PHARMACOLOGY FACULTY
Selected Publications
  • Higuchi M, Kieff E, Izumi KM. The Epstein-Barr virus latent membrane protein 1 (LMP1) putative Janus Kinase 3 (JAK3) binding domain does not mediate JAK3 association or activation in B-lymphoma or lymphoblastoid cell lines. J. Virol. 2002. 76:455-9.
  • Higuchi M, Izumi KM, Kieff E. Epstein-Barr virus latent-infection membrane proteins are palmitoylated and raft-associated: protien 1 binds to the cytoskeleton through TNF receptor cytoplasmic factors. Proc Natl. Acad. Sci. USA 2001. 98:4675-80.
  • Izumi KM, McFarland EC, Ting AT, Riley EA, Seed B, Kieff E. The Epstein-Barr virus oncoprotein latent membrane protein 1 (LMP1) engages TNF receptor associated proteins TRADD and RIP but does not induce apoptosis or require RIP for NF-Kappa B activation. Mol Cell Biol 1999. 19:5759-67.
  • Kaye KM, Izumi KM, Li H, Johanssen E, Davidson D, Longnecker R, Kieff E. An Epstein-Barr virus that expresses only the first 231 LMP1 amino acids efficiently initiates primary B-lymphocyte growth transformation. J. Virol. 1999. 73:10525-10530.
  • Izumi KM, Cahir-McFarland E, Chen Y, Riley EA, Rizzo D, Kieff E. The residues between the two transformation effector sites of Epstein-Barr virus latent membrane protein 1 are not critical for B-lymphocyte growth transformation. J. Virol. 1999. 73:9908-9916.
Kenneth M. Izumi
 

Kenneth M. Izumi

Associate Professor of Microbiology & Immunology
Ph.D., University of California - Los Angeles

Office: 210-567-3935
Email: izumi@uthscsa.edu

 

Keywords

KEYWORDS

 

Research Summary

Epstein-Barr virus (EBV) is associated with several human malignancies including a non-Hodgkin's lymphoma of AIDS patients and transplant recipients, Hodgkin's lymphoma, and Burkitt's lymphoma. In the malignant cells, EBV expresses nine proteins including latent infection membrane protein 1 (LMP1). LMP1 is required for EBV to transform primary B-lymphocytes into indefinitely proliferating cell lines and therefore is likely to be important in the pathogenesis of these lymphomas. The central hypothesis of our investigation is that LMP1 is constitutively activated receptor that drives B-cell proliferation by transducing signals that alter expression of specific cell genes. LMP1 transduces signals through tumor necrosis factor (TNF) receptor associated factors (TRAF), TNF receptor associated death domain protein (TRADD), and TNF receptor interacting protein (RIP) that activate NF-º?B and mitogen activated protein kinases (MAPK). Our goal is to delineate the role of these signals in driving B-cell proliferation and to identify the specific cell genes whose expression is altered by LMP1 signals to transform B-cell growth. It is expected that the knowledge gained from such analyses will reveal targets for treating or preventing EBV-associated malignancies. Such results will be of additional significance because of what is also learned about the signaling pathways and cell genes that regulate B-cell growth.