Stephen P. Goff

Columbia University


Primary Section: 44, Microbial Biology
Secondary Section: 21, Biochemistry
Membership Type:
Member (elected 2006)

Biosketch

Dr. Stephen P. Goff is Higgins Professor of Biochemistry at Columbia University Medical Center. He received the A.B. degree in Biophysics from Amherst College in 1973. His graduate work with Dr. Paul Berg at Stanford University focused on the use of SV40 as a viral vector for the expression of foreign DNAs in mammalian cells. He did postdoctoral work with Dr. David Baltimore at MIT on the replication of the murine leukemia viruses as a Jane Coffin Childs fellow, and joined the Columbia faculty in 1981. Goff was a Searle Scholar and has received two MERIT awards from the NIH.  He has been elected to membership in the National Academy of Science, the National Academy of Medicine, the American Academy of Arts and Sciences, and the American Academy of Microbiology, and is a fellow of the American Association for the Advancement of Science. He received an honorary Doctor of Science degree from Amherst College in 1997, and was the inaugural recipient of the Retrovirus Prize in 2005. He has mentored over 35 graduate students and 35 postdoctoral fellows in his laboratories at Columbia. He has authored or coauthored over 300 publications on viral replication and oncogenesis.

Research Interests

Goff's current work is centered on the study of the retrovirus life cycle and the host restriction systems that inhibit virus replication. His lab identified and characterized a novel host protein, termed ZAP for zinc finger antiviral protein, that blocks expression of many viruses, including the murine leukemia viruses (MLVs), Ebola, Sindbis, and HIV-1, by degrading CpG-rich viral mRNAs. The lab has also characterized a protein complex responsible for the silencing of MLV DNAs in embryonic stem (ES) cells, and identified a zinc finger protein, ZFP809, as an ES-cell specific recognition molecule that binds proviral DNA and brings TRIM28 to modify chromatin. The most recent finding is that unintegrated MLV DNAs are loaded with histones and then silenced by histone modifications mediated by NP220 and the so-called HUSH complex. The silencing is relieved upon integration into the host genome of permissive cells.

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