Linked Life Data

14517080

Source:http://linkedlifedata.com/resource/pubmed/id/14517080

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pubmed-article:14517080pubmed:abstractTextHepatitis C virus (HCV) is efficient in the establishment of persistent infection. We have previously shown that HCV core protein inhibits T cell proliferation through its interaction with the complement receptor, gC1qR. Here we show that HCV core-induced inhibition of T cell proliferation involves a G(0)/G(1) cell cycle arrest, which is reversible upon addition of anti-gC1qR antibody. Correspondingly, the expression of cyclin-dependent kinases (Cdk) 2/4 and cyclin E/D, as well as subsequent phosphorylation of retinoblastoma (pRb), is reduced in core-treated T cells in response to mitogenic stimulation. Remarkably, degradation of p27(Kip1), a negative regulator of both Cdk4/cyclin D and Cdk2/cyclin E complexes, is significantly diminished in T cells treated with HCV core upon mitogenic stimulation. These data indicate that the stability of p27(Kip1) by HCV core is associated with blocking activated T cells for the G(1) to S phase transition and inhibiting T cell proliferation.lld:pubmed
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pubmed-article:14517080pubmed:articleTitleHCV core/gC1qR interaction arrests T cell cycle progression through stabilization of the cell cycle inhibitor p27Kip1.lld:pubmed
pubmed-article:14517080pubmed:affiliationDepartment of Pathology, Beirne Carter Center for Immunology Research, University of Virginia, Charlottesville, VA 22908, USA.lld:pubmed
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pubmed-article:14517080pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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