The Gavathiotis laboratory investigates the structure and function of protein interactions to elucidate the molecular mechanisms that regulate cell death and survival signaling pathways and are deregulated in pathological processes such as cancer and cardiovascular disease. The overarching goal of our research is to translate mechanistic insights of protein interactions into novel pharmacologic strategies and develop therapeutics that can lead to cures.
A new paper from Anguiano et al. in Nature Chemical Biology demonstrates a structure-based design of RARα antagonists that leads to compounds that can selectively upregulate chaperone-mediated autophagy (CMA), yielding the first chemically tractable target for regulating CMA in cells!
Gabrielle's Angel Foundation For Cancer Research selects Dr. Gavathiotis as one of the 2012 Medical Research Award recipients! The Foundation funds innovative clinical or basic science research that will lead to novel therapeutic approaches that could replace, or be used in combination with existing effective therapies and improve the quality of life of patients with leukemia or lymphoma. "It is a great honor to receive this award that provides funding to explore a new and unconventional approach, which may lead to a significant advance against cancer".
Einstein's Wilf Family Cardiovascular Research Institute highlights work ongoing in our lab: "Escaping the Executioner Protein"
Denis will present a poster presentation at the Annual AACR meeting, April 6-10, 2013 on the development of BAX activator molecules for cancer therapy
Onyi presented her first WIP talk in Biochemistry.
Dat presented his first WIP talk in Biochemistry.
Tom gives a lighting talk and a poster presentation at Keystone Symposia "Frontiers of NMR in Biology". A few days later Tom gives another poster presentation at New York Structural Biology Discussion Group.
Harrington Discovery Institute announces funding of our collaborative project with Dr. Richard Kitsis about the creation of a first-in-class drug to reduce heart cell damage from acute myocardial infarction (heart attack).