Estela Jacinto, Ph.D.
Dept. of Biochemistry and Molecular Biology
Office Telephone: 732-235-4476
My research aims to understand how cells make a decision between growth and survival depending on extracellular signals. Elucidating the mechanisms that allow cells to survive under adverse growth conditions is crucial for understanding how cancer and other growth-related diseases occur. My research employs mammalian cell and mouse models to understand how the mammalian target of rapamycin (mTOR) plays a central role in controlling cellular signals that switch from growth to survival by regulating protein synthesis and folding. My studies currently address mTOR signaling in normal and cancer cells. Another research emphasis is the role of mTOR in T cell development and immune responses. Our goal is to identify critical and specific signals in the mTOR pathway that can be targeted for development of cancer therapeutics and in particular, immunotherapy.
The mammalian target of rapamycin (mTOR) regulates cell growth in response to nutrients. mTOR is a protein kinase that displays homology to lipid kinases. It is inhibited by the clinically important drug, rapamycin (used as an immunosuppressant, anti-fungal, to prevent restenosis in coronary stents, and as a potential anti-cancer drug). mTOR is part of two distinct protein complexes mTORC1 (mTOR complex 1) and mTORC2. mTORC1 regulates protein synthesis in response to growth signals. mTORC2 controls actin cytoskeleton organization and cell survival. Our long-term goal is to understand the cellular and physiological functions of the mTORC complexes and how we can manipulate the mTOR signaling pathway for treatment of growth-related disorders.
Graduate Program Membership