Geoffrey J. Clark, PhD


Associate Professor of Medicine; Scientist, James Graham Brown Cancer Center

Research Program
Molecular Targets

Education

Education/Training

B.Sc., University of Manchester, UK, Biochemistry & Applied Molecular Biology, 1982-1985

Ph.D., University of Manchester, UK, Molecular Oncology, 1985-1989

Postdoctoral Fellow, University of Southern California, Los Angeles, Viral Oncology, 1989-1990

Postdoctoral Fellow, La Jolla Cancer Research Foundation, California, Oncology, 1990-1992

Research and Professional Experience

1992-1995
Research Associate, Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina

1996-1998
Research Assistant Professor, Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina

1998-2006
Principal Investigator, Department of Cell and Cancer Biology, National Cancer Institute, Rockville, Maryland

2006-present
Associate Professor, Department of Medicine, University of Louisville, Kentucky

2006-present
Scientist, James Graham Brown Cancer Center, University of Louisville, Kentucky

Publications
Khosravi-Far R, Clark GJ, Abe K, Cox AD, McLain T, Lutz RJ, Sinensky M, Der CJ.  Ras (CXXX) and Rab (CC/CXC) prenylation signal sequences are unique and functionally distinct.  J Biol Chem 267(34):24363-8, 1992

Clark GJ, Quilliam LA, Hisaka MM, Der CJ.  Differential antagonism of Ras biological activity by catalytic and Src homology domains of Ras GTPase activation protein.  Proc Natl Acad Sci USA 90(11):4887-91, 1993

Khosravi-Far R, Solski PA, Clark GJ, Kinch MS, Der CJ.  Activation of Rac1, RhoA, and mitogen-activated protein kinases is required for Ras transformation.  Mol Cell Biol 15(11):6443-53, 1995

Clark GJ, Der CJ.  Aberrant function of the Ras signal transduction pathway in human breast cancer.  Breast Cancer Res Treat 35(1):133-44, 1995. Review.

Kinch MS, Clark GJ, Der CJ, Burridge K.  Tyrosine phosphorylation regulates the adhesions of ras-transformed breast epithelia.  J Cell Biol 130(2):461-71, 1995

Clark GJ, Cox AD, Graham SM, Der CJ.  Biological assays for Ras transformation.  Methods Enzymol 255:395-412, 1995.

Graham SM, Vojtek AB, Huff SY, Cox AD, Clark GJ, Cooper JA, Der CJ.  TC21 causes transformation by Raf-independent signaling pathways.  Molec Cell Biol 16(11):6132-40, 1996

Oldham SM, Clark GJ, Gangarosa LM, Coffey RJ Jr, Der CJ.  Activation of the Raf-1/MAP kinase cascade is not sufficient for Ras transformation of RIE-1 epithelial cells.  Proc Natl Acad Sci USA 93(14):6924-8, 1996

Clark GJ, Drugan JK, Terrell RS, Bradham C, Der CJ, Bell RM, Campbell S.  Peptides containing a consensus Ras binding sequence from Raf-1 and theGTPase activating protein NF1 inhibit Ras function.  Proc Natl Acad Sci USA 93(4):1577-81, 1996

Clark GJ, Kinch MS, Gilmer TM, Burridge K, Der CJ.  Overexpression of the Ras-related TC21/R-Ras2 protein may contribute to the development of human breast cancers.  Oncogene 12(1):169-76, 1996

Clark GJ, Drugan JK, Rossman KL, Carpenter JW, Rogers-Graham K, Fu H, Der CJ, Campbell SL.  14-3-3 zeta negatively regulates raf-1 activity by interactions with the Raf-1 cysteine-rich domain.  J Biol Chem 272(34):20990-3, 1997

Clark GJ, Kinch MS, Rogers-Graham K, Sebti SM, Hamilton AD, Der CJ.  The Ras-related protein Rheb is farnesylated and antagonizes Ras signaling and transformation.  J Biol Chem 272(16):10608-15, 1997

Westwick JK, Lambert QT, Clark GJ, Symons M, Van Aelst L, Pestell RG, Der CJ.  Rac regulation of transformation, gene expression, and actin organization by multiple, PAK-independent pathways.  Molec Cell Biol 17(3):1324-35, 1997

Clark GJ, Westwick JK, Der CJ.  p120 GAP modulates Ras activation of Jun kinases and transformation. J Biol Chem 272(3):1677-81, 1997

Campbell SL, Khosravi-Far R, Rossman KL, Clark GJ, Der CJ.  Increasing complexity of Ras signaling.  Oncogene 17(11 Reviews):1395-413, 1998. Review. 

Della Rocca GJ, Mukhin YV, Garnovskaya MN, Daaka Y, Clark GJ, Luttrell LM, Lefkowitz RJ, Raymond JR.  Serotonin 5-HT1A receptor-mediated Erk activation requires calcium/calmodulin-dependent receptor endocytosis.  J Biol Chem 274(8):4749-53, 1999

Vos MD, Ellis CA, Bell A, Birrer MJ, Clark GJ.  Ras uses the novel tumor suppressor RASSF1 as an effector t

Contact Information

CTR Building
505 South Hancock Street
Louisville, KY 40202
(502) 852-4485