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Neuromodulatory circuits and motivated behavior

September 9, 2013
Cori Bargmann, Ph.D., The Rockefeller University

Genetic variation, internal states, and environmental cues converge on shared neuronal circuits to regulate behaviors. In the nematode worm Caenorhabditis elegans, an anatomical wiring diagram provides an essential map for innate behaviors, such as preferences for specific stimuli. Superimposed on this detailed circuit diagram are neuromodulators reflecting internal states, which help select appropriate behavioral responses from a larger number of latent circuits, and lead to both rapid and long-lasting changes in behavior. Dr.

Proteoglycans: Arbiters of lipoprotein metabolism

September 11, 2013
Jeffrey D. Esko, Ph.D., University of California, San Diego

Recently, genetic experiments in mice identified the heparan sulfate proteoglycan syndecan-1 as an important receptor for the clearance of triglyceride-rich lipoprotein (TRL) in the liver. This binding site for the TRLs consists of a protein core and one or more heparan sulfate chains. Binding depends on the heparan sulfate chains based on the accumulation of plasma TRLs in mice bearing mutations in heparan sulfate biosynthesis. To identify the major apolipoproteins that mediate binding to the heparan sulfate chains, we developed a series of in vitro and in vivo assays.

Epidemiology: Back to translation

September 25, 2013
Moyses Szklo, M.D., The Johns Hopkins University

Epidemiology was born of the need to discover the evidence necessary for the practice of public health. Early generations of epidemiologists produced data with the objective of translating their findings into public health action. However, the need for epidemiology to establish its scientific credentials, and the fact that subsequent generations of epidemiologists lacked a public health background, eventually resulted in an almost exclusive focus on etiology.

Chromatin structure and the control of gene expression

October 30, 2013
Carl Wu, Ph.D., Howard Hughes Medical Institute

The Wu laboratory investigates the biochemical basis for histone H2A.Z exchange using the budding yeast model organism. They have identified the yeast SWR1 ATP-dependent chromatin remodeling complex as the responsible enzyme. In a purified system, SWR1 removes H2A-H2B dimers from nucleosomes and deposits free H2A.Z-H2B dimers in an ATP-dependent manner. Homologous enzymes have since been characterized in mammalian systems. How does SWR1 recognize promoters and enhancers genome-wide?

The structural basis of ebola viral pathogenesis

November 6, 2013
Erica Ollmann Saphire, Ph.D., The Scripps Research Institute

Dr. Saphire’s lab studies viruses with compact genomes that encode just four to seven genes each. Viruses with limited genomes offer a defined landscape of possible protein-protein interactions. Each protein is critical—many are obligated to perform multiple functions and some rearrange their structures to achieve those new functions. As a result, these few polypeptides accomplish a surprisingly complex set of biological functions including immune evasion, receptor recognition, cell entry, transcription, translation, assembly and exit. Dr.

Comprehensive molecular profiling to support treatment recommendations for advanced cancer

November 13, 2013
John D. Carpten, Ph.D., TGen

Prior to joining TGen, Dr. Carpten was an intramural tenure track investigator with the Cancer Genetics Branch of the National Human Genome Research Institute (NHGRI), NIH, a group that pioneered a number of innovative technologies and methods to study the underlying genetics of cancer. At NIH, he co-led the first published genome wide scan for prostate cancer susceptibility genes published in 1996 in Science. His lab subsequently discovered germ-line mutations in theRNASEL gene in HPC1-linked hereditary prostate cancer families.

The genetic basis of kidney cancer: targeting the metabolic basis of disease

November 20, 2013
W. Marston Linehan, M.D., National Cancer Institute

Dr. Linehan has had a long-standing interest in identification of the genetic basis of cancer of the kidney. Kidney cancer is not a single disease. It is made up of a number of different types of cancer, each of which has a different histology, a different clinical course, which respond differently to therapy and are caused by different genes. Studies of the kidney cancer gene pathways have revealed that kidney cancer is fundamentally a metabolic disease.

How bacteria and cancer cells regulate mutagenesis and their ability to evolve

December 4, 2013
Susan M. Rosenberg, Ph.D., Baylor College of Medicine

For 50 years the world believed that mutations occur at random. The discovery of stress-induced mutagenesis has changed ideas about mutation and evolution and revealed mutagenic programs that differ from standard spontaneous mutagenesis in rapidly proliferating cells. The stress-induced mutations occur during growth-limiting stress, and can include adaptive mutations that allow growth in the otherwise growth-limiting environment.

The protean manifestations of GATA2 deficiency across the lifespan

December 11, 2013
Steve M. Holland, M.D., National Institute of Allergy and Infectious Diseases (NIAID)

GATA binding factor 2 (GATA2) was initially cloned in 1991 as a critical regulator of murine endothelial development, the complete absence of which was incompatible with life. Subsequent work confirmed that it was also critical for hematopoiesis, erythropoiesis, and macrophage function. After almost 20 years of characterization of patients with disseminated mycobacterial infections who had monocytopenia, B cell and NK (natural killer) cell cytopenia, Steve Holland’s group found heterozygous mutations in the same transcription factor, GATA2, accounting for their disease.

Patient centered outcomes research: new directions; major challenges; transformative potential

December 18, 2013
Clyde W. Yancy, M.D., M.Sc., Northwestern University Feinberg School of Medicine

The Patient Centered Outcomes Research Institute (PCORI) was authorized by Congress — in legislation that was coincident with the Affordable Care Act — to conduct research to provide information about the best available evidence to help patients and their health-care providers make more informed decisions. Since 2010, a research infrastructure has been created to support a different model of clinical research. Practical questions impacting health-care delivery, unmet clinical needs, and health-care inequities are being explored through extensive measures of patient engagement.

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The page was last updated on Tuesday, March 31, 2015 - 12:28pm