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Stephen P. Goff

Stephen P. Goff
Stephen P.
Goff
Ph.D.
Higgins Professor of Biochemistry
Molecular Biophysics & Microbiology
Columbia University, College of Physicians and Surgeons
spg1@columbia.edu

Professor Goff is best known for the development of retroviruses as a genetic system. He has used mutagenesis to define the functional domains of the viral protease, reverse transcriptase, and integrase in the life cycle. His lab was also the first to express enzymatically active reverse transcriptase in bacteria, and to localize its two major enzymatic activities. Goff has been particularly active in applying the yeast two-hybrid method to study interactions between viral and cellular proteins, and to identify novel host factors for virus replication. His group has recently begun using somatic cell genetics to directly identify new cellular components utilized early in retrovirus infection.  Finally, the laboratory has maintained a long-standing interest in the Abelson oncogene, and in the downstream pathways that are activated by this tyrosine kinase.

Select Publications: 

Wolf D, Goff SP. Embryonic stem cells use ZFP809 to silence retroviral DNAs. Nature. 2009 Apr 30;458(7242):1201-4.

Wolf D, Hug K, Goff SP. TRIM28 mediates primer binding site-targeted silencing of Lys1,2 tRNA-utilizing retroviruses in embryonic cells. Proc Natl Acad Sci U S A. 2008 Aug 26;105(34):12521-6.

Wolf D, Cammas F, Losson R, Goff SP. Primer binding site-dependent restriction of murine leukemia virus requires HP1 binding by TRIM28. J Virol. 2008 May;82(9):4675-9.

Wolf D, Goff SP. TRIM28 mediates primer binding site-targeted silencing of murine leukemia virus in embryonic cells.  Cell. 2007 Oct 5;131(1):46-57.

Naghavi, MH, Valente, S, Hatziiouannou, T, de los Santos, K, Wen, Y, Mott, C, Gundersen, GG and Goff, SP. (2007) Moesin regulates stable microtubule formation and limits retroviral infection in cultured cells. EMBO J. 26, 41-52

Cang Y, Zhang J, Nicholas SA, Bastien J, Li B, Zhou P, Goff SP. Deletion of DDB1 in mouse brain and lens leads to p53-dependent elimination of proliferating cells.  Cell. 2006 Dec 1;127(5):929-40.