rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
4
|
pubmed:dateCreated |
2010-4-22
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pubmed:abstractText |
Histone deacetylase inhibitor n-butyrate induced proliferative unresponsiveness in antigen-stimulated murine CD4(+) T cells. T cells anergized by n-butyrate demonstrated reduced interleukin-2 (IL-2) secretion and decreased activating protein 1 (AP-1) activity upon restimulation. Mechanistic studies determined that the cyclin-dependent kinase (cdk) inhibitor p21(Cip1) was up-regulated in the anergic CD4(+) T cells. p21(Cip1) is known to inhibit the cell cycle through its interaction with cdk, proliferating cell nuclear antigen (PCNA) or c-Jun N-terminal kinase (JNK). p21(Cip1) did not preferentially associate with PCNA or cdk in anergic T helper type 1 (Th1) cells. Instead, among the three interaction partners, p21(Cip1) was found to interact with phospho-JNK and phospho-c-jun selectively in the anergic CD4(+) T cells. The activity of c-jun and downstream transcription factor AP-1 were suppressed in the anergic Th1 cells. In contrast, p21(Cip1) and the two phospho-proteins were never detected concurrently in the control CD4(+) T cells. The n-butyrate-induced p21(Cip1)-mediated inhibition of JNK and c-jun represents a novel potential mechanism by which proliferative unresponsiveness was maintained in CD4(+) T cells.
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
|
pubmed:status |
MEDLINE
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pubmed:month |
Apr
|
pubmed:issn |
1365-2567
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pubmed:author |
|
pubmed:issnType |
Electronic
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pubmed:volume |
129
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
589-99
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pubmed:dateRevised |
2011-7-27
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pubmed:meshHeading |
pubmed-meshheading:20102411-Animals,
pubmed-meshheading:20102411-Butyrates,
pubmed-meshheading:20102411-CD4-Positive T-Lymphocytes,
pubmed-meshheading:20102411-Clonal Anergy,
pubmed-meshheading:20102411-Cyclin-Dependent Kinase Inhibitor p21,
pubmed-meshheading:20102411-Histone Deacetylase Inhibitors,
pubmed-meshheading:20102411-Interleukin-2,
pubmed-meshheading:20102411-JNK Mitogen-Activated Protein Kinases,
pubmed-meshheading:20102411-Male,
pubmed-meshheading:20102411-Mice,
pubmed-meshheading:20102411-Mice, Inbred C57BL,
pubmed-meshheading:20102411-Protein Binding,
pubmed-meshheading:20102411-Proto-Oncogene Proteins c-jun,
pubmed-meshheading:20102411-Transcription Factor AP-1,
pubmed-meshheading:20102411-Up-Regulation
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pubmed:year |
2010
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pubmed:articleTitle |
p21(Cip1) up-regulated during histone deacetylase inhibitor-induced CD4(+) T-cell anergy selectively associates with mitogen-activated protein kinases.
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pubmed:affiliation |
Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Arkansas Children's Hospital Research Institute, Little Rock, AR 72202, USA. aselmad@yahoo.com
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
|