Estela Jacinto, Ph.D.

jacintes@umdnj.edu
Dept. of Physiology and Biophysics
UMDNJ-RWJ Med School
SPH/Research Building Rm 260
683 Hoes Lane
Piscataway, NJ 08854

Office Tel. 732-235-4476
Lab Tel. 732-235-4227
Fax 732-235-5038

LAB WEBPAGE

Research Interest:
 
Growth control, cancer, immunology, protein synthesis and processing

Description:

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.

Publications:

• Oh WJ, Wu C, Kim SJ, Facchinetti V, Julien LA, Finlan M, Roux PR, Su B, Jacinto E. (2010) mTORC2 can associate with ribosomes to promote cotranslational phosphorylation and stability of nascent Akt polypeptide. EMBO J.
• Facchinetti V, Ouyang W, Wei H, Soto N, Lazorchak A, Gould C, Lowry C, Newton AC, Mao Y, Miao RQ, Sessa WC, Qin J, Zhang P, Su B, Jacinto E. (2008) The mammalian target of rapamycin complex 2 controls folding and stability of Akt and protein kinase C. EMBO J. 27(14): 1932-43.
• Jacinto E. (2008) What controls TOR? IUBMBLife 60(8):483-96.
• Jacinto E, Lorberg A. (2008) TOR regulation of AGC kinases in yeast and mammals. Biochem J. 410(1):19-37.
• Jacinto E. (2007) Phosphatase targets in TOR signaling. Methods Mol Biol 365:323-34.
• Jacinto E, Facchinetti V, Liu D, Soto N, Wei S, Jung SY, Huang Q, Qin J, Su B. (2006)SIN1/MIP1 maintains rictor-mTOR complex integrity and regulates Akt phosphorylation and substrate specificity. Cell 127(1):125-37.
• Jacinto, E., Loewith, R., Schmidt, A., Lin, S., Ruegg, M.A., Hall, A., and Hall, M.N. (2004). Mammalian TOR complex 2 controls the actin cytoskeleton and is rapamycin insensitive. Nature Cell Biol. 6: 1122-1128.
• Jacinto, E., and Hall, M.N. (2003). TOR signaling in bugs, brain, and brawn. Nature Reviews (Mol.Cell.Biol) 4, 117-126.Nature Rev (Mol Cell Biol) 4, 117-126.
• Loewith, R., Jacinto, E., Wullschleger, S., Lorberg, A., Crespo, J.L., Bonenfant, D., Oppliger, W., Jenoe, P., and Hall, M.N. (2002). Two TOR complexes, only one of which is rapamycin sensitive, have distinct roles in cell growth control. Mol Cell 10:457-468.
• Bonenfant, D., Schmelzle, T., Jacinto, E., Crespo, J.L., Mini, T., Hall, M.N., and Jenoe, P. (2003). Quantitation of changes in site specific phosphorylation: a simple method based on stable isotope labelling and mass spectrometry. PNAS 100:880-885.
• Jacinto, E., Guo, B., Arndt, K.T., Schmelzle, T., and Hall, M.N. (2001). TIP41 interacts with TAP42 and negatively regulates the TOR signaling pathway. Mol Cell 8:1017-1026.
• Jacinto, E., Werlen G., and Karin, M. (1998). Cooperation between Syk and Rac1 leads to synergistic JNK activation in T lymphocytes. Immunity 8:31-41.

Graduate Program Membership

• Molecular Biosciences (Rutgers/UMDNJ)
• Physiology and Integrative Biology
• Cell and Developmental Biology
• Medical Scientist Training Program
• Biotechnology Training Program (Rutgers/UMDNJ)