C.A. Storke II Professor
Phone: (805) 893-3097
Office: 2119 LSB
Website: Samuel Lab
Molecular, Cellular, and Developmental Biology
University of California, Santa Barbara
Santa Barbara, CA 93106-9625
Charles Samuel is the C. A. Storke II Professor. He earned a B.S. in Chemistry from Montana State and his Ph.D. in Biochemistry from U.C. Berkeley. He was a Damon Runyon Scholar at Duke Univ. Med. Sch. where he began work on interferon. At UCSB he served as Director of the Interdepartmental Biochemistry & Molecular Biology Program (BMSE) from 1987-95, as Founding Chair of the Department of Molecular, Cellular & Developmental Biology from 1995-98, and again as MCDB Chair from 2001-04. He is an NIH Research Career Development Awardee, an NIH MERIT awardee, a FASEB Wellcome Professorship awardee, a Humboldt Forschungspreis recipient, and an elected Fellow of the American Association for the Advancement of Science and the American Academy of Microbiology. He is an Associate Editor of the Journal of Biological Chemistry, and serves on the editorial boards of Journal of Virology and Journal of Interferon and Cytokine Research.
The overall objective of the research in The Samuel Lab is to elucidate in molecular terms the mechanisms by which interferons exert their antiviral and cell growth control actions in mammalian cells. Present work includes biochemical and molecular genetic studies of two interferon-inducible enzymes, PKR and ADAR. PKR is a double-stranded RNA-dependent protein kinase induced by IFN, and activated by RNA-dependent autophosphorylation. PKR plays a major role in the regulation of translation of viral and cellular mRNAs and also modulates transcription and signaling. The ADAR1 deaminase is an RNA editing-enzyme that catalyzes the C-6 deamination of adenosine to yield inosine, thereby altering the genetic decoding and structure of RNAs. While PKR displays antiviral and proapoptic activities, ADAR1 is often proviral and antiapoptotic in virus-infected cells. Furthermore, PKR is not required for normal mouse embryogenesis, whereas ADAR1 is required.