Enhanced downregulation of Lck-mediated signal transduction by a Y114 mutation of herpesvirus Saimiri tip
Author:
Affiliation:
1. Department of Microbiology and Molecular Genetics, New England Regional Primate Research Center, Harvard Medical School, Southborough, Massachusetts 01772-9102, USA.
Abstract
Publisher
American Society for Microbiology
Subject
Virology,Insect Science,Immunology,Microbiology
Link
https://journals.asm.org/doi/pdf/10.1128/jvi.71.9.7092-7096.1997
Reference32 articles.
1. Molecular piracy of mammalian interleukin-8 receptor type B by herpesvirus saimiri;Ahuja S. K.;J. Biol. Chem.,1996
2. Primary structure of the herpesvirus saimiri genome;Albrecht J.;J. Virol.,1992
3. Herpesvirus saimiri has a gene specifying a homologue of the cellular membrane glycoprotein CD59;Albrecht J.;Virology,1992
4. The divergence between two oncogenic herpesvirus saimiri strains in a genomic region related to the transforming phenotype;Biesinger B.;Virology,1990
5. The product of the herpesvirus saimiri ORF1 (Tip) interacts with T cell specific kinase p56lck in transformed cells;Biesinger B.;J. Biol. Chem.,1995
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1. Modulating p56Lck in T-Cells by a Chimeric Peptide Comprising Two Functionally Different Motifs of Tip fromHerpesvirus saimiri;Journal of Immunology Research;2015
2. Species restriction of Herpesvirus saimiri and Herpesvirus ateles: Human lymphocyte transformation correlates with distinct signaling properties of viral oncoproteins;Virus Research;2012-05
3. Growth Transformation of Human T Cells by Herpesvirus Saimiri Requires Multiple Tip-Lck Interaction Motifs;Journal of Virology;2006-10-15
4. Regulation of intracellular signalling by the terminal membrane proteins of members of the Gammaherpesvirinae;Journal of General Virology;2006-05-01
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