipotent, unipotent stem cells produce a family of related cells. Pluripotent and multipoint produce only few organs or tissues, but all these cells forms, acell lineagewhose differentiation can be done by a master control gene. Likewise immune cells are produced from bone marrow; B-cells are responsible for antibody production. By Invivo production of B-cells, antibody diversity can be achieved as process follows differential gene expression. The prenatal and newborngenetic testingmarket were $1.12 billionin 2012 and expected to grow $8.37 billionin 2019 at a CAGR of 26.9% from 2013 to 2019 globally.

Related Conferences:

World congress on Human Genetics, October 31 - November 02, 2016 Valencia, Spain; International Conference on Genetics Counseling and Genomics Medicine, Aug 11-12, 2016 Birmingham, UK; International conference on Histocompatibility and Immunogenetics, November 28-30, 2016 San Antonio, USA; 6thInternational Conference on Genomics & Pharmacogenomics, September 12-14, 2016, Berlin, Germany; 5th International Conference on Cancer Genomics, Aug 8-9, 2016 Las Vegas, USA; 5thGeneticsand Genomics Conference, June 1-3, 2016, Nanjing, China; DNA Damage, Mutation & Cancer, March 13-18, 2016, Ventura, USA; Chromatin andEpigenetics, 20 March 2016, Dubrovnik, Croatia; Chromatin,Non-coding RNAsand RNAP II Regulation in Development and Disease Conference, 29 March 2016, Austin, USA; Maintenance ofGenome Stability2016, March 7-10, 2016, Panama, Central America

Track-10:Genetic Syndromes and Related Disorders

Genetic disorder is a genetic problem which is associated with the abnormalities in the genome, it may or may not be heritable. For example, cancer can be caused by some inherited genes or by newmutationsor it may be environmental cause in some patients. There are many genetic disorders among them Single-gene disorder is the one which is the resultant of a single mutated gene. It includes diseases like Cystic fibrosis,Sickle-cell-anemia, Polycystic kidney disease, Hemophilia-A, Albinism. Multifactorial diseases include diabetes and heart diseases. Most of the genetic disorders can be identified at birth or in childhood like Huntingtons disease. Treatment for these genetic disorders is still a battle where around 1800 clinical trials have been completed. Presently Gene therapy is followed in which a new gene is introduced to a patient which is very complicated. The market value of products to treatgenetic disorderswas $12.8 billion in 2009 and $17.3 in 2014 globally.

The market value for cancer treatment was about $51.2 billion in 2014 and is expected to reach $66.4 billion by 2019, with a CAGR of 5.4% from 2014 to 2019 globally.The autism spectrum disorders(ASD) market was about $346.2 million in 2013 and $360.9 million in 2014. The market value is expected to grow to $412.7 million by 2019, with a CAGR of 2.7 %.

Related Conferences:

World congress on Human Genetics, October 31 - November 02, 2016 Valencia, Spain; International Conference on Genetics Counseling and Genomics Medicine, Aug 11-12, 2016 Birmingham, UK; International conference on Histocompatibility and Immunogenetics, November 28-30, 2016 San Antonio, USA; 6thInternational Conference on Genomics & Pharmacogenomics, September 12-14, 2016, Berlin, Germany; 5th International Conference on Cancer Genomics, Aug 8-9, 2016 Las Vegas, USA; 5thGeneticsand Genomics Conference, June 1-3, 2016, Nanjing, China; DNA Damage, Mutation & Cancer, March 13-18, 2016, Ventura, USA; Chromatin andEpigenetics, 20 March 2016, Dubrovnik, Croatia; Chromatin,Non-coding RNAsand RNAP II Regulation in Development and Disease Conference, 29 March 2016, Austin, USA; Maintenance ofGenome Stability2016, March 7-10, 2016, Panama, Central America

Track-11: Genetics Market:

While the evidence base is still growing, genetic services industry leaders strongly believe that emerging testing capabilities will have significant clinical impact in the future. Many expressed opinions that genetic services will make significant contributions to prediction, detection, and care selection, leading to better quality care and increased affordability. Available genetic tests and genomic applications, can be categorized according to their clinical method of use across prediction, detection, and care selection. The prenatal and newborngenetic testingmarket were $1.12 billionin 2012 and expected to grow $8.37 billionin 2019 at a CAGR of 26.9% from 2013 to 2019 globally.

Related Conferences:

World congress onHuman Genetics, October 31 - November 02, 2016 Valencia, Spain; International Conference on Genetics Counseling andGenomicsMedicine, Aug 11-12, 2016 Birmingham, UK; International conference on Histocompatibility andImmunogenetics, November 28-30, 2016 San Antonio, USA; 6thInternational Conference on Genomics &Pharmacogenomics, September 12-14, 2016, Berlin, Germany; 5th International Conference onCancer Genomics, Aug 8-9, 2016 Las Vegas, USA; 5thGeneticsand Genomics Conference, June 1-3, 2016, Nanjing, China;DNA Damage, Mutation & Cancer, March 13-18, 2016, Ventura, USA; Chromatin andEpigenetics, 20 March 2016, Dubrovnik, Croatia; Chromatin,Non-coding RNAsand RNAP II Regulation in Development and Disease Conference, 29 March 2016, Austin, USA; Maintenance ofGenome Stability2016, March 7-10, 2016, Panama, Central America

Cell Therapy-2015

OMICS International Conferencessuccessfully hosted its premier4thInternational Conference and Exhibition on Cell & Gene Therapyduring August 10-12, 2015 at Crowne Plaza London-Heathrow, London, United Kingdom.

The conference brought together a comprehensive range of the cell and gene therapy researchers, educators from research universities as well as representatives from industry and professional cell and gene therapy societies.

Cell Therapy-2015is known for uplifting the future of cell and gene therapy and its allied areas by encouraging students and fellow researchers to present their work through poster presentations and young research forum. Students participated with great zeal and the best posters were awarded for their efforts and outstanding contribution to the cell and gene therapy research.

OMICS InternationalConferenceswishes to acknowledge with its deep sincere gratitude to all the supporters from the Editorial Board Members of our Open Access Journals, Keynote speakers, Honorable guests, valuable speakers, poster presenters, students, delegates and special thanks to the media partnersfor their promotion to make this event a huge success.

This4thInternational Conference and Exhibition on Cell & Gene Therapybased on the themeGenomic therapies from base pairs to bedsidewhich covered the below scientific sessions like Cell and Gene Therapy: Potential Applications, Plant Stem Cell Rejuvenation, Plant Stem Cells: Human Therapeutics, Stem Cell Therapies, Cellular Therapies, Advanced Gene Therapeutics, Molecular basis of epigenetics, Cancer Therapies, Nano-Therapy, Bioengineering Therapeutics, Clinical Trials and Research in Cell and Gene Therapies, Regulatory and Ethical Issues of Therapies.

The conference was greeted by the conference Moderator:Dr. Andrei Laikhter,Chemgenes Corporation, USA. The support was extended by the Keynote Speaker:Dr. James Koropatnic,Lawson Health Research Institute and Western University;Dr. Anelia Atanassova,BioGlobaX Inc., Canada;Dr. Noriyuki Kasahara,University of Miami, USA;Dr. Robert Hawkins,The Christie Hospital and University of Manchester, UK andDr. Paul L. Hermonat, Central Arkansas Veterans Healthcare System, USA

OMICSInternationalacknowledges the support of below Chairs and Co-chairs with whom we were able to run the scientific sessions smoothly it included:Dr. Ajan Reginald,Cell Therapy Limited, UK;Dr. Andrei Laikhter,Chemgenes Corporation, USA;Dr. Vasiliki Kalodimou,IASO Maternity Hospital, Greece;Dr. Geeta Shroff,Nutech Medicworld, India;Dr. Nady Golestaneh,Georgetown University School of Medicine, USA;Dr. James Koropatnick,Lawson Health Research Institute and Western University, Canada;Dr. Robert Hawkins,Christie Hospital and University of Manchester, UK.

This4thInternational Conference and Exhibition on Cell & Gene Therapywas uplifted with more than 32 oral presentations by researchers, scientists, professors, industry delegates and more than 15 poster participants around the globe. OMICS International has taken the privilege of felicitating Cell Therapy-2015 Organizing Committee Members, Editorial Board Members of the supported Journals and Keynote Speakers who supported for the success of this event.

With the enormous feedback from the participants and supporters 4thInternational Conference and Exhibition on Cell & Gene Therapy,OMICS International Conferencesis glad to announce its5thInternational Conference and Exhibition on Cell & Gene Therapy(Cell Therapy-2016) event from May 19-21, 2016 at San Antonio, USA

- See more at: http://cellgenetherapy.conferenceseries.com/#sthash.npJGo7Qv.dpuf

OMICS International Conferencessuccessfully hosted its premier4thInternational Conference and Exhibition on Cell & Gene Therapyduring August 10-12, 2015 at Crowne Plaza London-Heathrow, London, United Kingdom.

The conference brought together a comprehensive range of the cell and gene therapy researchers, educators from research universities as well as representatives from industry and professional cell and gene therapy societies.

Cell Therapy-2015is known for uplifting the future of cell and gene therapy and its allied areas by encouraging students and fellow researchers to present their work through poster presentations and young research forum. Students participated with great zeal and the best posters were awarded for their efforts and outstanding contribution to the cell and gene therapy research.

OMICS InternationalConferenceswishes to acknowledge with its deep sincere gratitude to all the supporters from the Editorial Board Members of our Open Access Journals, Keynote speakers, Honorable guests, valuable speakers, poster presenters, students, delegates and special thanks to the media partnersfor their promotion to make this event a huge success.

This4thInternational Conference and Exhibition on Cell & Gene Therapybased on the themeGenomic therapies from base pairs to bedsidewhich covered the below scientific sessions like Cell and Gene Therapy: Potential Applications, Plant Stem Cell Rejuvenation, Plant Stem Cells: Human Therapeutics, Stem Cell Therapies, Cellular Therapies, Advanced Gene Therapeutics, Molecular basis of epigenetics, Cancer Therapies, Nano-Therapy, Bioengineering Therapeutics, Clinical Trials and Research in Cell and Gene Therapies, Regulatory and Ethical Issues of Therapies.

The conference was greeted by the conference Moderator:Dr. Andrei Laikhter,Chemgenes Corporation, USA. The support was extended by the Keynote Speaker:Dr. James Koropatnic,Lawson Health Research Institute and Western University;Dr. Anelia Atanassova,BioGlobaX Inc., Canada;Dr. Noriyuki Kasahara,University of Miami, USA;Dr. Robert Hawkins,The Christie Hospital and University of Manchester, UK andDr. Paul L. Hermonat, Central Arkansas Veterans Healthcare System, USA

OMICSInternationalacknowledges the support of below Chairs and Co-chairs with whom we were able to run the scientific sessions smoothly it included:Dr. Ajan Reginald,Cell Therapy Limited, UK;Dr. Andrei Laikhter,Chemgenes Corporation, USA;Dr. Vasiliki Kalodimou,IASO Maternity Hospital, Greece;Dr. Geeta Shroff,Nutech Medicworld, India;Dr. Nady Golestaneh,Georgetown University School of Medicine, USA;Dr. James Koropatnick,Lawson Health Research Institute and Western University, Canada;Dr. Robert Hawkins,Christie Hospital and University of Manchester, UK.

This4thInternational Conference and Exhibition on Cell & Gene Therapywas uplifted with more than 32 oral presentations by researchers, scientists, professors, industry delegates and more than 15 poster participants around the globe. OMICS International has taken the privilege of felicitating Cell Therapy-2015 Organizing Committee Members, Editorial Board Members of the supported Journals and Keynote Speakers who supported for the success of this event.

With the enormous feedback from the participants and supporters 4thInternational Conference and Exhibition on Cell & Gene Therapy,OMICS International Conferencesis glad to announce its5thInternational Conference and Exhibition on Cell & Gene Therapy(Cell Therapy-2016) event from May 19-21, 2016 at San Antonio, USA

Cell Therapy-2014

3rdInternationalConferenceand Exhibition on Cell & Gene Therapywas held duringOctober 27-29, 2014 at Las Vegas, USAwith a theme Uncover the potential that lies within the cell brought together the International blend of people from Evolving Cell & Gene Therapies making it the largest endeavour from OMICS Group. All the papers presented at this conference were published in special issue ofJournal of Stem Cell Research & Therapy.

Cell Therapy-2014opened up new vistas and fostered collaborations in the industry and academia.

The conference was embarked with an opening ceremony followed by a series of lectures delivered by bothHonorable Guestsand members of theKeynote forum. The adepts who promulgated the theme with their exquisite talk were;

Dr. Paul L Hermonat,Central Arkansas Veterans Healthcare System, USA Dr. Peter J Quesenberry, The Warren Alpert Medical School of Brown University, USA Dr. Rafael Gonzalez,DaVinci Biosciences, LLC USA Dr. Paul J Davis, Albany Medical College, USA Dr. Stephen Lin,Thermo Fisher Scientifi c, USA

OMICS Grouphas taken the privilege of felicitatingCell Therapy-2014Organizing Committee, Editorial Board Members, Keynote Speakers and business delegates who supported for the success of this event.

OMICS Group, on behalf of the conference, congratulates the Best Poster awardees for their outstanding performance in the field of Cell & Gene and appreciates all the participants who put their efforts in poster presentations and sincerely wishes them success in future endeavours.Our warm gratitude to our sponsors exhibitors & media partners for associating with the conference.

Cell Therapy-2013

2ndInternationalConferenceand Exhibition on Cell & Gene Therapywas held duringOctober 23-25 2013,atOrlando-FL, USAwith a theme Innovative Strategies in Cell & Gene Therapies brought together the International blend of people from Evolving Cell & Gene Therapies making it the largest endeavour from OMICS Group. All the papers presented at this conference were published in special issue ofJournal of Stem Cell Research & Therapy.

Cell Therapy-2013opened up new vistas and fostered collaborations in the industry and academia.

Excerpt from:
International Conference on Clinical and Molecular Genetics

Wlodek Mandecki, Ph.D. Adjunct Professor Office: ICPH-E350V Tel: 973-972-8963 Lab: ICPH-E430L.1 Tel: 973-972-4679

Email: mandecwl@njms.rutgers.edu

The lab works on a method for acquiring sequence data from single nucleic acid molecules. The approach involves a fluorescence resonance energy transfer assay (FRET) based on molecules involved in protein biosynthesis. The fluorescence signal is acquired from single molecules using a fluorescence correlation spectroscope in several configurations, including measurements in solution and on surfaces. The project's goals are to: (i) perform site-directed labeling with a fluorescent dye and quencher; (ii) optimize the FRET assay; (iii) construct a synthetic template and demonstrate the performance of the system on this template; (iv) investigate nanostructures capable of enhancing fluorescence; (v) study the behavior of single molecules in the system; and (vi) demonstrate the capability of the system to acquire high volumes of sequence data. The method once fully developed will allow fast analyses of many types of nucleic acids. The project is funded by the NIH program on the "Revolutionary Genome Sequencing Technologies - the $1000 Genome".

EF-Tu (green) interacts with tRNA (pink) on the ribosome (not shown). Generated in PyMOL from data in 1mj1.pdb file. In addition, Dr. Mandecki's research interests include the mechanisms of frameshifting in ribosomal translation, phage display, protein structure and function, and innovative techniques in nucleic acid and protein analysis.

Consortium

The project is a collaboration between three investigators at the Department of Microbiology and Molecular Genetics of New Jersey Medical School:

as well as the following institutions and investigators:

University of Pennsylvania:

University of North Texas Health Sciences Center

Originally posted here:
Microbiology & Molecular Genetics - New Jersey Medical School

The Department of Genetics currently has 30 faculty members spanning all career stages including tenured, tenure-track, and research-track faculty. Our faculty are actively engaged in scholarship (conducting research, writing grants and peer-reviewed publications, and presenting research at national and international scientific meetings), teaching (teaching courses at Rutgers, lecturing in outside courses, hands-on teaching of post-doctoral fellows, graduate students, and undergraduate students within our laboratories, and participating in numerous activities aimed at educating the general public about the importance of our research), and service(serving on a wide variety of national and local committees, boards, participating in publication and grant peer-review groups).

The research interests of the 30 faculty members span such important areas as: DNA repair mechanisms, instability of cancer cells, molecular evolutionary processes (e.g. gene duplication, enhancer evolution) and evolutionary genetics, gene expression, cellular mechanisms of learning and memory, fertilization (gamete recognition, adhesion, signaling and fusion), and loss of heterozygosity (LOH) for tumor suppressor genes. Several laboratories are actively engaged in human genetics research including searching for genes linked with disease such as Schizophrenia, Autism, Tourette Syndrome, and Alzheimers disease. Other laboratories are applying molecular genetics techniques to model organisms, such as Caenorhabditis elegans (nematode worm), Drosophila melanogaster (fly), mouse, and Escherichia coli (bacterium), to study basic biological processes. We also have faculty working in computational and statistical genetics. For a complete faculty listing and their detailed research descriptions, see our list of faculty or faculty research page.

Members of the faculty have received competitive research grants from several institutes within the National Institutes of Health (NIH) as well as from the National Science Foundation (NSF), the State of New Jersey Commission on Science and Technology and the Commission on Cancer Research, and private foundations including the National Alliance for Research on Schizophrenia and Depression, the Simons Foundation, Autism Speaks, and the March of Dimes.

Our faculty are solely responsible for teaching several undergraduate and graduate courses at Rutgers and play a major role in other team-taught courses. These courses include Introduction to Cancer, Genetics, Genetics Lab, Genetic Analysis I and II, Seminar in Genetics, Genomes, Topics in Molecular Genetics, Topics in Human Genetics, Evolutionary Genetics, Cancer, Quantitative Biology and Bioinformatics, Introduction to Research in Genetics, General Microbiology, Pathogenic Microbiology, Genetics of Compulsive Behavior, Behavioral and Neural Genetics, and Bacterial Physiology.

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Faculty - Welcome to the Department of Genetics at Rutgers ...

The Molecular Genetics and GenomicsProgram in the Wake Forest School of Medicine is an interdisciplinary research and PhD training program composed of a diverse group of investigators employing molecular and genetic approaches to biomedical research.

The Program includes molecular biologists from each of the basic science departments of the School of Medicine as well as clinical faculty involved in laboratory research. Participating investigators include faculty from the departments of Biochemistry, Cancer Biology, Neurobiology and Anatomy, Medicine, Microbiology and Immunology, Pathology, Pediatrics, Physiology and Pharmacology, and Surgery. Many program faculty are also members of the Comprehensive Cancer Center of Wake Forest University.

Part of the first-year Molecular & Cellular Biosciences (MCB) track, the objective of the PhD training program is to provide an interdisciplinary curriculum that emphasizes the detailed analysis of fundamental biological processes using the tools of molecular biology and genetics. Individualized programs of study are designed to train students for independent careers in research and teaching. The first year MCB curriculum provides broad exposure to the fundamentals of molecular and cellular biology, biochemistry, and microbiology.

After the completion of the first year in the MCB track, students that select a Molecular Genetics & Genomics research advisor begin specialization in the research area of that laboratory. Areas of active investigation include the genetics of complex diseases, genetic epidemiology, epigenetics, and bioinformatics.

Click here to obtain information on the APPLICATION PROCESS for the Molecular Genetics and GenomicsProgram.

The rest is here:
Molecular Genetics and Genomics Program - Wake Forest ...

The Department of Genetics does not yet have its own graduate program. Faculty in the Genetics department generally belong to the graduate programs of Microbiology and Molecular Genetics or Cell and Developmental Biology. Students wishing to pursue a Ph.D. need to apply through the consolidated Graduate Programs in Molecular Biosciences at Rutgers, The State University of New Jersey, and the University of Medicine and Dentistry of New Jersey - Graduate School of Biomedical Sciences.

Students interested in pursuing a MS degree should contact the individual graduate programs for information.

Additional Information can be obtained from the Administrative Office:

Diane Murano 732-445-3430 This email address is being protected from spambots. You need JavaScript enabled to view it.

Nelson Biology Laboratories 604 Allison Road Rutgers - The State University of New Jersey Piscataway, N.J. 08854-8082

Nelson Biology Laboratories 604 Allison Road Rutgers - The State University of New Jersey Piscataway, N.J. 08854-8082

Jessica Joines, Director of the Genetic Counseling Master's Program This email address is being protected from spambots. You need JavaScript enabled to view it. Phone: (848) 445-9637

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Graduate Studies in Genetics - Rutgers University

Whether you're seeking a B.S. or a Ph.D. in Microbiology or Molecular Genetics, you'll find our department has broad research strengths ranging from molecular, structural, and computational biology to cellular and pathogenic microbiology. You will have access to a rich course curriculum and research laboratories where experienced and supportive faculty will guide your research and help you sharpen your scientific communication skills.

Our research addresses fundamental questions in eukaryotic and prokaryotic cell and molecular biology, using the methods of microbiology, genetics, biochemistry, bioinformatics, and structural biology. This work bears directly on crucial health-related problems such as cancer, AIDS, and infectious disease. Outstanding institutional core facilities provide access to the latest research technologies. The highly collaborative culture of the department is fostered by cross-departmental meetings and journal clubs on a variety of interdisciplinary topics, including DNA repair, parasitology and microbial pathogenesis, and by cross-college consortia such as the Vermont Center for Immunobiology and Infectious Disease. Learn More

The collaborative and interdisciplinary nature of our research programs means that a prospective graduate student is offered a wide choice of research opportunities. While all of our students take the same core curriculum, in their second year they choose to specialize in one of four advanced concentration areas. Our alumni have gone on to become university professors, journal editors and senior scientists and executives in the biotechnology industry. UVM is located in Burlington VT, consistently ranked one of the best places to live in the USA. Learn more

Unique opportunities await students majoring in Microbiology or Molecular Genetics at UVM. Our program is small, which permits our faculty to give each student the individual attention necessary to help them succeed. Our lecture and cutting-edge laboratory courses are challenging and provide each student with a strong foundation and the confidence to work at the bench. The flexibility of our curriculum is such that students can get credit for summer internships or for performing research in one of the many labs at UVM. Small classes foster long lasting camaraderie among our students: MMG'ers are quick to support each other, suggest study tips or point out where to find the best pizza. A student in MMG is never a face in the crowd; our students receive one-on-one mentoring and more often than not end up achieving more than they thought they could. Learn more

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Department of Microbiology and Molecular Genetics at the ...

The molecular genetics research interests are in human population genetics, anthropological genetics, immunogenetics, and the genetics of complex diseases. Ultimate goals surround elucidating questions of human variation, the evolutionary history of genes within populations and how these gene histories are involved in the etiology of complex diseases. While the laboratory's research goals have shared consequences for all humanity, specific interests focus on populations of African ancestry.

Operational Objectives:

1. Develop a SNP database for mapping functional mutations linked to diseases common in African peoples.

2. Utilization of evolutionary history of candidate genes to identify polymorphisms that are associated with diseases.

3. Exploit the linkage disquilibrium generated by admixture in the African American population for gene mapping.

CURRENT RESEARCH PROJECTS

The biological transition of enslaved Africans-to-African Americans is marked by the transition of environmental stresses from Africa to those in the Americas, and to a lesser extent, by The incorporation of non-African genes into the African American gene pool. The transition from the various African environments of origin to the diverse American environments is far from insignificant. The American environment imposed new selective pressures on the Africans. These selective pressures may have favored certain genes while eliminating others. This evolutionary hypothesis has been a controversial explanation for the high incidence of diseases such as hypertension in African Americans. Thus, African American biology has been significantly shaped by periods of intermixture creating high heterogeneity, and selective pressures emanating from the unique and particularly adverse social, economic, and political conditions in the US. All of these factors might contribute to the high incidence of diseases with a significant genetic component such as type 2 diabetes, asthma, hereditary cancer (prostate, breast and lung), and hypertension in African Americans.

Prostate cancer is the most common solid malignancy among men in the United States. African American men have the highest incidence of prostate cancer compared to other ethnic groups. This cohort also appears to present more commonly at an advanced stage with aggressive histology and increased cancer-related mortality. Thus, there is a critical need to explore the etiologic pathways (genetic and environmental factors) that contribute to this disparity. In on of our projects "Genes, environment and prostate cancer in populations of African descent" we seek to understand the relative contribution of allelic variations of candidate genes and environmental factors to determine an individuals risk of prostate cancer. The work is geared towards the African American population, for whom genomic studies are limited. African Americans share a common genetic background with West Africans yet vastly different environments. Comparative genetic and epidemiological research on the two populations reveal potential risk factors. This project will provide a better understanding of gene-gene (epistasis), and gene-environment effects on prostate cancer. At research sites in Washington, DC, Chicago, Illinois, and Benin City, Nigeria the goals of the project are to (1) recruit a well characterized cohort of 1200 cases and controls and collect blood for biochemical and molecular assays, along with diet and other environmental information; (2) use state of the art DHPLC technology to provide a formal evaluation of single nucleotide polymorphism (SNP) variation in 22 candidate genes for prostate cancer (androgen associated genes, apoptosis related genes, and diet related genes); (3) construct a web-based database of the SNPs discovered; (4) determine if haplotypic variation in candidate genes accounts for phenotypic variation in prostate cancer, prostate specific antigen (PSA) levels, and disease progression; and (5) assess whether gene-gene and gene-environment interactions exist by examining if prostate cancer risk is modified after stratification of genetic and/or environmental factors. This is the first study which examines SNP markers within the proposed candidate genes, diet, and other environmental variables in clinically evaluated African and African Americans and which evaluates their relative interactions and contribution, if any, to prostate cancer.

In another project, "Haplotype analyses of X chromosome variants: population genetics and implications for prostate cancer" the goals are to (1) provide a formal evaluation of X chromosome variation and linkage disequilibrium in the African American population, (2) determine the relationship of microsatellite alleles (CAG and GGN repeats) within the androgen receptor with the risk for prostate cancer and (3) exploit the evolutionary history of X chromosome haplotypes in order to determine if differences in X chromosome haplotypes account for phenotypic variation in prostate cancer and prostate specific antigen (PSA) levels.

While the molecular genetic research has shared consequences for all humanity, our specific interests focus on populations of African ancestry. Other areas of immediate interest are molecular evolutionary genetics, and biological anthropology. In another project, "the genetics of human pigmentation," we seek to understand the relative contribution of allelic variations of candidate genes responsible for variation in human pigmentation. Pigmentation is a classic anthropological trait that has been studied objectively using reflectance spectroscopy for over 50 years. Skin pigmentation is likely the trait that shows the largest degree of variability among human populations. That there are such dramatic differences in the levels of skin pigmentation among human populations is almost definite evidence for the action of natural selection. The identification of the genes that determine normal within-population variation in pigmentation and differences between populations is the first essential step in the elucidation of the molecular history of human pigmentation. The goals of this project are to (1) develop a database and sample collection that will allow for the delineation of the genes that determine pigmentation, and (2) genotype these individuals for a number of candidate genes to identify those which determine natural variation in pigmentation.

Mutation analyses of BRCA1 and BRCA2. We are analyzing the breast cancer predisposing genes, BRCA1 and BRCA2, for germline mutations in African American families at high-risk for hereditary breast cancer. Patients are considered high-risk if they have a family history of the disease, early onset breast cancer, bilateral breast cancer, breast and ovarian cancer, or a male affected with breast cancer. The entire BRCA1 and BRCA2 coding and flanking intron regions are being examined for mutation detection. In preliminary studies of BRCA1 using the technique of single strand conformation polymorphism, we identified 11 different germline mutations/ variations in 7 patients from 45 high-risk families. Two pathogenic, protein-truncating mutations were detected in exon 11. A ten base pair tandem duplication, 943ins10, was present in a woman with breast and ovarian cancer whose first-degree relatives had prostate cancer. A four base pair deletion, 3450del4, was detected in a breast cancer patient with five cases of breast cancer in the family; two of the proband's sisters with breast cancer also carried the same mutation. Four amino acid substitutions (Lys1183Arg, Leu1564Pro, Gln1785His, and Glu1794Asp) and four nucleotide substitutions in intron 22 (IVS22+78 C/A, IVS22+67 T/C, IVS22+8 T/A and IVS22+7 T/C) were observed in patients and not in control subjects. One early onset breast cancer patient carried five distinct BRCA1 variations, two amino acid substitutions and three substitutions in intron 22. An amino acid substitution in exon 11, Ser1140Gly, was identified in 3 different unrelated patients and in 6 of 92 control samples. The latter probably represents a benign polymorphism. BRCA1 and BRCA2 analyses for the detection of mutations are ongoing.

Genetic variation in asthma. Asthma families collected by HU investigators were part of the Collaborative Study on the Genetics of Asthma (CSGA) genome-wide search for asthma susceptibility loci in ethnically diverse populations. Asthma is an inflammatory airways disease associated with intermittent respiratory symptoms, bronchial hyper-responsiveness (BHR) and reversible airflow obstruction and is phenotypically heterogeneous. Patterns of clustering and segregation analyses in asthma families have suggested a genetic component to asthma. Previous studies reported linkage of BHR and atopy to chromosomes 5q, 6p, 11q, 14q, and 12q. One genome-wide search in atopic sib pairs had been reported, however, only 12% of their subjects had asthma. The CSGA conducted a genome-wide search in 140 families with > or = 2 asthmatic sibs, from three different populations and reported evidence for linkage to six novel regions: 5p15 (P = 0.0008) and 17p11.1-q11.2 (P = 0.0015) in African Americans; 11p15 (P = 0.0089) and 19q13 (P = 0.0013) in Caucasians; 2q33 (P = 0.0005) and 21q21 (P = 0.0040) in Hispanics. Evidence for linkage was also detected in five regions previously reported to be linked to asthma-associated phenotypes: 5q23-31 (P = 0.0187), 6p21.3-23 (P = 0.0129), 12q14-24.2 (P = 0.0042), 13q21.3-qter (P = 0.0014), and 14q11.2-13 (P = 0.0062) in Caucasians and 12q14-24.2 (P = 0.0260) in Hispanics.

Dermatophagoides pteronyssinus (Der p) is one of the most frequently implicated allergens in atopic diseases. Although HLA could play an important role in the development of the IgE response to the Der p allergens, genetic regulation by non-HLA genes influences certain HLA-associated IgE responses to complex allergens. To clarify genetic control for the expression of Der p-specific IgE responsiveness, a genome-wide search was conducted for genes influencing Der p-specific IgE antibody levels by using 45 Caucasian and 53 African American families ascertained as part of the Collaborative Study on the Genetics of Asthma (CSGA). Specific IgE antibody levels to the Der p crude allergen and to the purified allergens Der p 1 and Der p 2 were measured. Multipoint, nonparametric linkage analysis of 370 polymorphic markers was performed with the GENEHUNTER program. The best evidence of genes controlling specific IgE response to Der p was obtained in 2 novel regions: chromosomes 2q21-q23 (P = .0033 for Caucasian subjects) and 8p23-p21 (P = .0011 for African American subjects). Three regions previously proposed as candidate regions for atopy, total IgE, or asthma also showed evidence for linkage to Der p- specific IgE responsiveness: 6p21 (P = .0064) and 13q32-q34 (P = 0.0064) in Caucasian subjects and 5q23-q33 (P = 0.0071) in African American subjects. No single locus generated overwhelming evidence for linkage in terms of established criteria and guidelines for a genome-wide screening, which supports previous assertions of a heterogeneous etiology for Der p-specific IgE responsiveness. Two novel regions, 2q21-q23 and 8p23-p21, that were identified in this study merit additional study. In addition genome-wide screening was conducted for genes influencing Dermatophagoides pteronyssinus-specific IgE responsiveness as a part of the Collaborative Study on the Genetics of Asthma (CSGA). Evidence for linkage was found in some regions, including chromosomes 5131-q33 and 11q13 in African American families. Plans are underway to initiate an international study of the genetics of asthma in collaboration with medical scientists in Ghana and investigators at the NHGC. These investigations will target regions where associations with specific IgE responses have been indicated in African Americans.

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DEVELOPING PROJECTS

Characterization of African American Ancestral HLA Haplotypes in West Africa.

An important area of investigation at the NHGC is the inclusion of evolutionary history of genes as a diagnostic probe in tracing the history of disease in a population.

This project builds upon the foundation of research on the genetics of complex diseases common in African Americans already established with the NHGRI in partnership with the NIH Office of Research on Minority Health. More specifically, it would build upon African American Diabetes mellitus (AADM) an international human gnome research initiative to map genes for type 2 diabetes in ancestral populations of African Americans. Because of the overlap in clinical phenotype of some subsets of types 1 and 2 diabetes, the rationale for this study is that characterization of HLA class II haplotypes in the west African study population may assist in refining the clinical phenotype of a subset of type 2 diabetes patients.

The association of HLA class II genes with susceptibility to type 1 diabetes is well documented in many populations. In African Americans type 1 diabetes patients, unique HLA class II polymorphisms have been instructive in determining risk assessment of closely linked HLA loci. We have reported the association of a unique HLA-DR3 haplotype in African Americans that appears to be associated with resistance to type 1 diabetes. The higher frequency of this haplotype among controls raises questions about the frequency of this haplotype in west African ancestral populations of African Americans.

The long range goal of research at the NHGC is to improve the health status of African Americans through research on human DNA sequence variation and to apply the knowledge gained to better understand the biomedical significance of gene-based differences already known to exist among populations in the immune response to organ transplants; sensitivity to drugs; influence of environment on health, and susceptibility to complex diseases, such as cancer and diabetes.

The research goals of the molecular genetics component are predicated upon the two broad hypotheses of population variation in DNA polymorphic markers used to map genes and the correlation of population-based variation in DNA polymorphic markers with disease.Studies of human leukocyte antigen (HLA) polymorphisms and other genetic polymorphic systems have consistently shown greater genetic variability in African populations. The biomedical implications of population-based variation in HLA genes are seen in association in the arena of clinical transplantation, where decisions regarding the distribution of limited donor organs must be informed by science and balanced by the ethical concerns of the larger society.

The goal of this study is to define HLA alleles and haplotypes in the study population and determine whether allele and haplotype frequencies in diabetics differ from controls. If a difference is found, the implication of HLA associations with the clinical phenotype of type 2 diabetes will be investigated. The study of HLA haplotypes in west African ancestral populations of African Americans will help identify HLA polymorphisms that are common in this population.Since HLA has been associated with a variety of autoimmune diseases, the results of this study should not only be useful in the analysis of HLA haplotypes in type 2 diabetes, but also informative for population-based HLA evolutionary studies.

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Linkage disequilibrium (LD) in African Americans.

Linkage disequilibrium is a population genetic phenomenon that has been useful for gene mapping efforts. LD can usually be found in populations for genes that are tightly (close genetic distance) linked, and can be generated by mutation, selection, or admixture of populations with different allele frequencies. Generally, disequilibrium is dependent on population size, time (generations), and distance between genetic markers. Normally, the greater the distance between markers, the faster the decay of disequilibrium. The nonrandom association of alleles at different genetic loci can be measured by a variety of linkage disequilibrium measures.

Within the African American population one would expect to find short genomic areas of tight LD, a legacy of this population's roots in the antiquity of African human history, together with large areas of LD, a legacy of more recent admixture with Europeans and Native Americans. Assessment of the level of genetic variation and LD in the African American population is important for several reasons. It will allow us to better understand the mechanisms responsible for the creation and maintenance of LD over genomic regions.

This better understanding will aid in the mapping of genes responsible for complex diseases. We expect to observe a diverse pattern of LD among the African American chromosomes when compared to other populations. While the pattern observed among African Americans is not restricted to the population, it is observed at higher frequency than others with diffferent populatioin histories. African American chromosomes with ancestry in West Africa should exhibit closely linked disequilibrium while chromosomes with ultimate ancestry from Europe will reveal broader regions of disequilibrium. What this study will do is assess patterns and level of LD among chromosomal regions within the African American population.

Significance of the African American population for gene mapping

As stated above, LD can be generated by admixture between divergent populations. Thus, a genetic consequence of the unique population history of African Americans is increased LD. We caution that much of the disequilibrium may not actually be due to genetic linkage, but are artifacts of divergent allele frequencies in the parental populations. However, it is expected that linked loci will also show significant disequilibrium in the African American population. The analysis of LD between marker and disease loci has proven to be a powerful tool for positional cloning of disease genes.

When a disease or trait manifests variation between populations, admixed populations provide a population based approach to evaluate the relative importance of genetic factors. A variety of statistical genetic methods for disease studies exploit the LD created by admixture. These include the Transmission Disequilibrium Test (TDT) and Mapping by Admixture Linkage Disequilibrium (MALD). An important assumption of many of these methods is that the ancestry of alleles at each locus be assigned to one of the two founding populations. The assignment of alleles to parent populations is problematic at times, however as more informative genetic markers are found and more individuals and populations sampled, the statistical power to assign alleles increases.

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RESOURCES

The Molecular Genetics Laboratory in the National Human Genome Center is newly renovated and is located on the 6th floor of the Howard University Cancer Center. This facility is approximately 7,500 square feet. There are two large laboratories (~1500 sq. ft. each), a DNA sequencing and genotyping room (~800 sq. ft.), two cold rooms, dark room, and a walk-in freezer. The laboratory space is equipped with benches, tables, sinks, distilled water, fume hoods and separate areas for tissue culture, PCR, and radioisotope use.

Four Pentium III NT Workstations (400-500 mHz) and four Power Macintosh G4's provide the computational hardware for the Molecular Genetics laboratory. The eight computers are networked together via the Genome Center NT server with the 5 computers operating three ABI 377 DNA sequencers and two DNA Wave Machines in addition to the computers used by the Genetic Epidemiology and Statistical Genetics units. The molecular genetics laboratory contains all the standard equipment necessary for large-scale, high throughput molecular analysis of DNA variation. These items include centrifuges, waterbaths, gel electrophoresis apparatus, pipettes, glassware, balances, etc. The laboratory also has two Transgenomics DNA Wave machines for SNP detection using dHPLC. The genotyping room contains three ABI 377 automated sequencers, ten Perkin Elmer 9700 thermocyclers, and the PSQ 96 Pyrosequencing platform for SNP genotyping.

Molecular genetics laboratory space on the 5th floor of the cancer center, contains two ABI 373 automated sequencers. The immunogenetics core research laboratory, also on the 5thfloor of the cancer center, provides approximately 800 sq ft of additional laboratory space for molecular genetics work.

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CORE SERVICES

The Molecular Genetics Laboratory will utilize current SNP technologies to:

1) identify and characterize DNA sequence variation in the NHGC African American population resource,

2) generate databases for locating functional mutations in candidate genes involved in the biology and pathophysiology of complex diseases common in African Americans and other populations in the African Diaspora,

3) develop a database of allele and haplotype frequencies for a reference panel of SNP variants in the NHGC population resource. This will include a set of candidate genes for complex diseases common in African Americans,

Prostate Cancer

Breast cancer

Asthma

Type 2 diabetes

Hypertension

HIV aids

4) Use coalescence models to construct phylogenies of the candidate genes in order to evaluate the evolutionary history of the genes in various populations. Construct haplotype phylogenies for a reference set of DNA loci/markers representative of various types of polymorphic systems found in the genome. This will include but is not limited to the following:

Single nucleotide polymorphisms (SNPs)

Microsatellites (mono, di, tri, and tetra nucleotide repeats)

Minisatellites (variable number of tandem repeats/VNTRs)

Nucleotide insertions and deletions

Alu repeats

MOLECULAR GENETICS UNIT GROUP PICTURE

06-Jan-2008

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See the article here:
Howard University National Human Genome Center

Nikhat Parveen, Ph.D. Associate Professor Office: ICPH-E350T Tel: 973-972-5218 Lab: ICPH-E-310N.1 Tel: 973-972-4437

Email: parveeni@njms.rutgers.edu

My laboratory is studying the molecular basis of pathogenesis of bacterial species, Borrelia burgdorferi, Treponema pallidum and Pseudomonas aeruginosa. These clinically important bacterial pathogens are transmitted to humans using different mechanisms and also show different disease manifestations. B. burgdorferi is transmitted by Ixodes tick vector, T. pallidum by sexual contact and P. aeruginosa, a ubiquitously present organism, is transmitted through ventilation or by direct contact of the patient with the contaminated source.

B. burgdorferi, a spirochete, is causative agent of Lyme disease, a multisystemic illness that affects various organs including joints, heart, nervous system and skin. If untreated, it may result in chronic disease with the symptoms including arthritis, acrodermatitis or neuroborreliosis. It is an extracellular pathogen often found adhering to the host cells in the biopsy specimens of the patients. We have been studying the molecular mechanisms involved in the attachment of Lyme disease spirochetes to a variety of host cells. The specific interaction between the spirochete and host cells may be responsible for the tissue tropism exhibited by B. burgdorferi. Our objective is to understand whether different B.burgdorferi adhesins show affinity for different host receptors on various host cells. We use genetics, biochemical techniques and tissue culture system to identify and characterize the bacterial and host molecules involved in this interaction in vitro. We have already identified two types of glycosaminoglycan receptors on mammalian cells that are recognized by several B. burgdorferi proteins and we are further characterizing this interaction. Mouse is a natural host of B. burgdorferi and C3H mice show several manifestations of Lyme disease observed in humans. We have recently adapted firefly luciferase-based detection system for B. burgdorferi. Using a combination of bioluminescent B. burgdorferi and mouse model of infection, we will further analyze the contribution of each bacterial ligand-host receptor interaction in Lyme pathogenesis. Tissue colonization by the spirochetes will be monitored non-invasively by employing in vivo imaging system. Recently, we have initiated studies to understand molecular basis of T. pallidum pathogenesis using this as a surrogate system.

P. aeruginosa is an opportunistic pathogen and produces a wide variety of virulence factors. It results in a variety of illnesses and is responsible for high morbidity and mortality in immunocompromised and elderly patients. Due to a highly adaptable nature of P. aeruginosa and its ability to survive even in detergents, it is a major contributor to infections in the hospital environment. We have been studying the quorum-sensing mediated induction of several virulence factors in this organism both as free-living organism and in association with its different hosts. We will assess the role of selected virulence factors in biofilm formation while P. aeruginosa is present in communities along with the other organisms. Our current focus is to investigate genetics of production and regulation of PrpL protease and pyocyanin pigment of P. aeruginosa and examine the roles of these virulence factors in tissue destruction. The roles of these two virulence factors in corneal damage, in burn wounds and in the cystic fibrosis patients will then be examined.

1988-1991 Scientist at IARI, New Delhi and Investigator in Indo-US Bilateral Program

1991-1995 Ph.D. in Microbiology, University of Hawaii at Manoa, Honolulu, HI

1996-Nov.00 Postdoctoral Fellow, mentor: John Leong, Univ. Mass. Med. School, MA

2000-May 05 Research Assistant Professor, Univ. Mass. Med. School, MA

Original post:
Microbiology & Molecular Genetics - Rutgers New Jersey ...

Molecular evolution is a change in the sequence composition of cellular molecules such as DNA, RNA, and proteins across generations. The field of molecular evolution uses principles of evolutionary biology and population genetics to explain patterns in these changes. Major topics in molecular evolution concern the rates and impacts of single nucleotide changes, neutral evolution vs. natural selection, origins of new genes, the genetic nature of complex traits, the genetic basis of speciation, evolution of development, and ways that evolutionary forces influence genomic and phenotypic changes.

The content and structure of a genome is the product of the molecular and population genetic forces which act upon that genome. Novel genetic variants will arise through mutation and will spread and be maintained in populations due to genetic drift or natural selection.

Mutations are permanent, transmissible changes to the genetic material (DNA or RNA) of a cell or virus. Mutations result from errors in DNA replication during cell division and by exposure to radiation, chemicals, and other environmental stressors, or viruses and transposable elements. Most mutations that occur are single nucleotide polymorphisms which modify single bases of the DNA sequence. Other types of mutations modify larger segments of DNA and can cause duplications, insertions, deletions, inversions, and translocations.

Most organisms display a strong bias in the types of mutations that occur with strong influence in GC-content. Transitions (A G or C T) are more common than transversions (purine pyrimidine)[1] and are less likely to alter amino acid sequences of proteins.

Mutations are stochastic and typically occur randomly across genes. Mutation rates for single nucleotide sites for most organisms are very low, roughly 109 to 108 per site per generation, though some viruses have higher mutation rates on the order of 106 per site per generation. Among these mutations, some will be neutral or beneficial and will remain in the genome unless lost via Genetic drift, and others will be detrimental and will be eliminated from the genome by natural selection.

Because mutations are extremely rare, they accumulate very slowly across generations. While the number of mutations which appears in any single generation may vary, over very long time periods they will appear to accumulate at a regular pace. Using the mutation rate per generation and the number of nucleotide differences between two sequences, divergence times can be estimated effectively via the molecular clock.

Recombination is a process that results in genetic exchange between chromosomes or chromosomal regions. Recombination counteracts physical linkage between adjacent genes, thereby reducing genetic hitchhiking. The resulting independent inheritance of genes results in more efficient selection, meaning that regions with higher recombination will harbor fewer detrimental mutations, more selectively favored variants, and fewer errors in replication and repair. Recombination can also generate particular types of mutations if chromosomes are misaligned.

Gene conversion is a type of recombination that is the product of DNA repair where nucleotide damage is corrected using orthologous genomic regions as a template. Damaged bases are first excised, the damaged strand is then aligned with an undamaged homolog, and DNA synthesis repairs the excised region using the undamaged strand as a guide. Gene conversion is often responsible for homogenizing sequence of duplicate genes over long time periods, reducing nucleotide divergence.

Genetic drift is the change of allele frequencies from one generation to the next due to stochastic effects of random sampling in finite populations. Some existing variants have no effect on fitness and may increase or decrease in frequency simply due to chance. "Nearly neutral" variants whose selection coefficient is close to a threshold value of 1 / the effective population size will also be affected by chance as well as by selection and mutation. Many genomic features have been ascribed to accumulation of nearly neutral detrimental mutations as a result of small effective population sizes.[2] With a smaller effective population size, a larger variety of mutations will behave as if they are neutral due to inefficiency of selection.

Selection occurs when organisms with greater fitness, i.e. greater ability to survive or reproduce, are favored in subsequent generations, thereby increasing the instance of underlying genetic variants in a population. Selection can be the product of natural selection, artificial selection, or sexual selection. Natural selection is any selective process that occurs due to the fitness of an organism to its environment. In contrast sexual selection is a product of mate choice and can favor the spread of genetic variants which act counter to natural selection but increase desirability to the opposite sex or increase mating success. Artificial selection, also known as selective breeding, is imposed by an outside entity, typically humans, in order to increase the frequency of desired traits.

More here:
Molecular evolution - Wikipedia, the free encyclopedia

Dr. Jeffrey Noebels, professor of neurology and molecular and human genetics, is leading a new research center of international scientists who seek to answer questions that arise from the mystery of sudden unexpected death in epilepsy (SUDEP).

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molecular and human genetics | Momentum - The Baylor ...

Table of Contents

The physical carrier of inheritance | The structure of DNA | DNA Replication

While the period from the early 1900s to World War II has been considered the "golden age" of genetics, scientists still had not determined that DNA, and not protein, was the hereditary material. However, during this time a great many genetic discoveries were made and the link between genetics and evolution was made.

Friedrich Meischer in 1869 isolated DNA from fish sperm and the pus of open wounds. Since it came from nuclei, Meischer named this new chemical, nuclein. Subsequently the name was changed to nucleic acid and lastly to deoxyribonucleic acid (DNA). Robert Feulgen, in 1914, discovered that fuchsin dye stained DNA. DNA was then found in the nucleusof all eukaryoticcells.

During the 1920s, biochemist P.A. Levene analyzed the components of the DNA molecule. He found it contained four nitrogenous bases: cytosine, thymine, adenine, and guanine; deoxyribose sugar; and a phosphate group. He concluded that the basic unit (nucleotide) was composed of a base attached to a sugar and that the phosphate also attached to the sugar. He (unfortunately) also erroneously concluded that the proportions of bases were equal and that there was a tetranucleotide that was the repeating structure of the molecule. The nucleotide, however, remains as the fundemantal unit (monomer) of the nucleic acid polymer. There are four nucleotides: those with cytosine (C), those with guanine (G), those with adenine (A), and those with thymine (T).

Molecular structure of three nirogenous bases. In this diagram there are three phosphates instead of the single phosphate found in the normal nucleotide. Images from Purves et al., Life: The Science of Biology, 4th Edition, by Sinauer Associates (www.sinauer.com) and WH Freeman (www.whfreeman.com), used with permission.

During the early 1900s, the study of genetics began in earnest: the link between Mendel's work and that of cell biologists resulted in the chromosomal theory of inheritance; Garrod proposed the link between genes and "inborn errors of metabolism"; and the question was formed: what is a gene? The answer came from the study of a deadly infectious disease: pneumonia. During the 1920s Frederick Griffith studied the difference between a disease-causing strain of the pneumonia causing bacteria (Streptococcus peumoniae) and a strain that did not cause pneumonia. The pneumonia-causing strain (the S strain) was surrounded by a capsule. The other strain (the R strain) did not have a capsule and also did not cause pneumonia. Frederick Griffith (1928) was able to induce a nonpathogenic strain of the bacterium Streptococcus pneumoniae to become pathogenic. Griffith referred to a transforming factor that caused the non-pathogenic bacteria to become pathogenic. Griffith injected the different strains of bacteria into mice. The S strain killed the mice; the R strain did not. He further noted that if heat killed S strain was injected into a mouse, it did not cause pneumonia. When he combined heat-killed S with Live R and injected the mixture into a mouse (remember neither alone will kill the mouse) that the mouse developed pneumonia and died. Bacteria recovered from the mouse had a capsule and killed other mice when injected into them!

Hypotheses:

1. The dead S strain had been reanimated/resurrected.

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DNA and Molecular Genetics - Estrella Mountain Community ...

The term molecular genetics is now redundant because contemporary genetics is thoroughly molecular. Genetics is not made up of two sciences, one molecular and one non-molecular. Nevertheless, practicing biologists still use the term. When they do, they are typically referring to a set of laboratory techniques aimed at identifying and/or manipulating DNA segments involved in the synthesis of important biological molecules. Scientists often talk and write about the application of these techniques across a broad swath of biomedical sciences. For them, molecular genetics is an investigative approach that involves the application of laboratory methods and research strategies. This approach presupposes basic knowledge about the expression and regulation of genes at the molecular level.

Philosophical interest in molecular genetics, however, has centered, not on investigative approaches or laboratory methods, but on theory. Early philosophical research concerned the basic theory about the make-up, expression, and regulation of genes. Most attention centered on the issue of theoretical reductionism. The motivating question concerned whether classical genetics, the science of T. H. Morgan and his collaborators, was being reduced to molecular genetics. With the rise of developmental genetics and developmental biology, philosophical attention has subsequently shifted towards critiquing a fundamental theory associated with contemporary genetics. The fundamental theory concerns not just the make-up, expression, and regulation of genes, but also the overall role of genes within the organism. According to the fundamental theory, genes and DNA direct all life processes by providing the information that specifies the development and functioning of organisms.

This article begins by providing a quick review of the basic theory associated with molecular genetics. Since this theory incorporates ideas from the Morgan school of classical genetics, it is useful to sketch its development from Morgan's genetics. After reviewing the basic theory, I examine four questions driving philosophical investigations of molecular genetics. The first question asks whether classical genetics has been or will be reduced to molecular genetics. The second question concerns the gene concept and whether it has outlived its usefulness. The third question regards the tenability of the fundamental theory. The fourth question, which hasn't yet attracted much philosophical attention, asks why so much biological research is centered on genes and DNA.

The basic theory associated with classical genetics provided explanations of the transmission of traits from parents to offspring. Morgan and his collaborators drew upon a conceptual division between the genetic makeup of an organism, termed its genotype, and its observed manifestation called its phenotype (see the entry on the genotype/phenotype distinction). The relation between the two was treated as causal: genotype in conjunction with environment produces phenotype. The theory explained the transmission of phenotypic differences from parents to offspring by following the transmission of gene differences from generation to generation and attributing the presence of alternative traits to the presence of alternative forms of genes.

I will illustrate the classical mode of explanatory reasoning with a simple historical example involving the fruit fly Drosophila melanogastor. It is worth emphasizing that the mode of reasoning illustrated by this historical example is still an important mode of reasoning in genetics today, including what is sometimes called molecular genetics.

Genes of Drosophila come in pairs, located in corresponding positions on the four pairs of chromosomes contained within each cell of the fly. The eye-color mutant known as purple is associated with a gene located on chromosome II. Two copies of this gene, existing either in mutated or normal wild-type form, are located at the same locus (corresponding position) in the two second-chromosomes. Alternative forms of a gene occurring at a locus are called alleles. The transmission of genes from parent to offspring is carried out in a special process of cellular division called meiosis, which produces gamete cells containing one chromosome from each paired set. The half set of chromosomes from an egg and the half set from a sperm combine during fertilization, which gives each offspring a copy of one gene from each gene pair of its female parent and a copy of one gene from each gene pair of its male parent.

Explanations of the transmission of traits relate the presence of alternative genes (genotype) to the presence of alternative observable traits (phenotype). Sometimes this is done in terms of dominant/recessive relations. Purple eye-color, for example, is recessive to the wild-type character (red eye-color). This means that flies with two copies of the purple allele (the mutant form of the gene, which is designated pr) have purple eyes, but heterozygotes, flies with one copy of the purple allele and one copy of the wild-type allele (designated +), have normal wild-type eyes (as do flies with two copies of the wild-type allele). See Table 1.

To see how the classical theory explains trait transmission, consider a cross of red-eyed females with purple-eyed males that was carried out by Morgan's collaborators. The offspring all had red eyes. So the trait of red eyes was passed from the females to all their offspring even though the offspring's male parents had purple eyes. The classical explanation of this inheritance pattern proceeds, as do all classical explanations of inheritance patterns, in two stages.

The first stage accounts for the transmission of genes and goes as follows (Figure 1): each offspring received one copy of chromosome II from each parent. The maternally derived chromosomes must have contained the wild-type allele (since both second-chromosomes of every female parent used in the experiment contained the wild-type allele -- this was known on the basis of previous experiments). The paternally derived chromosomes must have contained the purple allele (since both second-chromosomes of every male parent contained the purple allele -- this was inferred from the knowledge that purple is recessive to red eye-color). Hence, all offspring were heterozygous (pr / +). Having explained the genetic makeup of the progeny by tracing the transmission of genes from parents to offspring, we can proceed to the second stage of the explanation: drawing an inference about phenotypic appearances. Since all offspring were heterozygous (pr / +), and since purple is recessive to wild-type, all offspring had red eye-color (the wild-type character). See Figure 1.

Notice that the reasoning here does not depend on identifying the material make-up, mode of action, or general function of the underlying gene. It depends only on the ideas that copies of the gene are distributed from generation to generation and that the difference in the gene (i.e., the difference between pr and +), whatever this difference is, causes the phenotypic difference. The idea that the gene is the difference maker needs to be qualified: differences in the gene cause phenotypic differences in particular genetic and environmental contexts. This idea is so crucial and so often overlooked that it merits articulation as a principle (Waters 1994):

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Molecular Genetics (Stanford Encyclopedia of Philosophy)

Molecular genetics is the field of biology and genetics that studies the structure and function of genes at a molecular level. Molecular genetics employs the methods of genetics and molecular biology to elucidate molecular function and interactions among genes. It is so called to differentiate it from other sub fields of genetics such as ecological genetics and population genetics.

Along with determining the pattern of descendants, molecular genetics helps in understanding developmental biology, genetic mutations that can cause certain types of diseases. Through utilizing the methods of genetics and molecular biology, molecular genetics discovers the reasons why traits are carried on and how and why some may mutate.

One of the first tools available to molecular geneticists is the forward genetic screen. The aim of this technique is to identify mutations that produce a certain phenotype. A mutagen is very often used to accelerate this process. Once mutants have been isolated, the mutated genes can be molecularly identified.

Forward saturation genetics is a method for treating organisms with a mutagen, then screens the organism's offspring for particular phenotypes. This type of genetic screening is used to find and identify all the genes involved in a trait.[1]

While forward genetic screens are productive, a more straightforward approach is to simply determine the phenotype that results from mutating a given gene. This is called reverse genetics. In some organisms, such as yeast and mice, it is possible to induce the deletion of a particular gene, creating what's known as a gene "knockout" - the laboratory origin of so-called "knockout mice" for further study. In other words this process involves the creation of transgenic organisms that do not express a gene of interest. Alternative methods of reverse genetic research include the random induction of DNA deletions and subsequent selection for deletions in a gene of interest, as well as the application of RNA interference.

A mutation in a gene can result in a severe medical condition. A protein encoded by a mutated gene may malfunction and cells that rely on the protein might therefore fail to function properly. This can cause problems for specific tissues or organs, or for the entire body. This might manifest through the course of development (like a cleft palate) or as an abnormal response to stimuli (like a peanut allergy). Conditions related to gene mutations are called genetic disorders. One way to fix such a physiological problem is gene therapy. By adding a corrected copy of the gene, a functional form of the protein can be produced, and affected cells, tissues, and organs may work properly. As opposed to drug-based approaches, gene therapy repairs the underlying genetic defect.

One form of gene therapy is the process of treating or alleviating diseases by genetically modifying the cells of the affected person with a new gene that's functioning properly. When a human disease gene has been recognized molecular genetics tools can be used to explore the process of the gene in both its normal and mutant states. From there, geneticists engineer a new gene that is working correctly. Then the new gene is transferred either in vivo or ex vivo and the body begins to make proteins according to the instructions in that gene. Gene therapy has to be repeated several times for the infected patient to continually be relieved, however, as repeated cell division and cell death slowly randomizes the body's ratio of functional-to-mutant genes.

Currently, gene therapy is still being experimented with and products are not approved by the U.S. Food and Drug Administration. There have been several setbacks in the last 15 years that have restricted further developments in gene therapy. As there are unsuccessful attempts, there continue to be a growing number of successful gene therapy transfers which have furthered the research.

Major diseases that can be treated with gene therapy include viral infections, cancers, and inherited disorders, including immune system disorders.[citation needed]

Classical gene therapy is the approach which delivers genes, via a modified virus or "vector" to the appropriate target cells with a goal of attaining optimal expression of the new, introduced gene. Once inside the patient, the expressed genes are intended to produce a product that the patient lacks, kill diseased cells directly by producing a toxin, or activate the immune system to help the killing of diseased cells. [2]

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Molecular genetics - Wikipedia, the free encyclopedia

This article is about the general scientific term. For the scientific journal, see Genetics (journal).

Genetics is the study of genes, heredity, and genetic variation in living organisms.[1][2] It is generally considered a field of biology, but it intersects frequently with many of the life sciences and is strongly linked with the study of information systems.

The father of genetics is Gregor Mendel, a late 19th-century scientist and Augustinian friar. Mendel studied 'trait inheritance', patterns in the way traits were handed down from parents to offspring. He observed that organisms (pea plants) inherit traits by way of discrete "units of inheritance". This term, still used today, is a somewhat ambiguous definition of what is referred to as a gene.

Trait inheritance and molecular inheritance mechanisms of genes are still a primary principle of genetics in the 21st century, but modern genetics has expanded beyond inheritance to studying the function and behavior of genes. Gene structure and function, variation, and distribution are studied within the context of the cell, the organism (e.g. dominance) and within the context of a population. Genetics has given rise to a number of sub-fields including epigenetics and population genetics. Organisms studied within the broad field span the domain of life, including bacteria, plants, animals, and humans.

Genetic processes work in combination with an organism's environment and experiences to influence development and behavior, often referred to as nature versus nurture. The intra- or extra-cellular environment of a cell or organism may switch gene transcription on or off. A classic example is two seeds of genetically identical corn, one placed in a temperate climate and one in an arid climate. While the average height of the two corn stalks may be genetically determined to be equal, the one in the arid climate only grows to half the height of the one in the temperate climate, due to lack of water and nutrients in its environment.

The word genetics stems from the Ancient Greek genetikos meaning "genitive"/"generative", which in turn derives from genesis meaning "origin".[3][4][5]

The modern working definition of a gene is a portion (or sequence) of DNA that codes for a known cellular function or process (e.g. the function "make melanin molecules"). A single 'gene' is most similar to a single 'word' in the English language. The nucleotides (molecules) that make up genes can be seen as 'letters' in the English language. Nucleotides are named according to which of the four nitrogenous bases they contain. The four bases are cytosine, guanine, adenine, and thymine. A single gene may have a small number of nucleotides or a large number of nucleotides, in the same way that a word may be small or large (e.g. 'cell' vs. 'electrophysiology'). A single gene often interacts with neighboring genes to produce a cellular function and can even be ineffectual without those neighboring genes. This can be seen in the same way that a 'word' may have meaning only in the context of a 'sentence.' A series of nucleotides can be put together without forming a gene (non coding regions of DNA), like a string of letters can be put together without forming a word (e.g. udkslk). Nonetheless, all words have letters, like all genes must have nucleotides.

A quick heuristic that is often used (but not always true) is "one gene, one protein" meaning a singular gene codes for a singular protein type in a cell (enzyme, transcription factor, etc.)

The sequence of nucleotides in a gene is read and translated by a cell to produce a chain of amino acids which in turn folds into a protein. The order of amino acids in a protein corresponds to the order of nucleotides in the gene. This relationship between nucleotide sequence and amino acid sequence is known as the genetic code. The amino acids in a protein determine how it folds into its unique three-dimensional shape, a structure that is ultimately responsible for the protein's function. Proteins carry out many of the functions needed for cells to live. A change to the DNA in a gene can alter a protein's amino acid sequence, thereby changing its shape and function and rendering the protein ineffective or even malignant (e.g. sickle cell anemia). Changes to genes are called mutations.

The observation that living things inherit traits from their parents has been used since prehistoric times to improve crop plants and animals through selective breeding.[6] The modern science of genetics, seeking to understand this process, began with the work of Gregor Mendel in the mid-19th century.[7]

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Genetics - Wikipedia, the free encyclopedia

Public release date: 15-Oct-2012 [ | E-mail | Share ]

Contact: Jennifer Hilliard Scott jscott1@georgiahealth.edu 706-721-8604 Georgia Health Sciences University

AUGUSTA, Ga. Georgia Health Sciences University researchers have developed a mouse that errs on the side of making bone rather than fat, which could eventually lead to better drugs to treat inflammatory diseases such as rheumatoid arthritis.

Drugs commonly used to treat those types of conditions called glucocorticoids work by turning down the body's anti-inflammatory response, but simultaneously turn on other pathways that lead to bone loss. The result can lead to osteoporosis and an accumulation of marrow fat, says Dr. Xingming Shi, bone biologist at the GHSU Institute of Molecular Medicine and Genetics.

The key to the body developing bone instead of fat, a small protein called GILZ, was shown in cell cultures in 2008. Now, with work by GHSU Graduate Student Guodong Pan, the work has been replicated in an animal model. Pan received the American Society for Bone and Mineral Research's Young Investigator Award for his work at the society's annual meeting Oct. 12-15 in Minneapolis.

Bone and marrow fat come from the same biological precursor mesynchymal stem cells. "The pathways for bone and fat have a reciprocal relationship, so we needed to find the key that disrupts the fat production pathway, which would then instead encourage bone growth," Shi says.

GILZ, Shi and Pan say, was already a known mediator of the anti-inflammatory response of glucocorticoids, and the protein also mediates bone production. Shi's early research had shown that glucocorticoids enhance bone formation in the lab because of a short "burst" of GILZ.

The protein works by inhibiting the way cells regulate fat production and turn on fat-producing genes, Shi says. "When you permanently express GILZ, the fat pathway is suppressed, so the body chooses to produce bone instead."

"We found that when we overexpressed the protein in these mice, it increased bone formation," Pan added. "This supports our original hypothesis that GILZ mediates the body's response to glucocorticoids and encourages bone growth." In fact, the genetically modified mice showed a significant increase in bone mineral density and bone volume as well, he found.

"That means GILZ is a potential new anti-inflammatory drug candidate that could spare people from the harmful effects associated with glucocorticoid therapy," Pan said

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Protein could be key for drugs that promote bone growth