Cytomegalovirus M45 cell death suppression requires receptor-interacting protein (RIP) homotypic interaction motif (RHIM)-dependent interaction with RIP1

Jason W. Upton, William J. Kaiser, Edward S. Mocarski

Research output: Contribution to journalArticle

121 Scopus citations

Abstract

Herpesviruses such as cytomegaloviruses encode functions that modulate the innate response in diverse ways to counteract host sensing and delay host clearance during infection. The murine cytomegalovirus M45 protein interacts with receptor-interacting protein (RIP) 1 and RIP3 via a RIP homotypic interaction motif. Cell death suppression by M45 requires RIP homotypic interaction motif-dependent interaction with RIP1. This interaction also underlies the cell tropism role of M45 in preventing premature death of endothelial cells during murine cytomegalovirus infection. Thus, M45 is a viral inhibitor of RIP activation that provides a direct cell type-dependent replication benefit to the virus while modulating other biological processes signaling via the RIP1 adaptor such as activation of Toll-like receptor (TLR)3 as well as other mediators of cell death.

Original languageEnglish (US)
Pages (from-to)16966-16970
Number of pages5
JournalJournal of Biological Chemistry
Volume283
Issue number25
DOIs
StatePublished - Jun 20 2008

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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