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rdf:type |
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lifeskim:mentions |
umls-concept:C0007586,
umls-concept:C0007634,
umls-concept:C0039194,
umls-concept:C0169665,
umls-concept:C0220847,
umls-concept:C0237477,
umls-concept:C0444669,
umls-concept:C1332737,
umls-concept:C1412933,
umls-concept:C1516334,
umls-concept:C1704675,
umls-concept:C1705523,
umls-concept:C1999216
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pubmed:issue |
1
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pubmed:dateCreated |
2003-9-30
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pubmed:abstractText |
Hepatitis 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.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD44,
http://linkedlifedata.com/resource/pubmed/chemical/C1QBP protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Carrier Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Cell Cycle Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclin-Dependent Kinase Inhibitor...,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Mitochondrial Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Complement,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Suppressor Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Viral Core Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/complement 1q receptor,
http://linkedlifedata.com/resource/pubmed/chemical/nucleocapsid protein, Hepatitis C...
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0042-6822
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
314
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
271-82
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:14517080-Antigens, CD44,
pubmed-meshheading:14517080-Carrier Proteins,
pubmed-meshheading:14517080-Cell Cycle,
pubmed-meshheading:14517080-Cell Cycle Proteins,
pubmed-meshheading:14517080-Cyclin-Dependent Kinase Inhibitor p27,
pubmed-meshheading:14517080-G0 Phase,
pubmed-meshheading:14517080-G1 Phase,
pubmed-meshheading:14517080-Hepacivirus,
pubmed-meshheading:14517080-Humans,
pubmed-meshheading:14517080-Lymphocyte Activation,
pubmed-meshheading:14517080-Membrane Glycoproteins,
pubmed-meshheading:14517080-Mitochondrial Proteins,
pubmed-meshheading:14517080-Receptors, Complement,
pubmed-meshheading:14517080-S Phase,
pubmed-meshheading:14517080-T-Lymphocytes,
pubmed-meshheading:14517080-Tumor Suppressor Proteins,
pubmed-meshheading:14517080-Viral Core Proteins
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pubmed:year |
2003
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pubmed:articleTitle |
HCV core/gC1qR interaction arrests T cell cycle progression through stabilization of the cell cycle inhibitor p27Kip1.
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pubmed:affiliation |
Department of Pathology, Beirne Carter Center for Immunology Research, University of Virginia, Charlottesville, VA 22908, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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