Charles Samuel is the C. A. Storke II Professor at the U. C. Santa Barbara. He earned a B.S. in Chemistry from Montana State University and his Ph.D. in Biochemistry from U.C. Berkeley. He was a Damon Runyon Scholar at Duke University Medical School where he began work on interferon. At U.C. Santa Barbara he served as Director of the 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. Dr. Samuel is an NIH Research Career Development Awardee, an NIH MERIT awardee, a FASEB Wellcome Professorship awardee, a Humboldt Forschungspreis recipient, and an elected Member of the the American Academy of Microbiology and Fellow of the American Association for the Advancement of Science. He is an Associate Editor of the Journal of Biological Chemistry and of the Journal of Interferon and Cytokine Research, and serves on the editorial board of Journal of Virology. Chuck was President of ISICR in 2012 and Founding co-President of ICIS in 2013. The overall goal of The Samuel Lab's research is to elucidate in molecular terms the mechanisms by which interferons exert their antiviral and cell growth control actions, with focus on 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. ADAR1 is an RNA adenosine deaminase that catalyzes the C6 deamination of adenosine to yield inosine, a process known as A-to-I editing that thereby alters the genetic decoding and structure of RNAs. While PKR displays antiviral and proapoptic activities, ADAR1 is often proviral and antiapoptotic. Furthermore, PKR is not required for normal mouse embryogenesis, whereas ADAR1 is required.