You are here

Home » People » Faculty
Photo

Charles E. Samuel

C.A. Storke II Professor

Contact Information

Phone: (805) 893-3097
Email: samuel@lifesci.ucsb.edu
Office: 2119 LSB
Website: Samuel Lab

Address

Molecular, Cellular, and Developmental Biology
University of California, Santa Barbara
Santa Barbara, CA 93106-9625

Bio

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.

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.

Selected Publications

  • Okonski, K.M., Samuel, C.E. (2013) Stress Granule Formation Induced by Measles Virus is Protein Kinase PKR-dependent and Impaired by RNA Adenosine Deaminase ADAR1. J. Virol. 87: 756-766
  • McAllister, C.S., Taghavi, N., Samuel, C.E. (2012) Protein Kinase PKR Amplification of Interferon β Induction Occurs through Initiation Factor eIF-2α-mediated Translational Control. J. Biol. Chem. 287:36384-36392.
  • Ruggieri A, Dazert E, Metz P, Hofmann S, Bergeest JP, Mazur J, et al. (2012) Dynamic oscillation of translation and stress granule formation mark the cellular response to virus infection. Cell Host Microbe 12:71-85.
  • Li, Z., Okonski, K. M., and Samuel, C. E. (2012) Adenosine Deaminase Acting on RNA 1 (ADAR1) Suppresses the Induction of Interferon by Measles Virus. J Virol. 86: 3787-3794.
  • Samuel CE (2012) Understanding human Immunodeficiency virus-host interactions at the biochemical level. J. Biol. Chem. 287: 40838-40840.
  • Taghavi, N., and Samuel C. E. (2012) Protein kinase PKR catalytic activity is required for the PKR-dependent activation of mitogen-activated protein kinases and amplification of interferon beta induction following virus infection. Virology 427: 208-216.
  • Samuel, C.E. (2011) Adenosine Deaminases Acting on RNAs (ADARs) are both Antiviral and Proviral. Virology 411: 180-193.
  • Ward, S.V., George, C.X., Welch,M.J., Liou, L-Y, Hahm, B., Lewicki, H, de la Torre, J.C., Samuel, C.E., and Oldstone, M.B. (2011) RNA Editing Enzyme Adenosine Deaminase is a Restriction Factor for Controlling Measles Virus Replication that also is Required for Embryogenesis. Proc. Natl. Acad. Sci. USA 108: 331-336.
  • George, C.X., and Samuel, C.E. (2011) Host Response to Polyoma Virus Infection is Modulated by RNA Adenosine Deaminse ADAR1 but not by ADAR2. J. Virol. 85: 8338-8347.
  • Bouxsein, N.F., Leal, C., McAllister, C.S., Ewert, K.K., Li, Y., Samuel, C.E., and Safinya, C.S. (2011) Two-dimensional Packing of Short DNA with Non-pairing Overhangs in Cationic Liposome-DNA Complexes: From Onsager Nematics to Columnar Nematics with Finite-length Columns. J. Am. Chem. Soc. 133: 7585-7595.
  • Pfaller CK, Li Z, George CX, Samuel CE. (2011) Protein kinase PKR and RNA adenosine deaminase ADAR1: new roles for old players as modulators of the interferon response. Curr Opin Immunol. 23: 573-582
  • McAllister, C.S., Toth, A.M., Zhang, P., Devaux, P., Cattaneo, R., and Samuel, C.E. (2010) Mechanisms of Protein Kinase PKR-mediated Amplification of Beta Interferon Induction by C Protein-deficient Measles Virus. J. Virol. 84 : 380-386.
  • Li, Z., Wolff, K.C., and Samuel, C.E. (2010) RNA Adenosine Deaminase ADAR1 Deficiency Leads to Increased Activation of Protein Kinase PKR and Reduced Vesicular Stomatitis Virus Growth following Interferon Treatment. Virology 396: 316-322.
  • Toth, A.M., Li, Z., Cattaneio, R., and Samuel, C.E. (2009) RNA-specific adenosine deaminae ADAR1 suppresses measles virus-induced apoptosis and activation of protein kinase PKR. J. Biol. Chem. 284: 29350-29356.
  • Zhang, P., Langland, J.O., Jacobs, B.L., Samuel, C.E. (2009) Protein kinase PKR-dependent activation of mitogen-activated protein kinases occurs through mitochondrial adapter IPS-1 and is antagonized by vaccinia virus E3L. J. Virol. 83: 5718-5725.
  • McAllister, C.S., Samuel, C.E. (2009) Protein kinase PKR enhances the induction of interferon-beta and apoptosis mediated by cytoplasmic RNA sensors. J. Biol. Chem. 284: 1644-1651.
PubMed Database