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Peter SarnowAcademic Appointments
Appointment
Organization
Professor
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Honors & Awards
Title
Organization
Date(s)
Editor
Virology
2003-present
The Sidney and Skippy Frank Prize
Institute for Immunity, Transplantation and Infection, Stanford University
2006
Faculty Research Award
American Cancer Society
1992-1997
Postdoctoral Fellowship
Deutsche Forschungsgemeinschaft
1982-1985
Predoctoral Fellowship
Studienstiftung des Deutschen Volkes
1979-1982
Administrative Appointments
Title
Organization
Start Year
End Year
Member of School of Medicine Awards Committee
Stanford University School of Medicine
2005
-
Member of the Committee on Graduate Studies
Stanford University
2001
2004
Director of Graduate Program, Dept. Microbiology and Immunology
Stanford University School of Medicine
2002
-
Professional Education
Degree
Awarding Institution
Field of Study
Year of Graduation
Ph.D.
SUNY at Stony Brook
Molecular Virology
1982
B.S.
University of Konstanz
Molecular Genetics
1979
Postdoctoral Advisees
Teresa Abraham,
Cara Belsham,
Randal Cevallos,
Gabriele Fuchs,
Kara Lee Norman,
Karen Wehner
Web Site Links
Research/Lab website:
http://cmgm.stanford.edu/micro/sarnow_lab/index.html
Research Interests
Our laboratory has been been studying the mechanism by which a liver-specific microRNA, miR-122, regulates the amplification of the hepatitis C virus (HCV) genome in cultured cells. Specifically, we have found that miR-122 interacts with the 5' end of the viral RNA and is essential for viral replication. Consequently, sequestration of miR-122 by antisense-oligonucleotides results in rapid loss of viral RNA. We are currently examining the mechanism by which miR-122 helps HCV RNA replication and are searching for cellular targets of miR-122 and their regulation by miR-122. These lines of investigations will lead to new insights how these small noncoding RNAs regulate expression of cellular and viral mRNAs and may point to new venues for antiviral therapeutics against HCV.
In a second line of investigation, we are studying the unusual mechanism of translation initiation by internal ribosome entry in certain viral (i.e. HCV, picornavirsues and some insect viruses) and cellular mRNA molecules. In the conventional scanning mechanism of translation initiation, which operates on most mRNA molecules, 40S subunits are recruited at or near the 5' end of the mRNA. Subsequently, the 40S ribosomal subunits are predicted to scan the mRNA in a 5' to 3' direction until the first AUG codon is encountered as start site for protein synthesis. However, certain viral and cellular mRNAs, notably encoding proto-oncogenes and regulatory genes, contain long 5' noncoding regions with multiple AUG codons. Thus, the translation initiation rate in these mRNAs is predicted to be low according to the scanning model; alternatively, other translation initiation mechanisms may operate to ensure efficient translation. Indeed, some of such mRNAs with long leaders contain internal ribosome entry sites which can bind ribosomes directly. Much of our work has been focussing on the mechanism and prevalence of internal ribosome binding. Specifically, we are addressing the following questions: Which cellular and viral mRNAs can be translated by internal ribosome binding? What are the cellular gene products that mediate internal ribosome binding? Is internal initiation regulated in the cell? What is the molecular basis for designating a given AUG codon as start site codon?
In a second line of investigation, we are studying the unusual mechanism of translation initiation by internal ribosome entry in certain viral (i.e. HCV, picornavirsues and some insect viruses) and cellular mRNA molecules. In the conventional scanning mechanism of translation initiation, which operates on most mRNA molecules, 40S subunits are recruited at or near the 5' end of the mRNA. Subsequently, the 40S ribosomal subunits are predicted to scan the mRNA in a 5' to 3' direction until the first AUG codon is encountered as start site for protein synthesis. However, certain viral and cellular mRNAs, notably encoding proto-oncogenes and regulatory genes, contain long 5' noncoding regions with multiple AUG codons. Thus, the translation initiation rate in these mRNAs is predicted to be low according to the scanning model; alternatively, other translation initiation mechanisms may operate to ensure efficient translation. Indeed, some of such mRNAs with long leaders contain internal ribosome entry sites which can bind ribosomes directly. Much of our work has been focussing on the mechanism and prevalence of internal ribosome binding. Specifically, we are addressing the following questions: Which cellular and viral mRNAs can be translated by internal ribosome binding? What are the cellular gene products that mediate internal ribosome binding? Is internal initiation regulated in the cell? What is the molecular basis for designating a given AUG codon as start site codon?
Publications
- Almstead LL, Sarnow P "Inhibition of U snRNP assembly by a virus-encoded proteinase." Genes Dev 2007; 21: 9: 1086-97 More »
- Schütz S, Sarnow P "Interaction of viruses with the mammalian RNA interference pathway." Virology 2006; 344: 1: 151-7 More »
- Lancaster AM, Jan E, Sarnow P "Initiation factor-independent translation mediated by the hepatitis C virus internal ribosome entry site." RNA 2006; More »
- Bushell M, Stoneley M, Kong YW, Hamilton TL, Spriggs KA, Dobbyn HC, Qin X, Sarnow P, Willis AE "Polypyrimidine Tract Binding Protein Regulates IRES-Mediated Gene Expression during Apoptosis." Mol Cell 2006; 23: 3: 401-12 More »
- Jopling CL, Norman KL, Sarnow P "Positive and Negative Modulation of Viral and Cellular mRNAs by Liver-specific MicroRNA miR-122." Cold Spring Harb Symp Quant Biol 2006; 71: 369-76 More »
78 publications: view full list
