Natasha J. Caplen | |
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Alma mater | King's College Hospital Medical School (PhD) |
Scientific career | |
Fields | Genetics, cancer biology |
Institutions | National Human Genome Research Institute National Cancer Institute |
Thesis | A Study of the Genetics of Insulin-Dependent Diabetes Mellitus and its Microvascular Complications (1991) |
Natasha Jane Caplen is a British-American geneticist who discovered RNA interference (RNAi) in mammalian cells. She is a senior investigator and head of the functional genetics section at the National Cancer Institute.
Caplen completed a Ph.D. from the King's College Hospital Medical School where she studied the genetics of type I diabetes and its complications. [1] Her dissertation in 1991 was titled, A Study of the Genetics of Insulin-Dependent Diabetes Mellitus and its Microvascular Complications. [2] Caplen's postdoctoral training began at St Mary's Hospital Medical School where she focused on the development of gene therapy approaches for cystic fibrosis (CF) during which she was involved in some of the first pre-clinical and clinical studies of cationic lipid mediated gene therapy for CF. [1] [3]
In 1996, Caplen came to the National Human Genome Research Institute (NHGRI) at NIH as a visiting fellow, where she initially conducted studies investigating hybrid viral vector systems. It was while at NHGRI that Caplen developed a research interest in the newly identified gene silencing mechanism, RNA interference (RNAi) leading to her studies that establish the presence of RNAi in mammalian cells. Caplen joined the Center for Cancer Research (CCR) at the National Cancer Institute (NC) in 2004 as a Senior Scientist, where she pioneered approaches for exploiting RNAi to investigate cancer biology and treatment and helped establish a trans-NIH facility for genome-wide RNAi screening. Caplen was appointed a tenure-track investigator in CCR's Genetics Branch in January 2016. She is head of the functional genetics section. Her research focuses on using functional genetic methods to interrogate specific aspects of the genetic, transcriptional, and signaling alterations observed in cancers driven by fusion oncogenes. [1]
Gene knockdown is an experimental technique by which the expression of one or more of an organism's genes is reduced. The reduction can occur either through genetic modification or by treatment with a reagent such as a short DNA or RNA oligonucleotide that has a sequence complementary to either gene or an mRNA transcript.
Functional genomics is a field of molecular biology that attempts to describe gene functions and interactions. Functional genomics make use of the vast data generated by genomic and transcriptomic projects. Functional genomics focuses on the dynamic aspects such as gene transcription, translation, regulation of gene expression and protein–protein interactions, as opposed to the static aspects of the genomic information such as DNA sequence or structures. A key characteristic of functional genomics studies is their genome-wide approach to these questions, generally involving high-throughput methods rather than a more traditional "candidate-gene" approach.
The National Human Genome Research Institute (NHGRI) is an institute of the National Institutes of Health, located in Bethesda, Maryland.
Mitochondrially encoded tRNA leucine 1 (UUA/G) also known as MT-TL1 is a transfer RNA which in humans is encoded by the mitochondrial MT-TL1 gene.
Mitochondrially encoded tRNA glutamic acid also known as MT-TE is a transfer RNA which in humans is encoded by the mitochondrial MT-TE gene. MT-TE is a small 69 nucleotide RNA that transfers the amino acid glutamic acid to a growing polypeptide chain at the ribosome site of protein synthesis during translation.
Complications of diabetes are secondary diseases that are a result of elevated blood glucose levels that occur in diabetic patients. These complications can be divided into two types: acute and chronic. Acute complications are complications that develop rapidly and can be exemplified as diabetic ketoacidosis (DKA), hyperglycemic hyperosmolar state (HHS), lactic acidosis (LA), and hypoglycemia. Chronic complications develop over time and are generally classified in two categories: microvascular and macrovascular. Microvascular complications include neuropathy, nephropathy, and retinopathy; while cardiovascular disease, stroke, and peripheral vascular disease are included in the macrovascular complications.
Most cases of type 2 diabetes involved many genes contributing small amount to the overall condition. As of 2011 more than 36 genes have been found that contribute to the risk of type 2 diabetes. All of these genes together still only account for 10% of the total genetic component of the disease.
John B. Hogenesch is an American chronobiologist and Professor of Pediatrics at the Cincinnati Children's Hospital Medical Center. The primary focus of his work has been studying the network of mammalian clock genes from the genomic and computational perspective to further the understanding of circadian behavior. He is currently the Deputy Director of the Center for Chronobiology, an Ohio Eminent Scholar, and Professor of Pediatrics in the Divisions of Perinatal Biology and Immunobiology at the Cincinnati Children's Hospital Medical Center.
Elaine Ann Ostrander is an American geneticist at the National Human Genome Research Institute (NHGRI) of the National Institutes of Health (NIH) in Bethesda, Maryland. She holds a number of professional academic appointments, currently serving as Distinguished and Senior Investigator and head of the NHGRI Section of Comparative Genomics; and Chief of the Cancer Genetics and Comparative Genomics Branch. She is known for her research on prostate cancer susceptibility in humans and for conducting genetic investigations with the Canis familiaris —the domestic dog— model, which she has used to study disease susceptibility and frequency and other aspects of natural variation across mammals. In 2007, her laboratory showed that much of the variation in body size of domestic dogs is due to sequence changes in a single gene encoding a growth-promoting protein.
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