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Jonathan
Chernoff
Senior Member, Fox Chase Cancer Center
Director, Tumor Cell Biology Program, Fox Chase Cancer Center
Cancer Biology Program
Address
Fox Chase Cancer Center
W451
333 Cottman Ave
Philadelphia, PA 19111
Office tel.: 215 728 5319
Lab tel.: 215 728 5320
Fax: 215 728 3616
E-mail: J_Chernoff@fccc.edu
Education
Yale: BA (Molecular Biochem & Biophys), 1978.
Mt Sinai School of Medicine: PhD (Biochemistry), 1984.
Mt Sinai School of Medicine: MD, 1984.
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Research
Interests
- Role of protein phosphorylation in adhesion-dependent
signaling pathways.
Key words: Protein
tyrosine Phosphatase, GTPase, protein kinase, Pak, cell motility
Search PubMed for articles
Description
of Research
The process of neoplastic transformation can
be conceptually divided into two components. The first of
these, proliferative transformation, refers to the ability
of transformed cells to bypass growth suppression signals,
dividing when normal cells would not. The second, morphologic
transformation, refers to loss of normal cytoskeletal architecture,
often accompanied by decreased adhesion and acquisition of
the ability to invade surrounding tissues. These two fundamental
properties are intimately linked to one another, although
experimentally they can be dissected apart through the use
of mutant oncogenes and other abnormal signaling molecules.
The overall focus of my research interests is in uncovering
the roles of protein phosphorylation in governing these two
fundamental aspects of cancer biology.
Recent
Publications
Beeser, A., Jaffer, Z.M., Hofmann, C., and Chernoff,
J. (2005). Role of group A p21-activated kinases
in activation of extracellular-regulated kinase by growth
factors. J. Biol. Chem., 280, 36609-36615.
Cotteret, S. and Chernoff, J.
(2006). Nucleocytoplasmic shuttling of Pak5 regulates its
anti-apoptotic properties. Mol.Cell Biol. 26, 3215-3230.
Pirruccello, M., Sondermann, H., Pelton, J.G.,
Pellicena, P., Hoelz, A., Chernoff, J., Wemmer,
D.E., and Kuriyan, J. (2006). Dimeric kinase assembly underlying autophosphorylation
in the p21 activated kinases. J. Mol. Biol., 361,
312-326.
Thullberg, M., Gad, A., Beeser, A., Chernoff,
J., and Strömblad, S. (2007). The Kinase-inhibitory
domain of p21-activated kinase 1 (PAK1) inhibits cell cycle
progression independent of PAK1 kinase activity. Oncogene.
26, 1820-1828, 2007.
Dadke, S., Cotteret, S., Yip, S.-C., Jaffer,
Z.M., Haj, F., Ivanov A., Rauscher III, F., Shuai, K., Ng,
T., Neel, B.G., and Chernoff, J. (2007).
Regulation of Protein-Tyrosine Phosphatase (PTP) 1B by sumoylation.
Nat. Cell Biol. 9, 80-85.
Lab
Rotation
projects:
- Substrates of p21-activated kinases.
- Role of PTP1B in insulin signaling.
- Regulation of protein phosphatases by sumoylation
- Genetic analysis of Pak function.
- Rho GTPases in formation of breast acini
in 3D cultures.
- Role of p21-activated kinases in cell cycle
and apoptosis.
- Personnel:
- Luis Arias, Ph.D., Postdoctoral Fellow
Sophie Cotteret, Ph.D., Postdoctoral Fellow
Clemens Hofmann, Ph.D., Postdoctoral Fellow
Zahara Jaffer, Ph.D., Postdoctoral Fellow
Jenny Yip, Ph.D., Postdoctoral Fellow
Dina Stepanova, M.S., Russian Medical State University
Mikhail Shepelev, M.S., Russian Medical State University
Jorden Valens, Chentenham High School
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last updated 7/2007
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