Our lab is primarily focused on studying regulatory mechanisms controlling the balance between cell life and death. In the first line of research, we are exploring the activities of the pro-apoptotic BID protein at the mitochondria by studying its interaction with a novel and uncharacterized protein named mitochondrial carrier homolog 2 (MTCH2)/Met-induced mitochondrial protein (MIMP). We have recently revealed that MTCH2/MIMP is a critical component of the tBID-death pathway in vivo using a MTCH2/MIMP conditional knockout mouse. Our future goals are to determine its exact function at the mitochondria and how this function is regulated during the apoptotic process.

In a second line of research, we are exploring the activities of BID in the response of cells to DNA damage. We have previously revealed that DNA damage induces the phosphorylation of BID by the ataxia-telangiectasia mutated (ATM) kinase, and that this phosphorylation is important for cell cycle arrest at the S phase and for inhibition of apoptosis. We have recently revealed that ATM-mediated BID phosphorylation plays a critical role in the DNA damage response in vivo using a BID knock-in mouse, in which the endogenous BID gene has been replaced with a gene that drives the expression of a non-phosphorylatable BID protein. Our future goals are to determine the mechanistic details of BID’s activities in the DNA damage pathway and how this activity relates to its pro-apoptotic function at the mitochondria.