IMMUNOBIOLOGY HSV ICP0 recruits USP7 to modulate TLR-mediated innate response
نویسندگان
چکیده
1Institut de Pharmacologie et de Biologie Structurale (IPBS), Centre National de Recherche Scientifique (CNRS), Unité Mixte de Recherche 5089 (UMR), Toulouse, France; 2Division of Hematology-Oncology, Department of Medicine, Sylvester Comprehensive Cancer Center, University of Miami, FL; 3Georgetown University Medical Center, Washington, DC; and 4Department of Neurology, Center for Aging and Developmental Biology, University of Rochester School of Medicine and Dentistry, NY
منابع مشابه
HSV ICP0 recruits USP7 to modulate TLR-mediated innate response.
Pattern recognition receptors represent the first line of defense against invading pathogens. Herpes simplex virus (HSV) encodes multiple ligands detected by these receptors, yet persists in the majority of infected individuals indicating a breakdown in host defense against the virus. Here we identify a novel mechanism through which HSV immediate-early protein ICP0 inhibits TLR-dependent inflam...
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The herpes simplex virus type 1 (HSV-1) encoded E3 ubiquitin ligase, infected cell protein 0 (ICP0), is required for efficient lytic viral replication and regulates the switch between the lytic and latent states of HSV-1. As an E3 ubiquitin ligase, ICP0 directs the proteasomal degradation of several cellular targets, allowing the virus to counteract different cellular intrinsic and innate immun...
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Herpes simplex virus type 1 (HSV-1) regulatory protein ICP0 stimulates lytic infection and the reactivation of quiescent viral genomes. These roles of ICP0 require its RING finger E3 ubiquitin ligase domain, which induces the degradation of several cellular proteins, including components of promyelocytic leukemia nuclear bodies and centromeres. ICP0 also interacts very strongly with the cellula...
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تاریخ انتشار 2009