The objectives of this program are to train graduate students for a research career in academia, pharmaceutical companies, or government research agencies in the general area of pharmacology, with a focus on signal transduction, structural biology, neuropharmacology, and drug discovery. The program is designed to adapt to students'interest a will provide a strong biochemical, neuroscience, biophysical, and physiological background that will enable the student (1) to understand the molecular basis of currently used therapeutics;(2) to design experiments (a) to identify potential targets;and (b) t elucidate signal transduction mechanisms of new physiological agents or new therapeutics, (c) to solve macromolecular structures of interest in pharmacology, and (d) use modern tools for drug discovery. To achieve these ends, the pharmacology program at Yale was changed with new faculty and courses. Modern techniques in molecular pharmacology, cell and molecular biology, structural biology, chemistry, biochemistry, physiology and biophysics will be available to the trainee to achieve these goals. The trainee will have constant exposure to a variety of research programs of the faculty and over one hundred senior postdoctoral fellows who provide an additional resource for the trainees.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Institutional National Research Service Award (T32)
Project #
5T32GM007324-38
Application #
8681449
Study Section
National Institute of General Medical Sciences Initial Review Group (BRT)
Program Officer
Okita, Richard T
Project Start
1975-07-01
Project End
2017-06-30
Budget Start
2014-07-01
Budget End
2015-06-30
Support Year
38
Fiscal Year
2014
Total Cost
Indirect Cost
Name
Yale University
Department
Pharmacology
Type
Schools of Medicine
DUNS #
City
New Haven
State
CT
Country
United States
Zip Code
06510
Wali, Vikram B; Langdon, Casey G; Held, Matthew A et al. (2016) Systematic drug screening identifies tractable targeted combination therapies in triple-negative breast cancer. Cancer Res :
Lin, Tiffany V; Hsieh, Lawrence; Kimura, Tomoki et al. (2016) Normalizing translation through 4E-BP prevents mTOR-driven cortical mislamination and ameliorates aberrant neuron integration. Proc Natl Acad Sci U S A 113:11330-11335
Goldberg, Allison B; Turk, Benjamin E (2016) Inhibitors of the Metalloproteinase Anthrax Lethal Factor. Curr Top Med Chem 16:2350-8
Creixell, Pau; Schoof, Erwin M; Simpson, Craig D et al. (2015) Kinome-wide decoding of network-attacking mutations rewiring cancer signaling. Cell 163:202-17
Fisher, Oriana S; Liu, Weizhi; Zhang, Rong et al. (2015) Structural basis for the disruption of the cerebral cavernous malformations 2 (CCM2) interaction with Krev interaction trapped 1 (KRIT1) by disease-associated mutations. J Biol Chem 290:2842-53
Iwamoto, Daniel V; Calderwood, David A (2015) Regulation of integrin-mediated adhesions. Curr Opin Cell Biol 36:41-7
Frey, Kathleen M; Puleo, David E; Spasov, Krasimir A et al. (2015) Structure-based evaluation of non-nucleoside inhibitors with improved potency and solubility that target HIV reverse transcriptase variants. J Med Chem 58:2737-45
Gray, William T; Frey, Kathleen M; Laskey, Sarah B et al. (2015) Potent Inhibitors Active against HIV Reverse Transcriptase with K101P, a Mutation Conferring Rilpivirine Resistance. ACS Med Chem Lett 6:1075-9
Langdon, Casey G; Held, Matthew A; Platt, James T et al. (2015) The broad-spectrum receptor tyrosine kinase inhibitor dovitinib suppresses growth of BRAF-mutant melanoma cells in combination with other signaling pathway inhibitors. Pigment Cell Melanoma Res 28:417-30
Sohl, Christal D; Ryan, Molly R; Luo, BeiBei et al. (2015) Illuminating the molecular mechanisms of tyrosine kinase inhibitor resistance for the FGFR1 gatekeeper mutation: the Achilles' heel of targeted therapy. ACS Chem Biol 10:1319-29

Showing the most recent 10 out of 40 publications