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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
32
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pubmed:dateCreated |
2001-8-6
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pubmed:abstractText |
FADD is an adapter protein that was originally isolated as a transducer of apoptotic signals for death domain-containing receptors. However, FADD-deficient mice are embryonic lethal and FADD(-/-) T cells developed from FADD(-/-) embryonic stem cells in the RAG-1(-/-) hosts lack the full potential to proliferate when stimulated through their T-cell receptor complex, suggesting that FADD protein might play a dualistic role in mediating not only cell death signaling but other non-apoptotic cellular pathways as well. Here we show that a substantial number of freshly isolated FADD(-/-) peripheral T cells are cycling but are defective in their co-stimulatory response when stimulated. Analysis of several cell cycle proteins shows normal down-regulation of p27 inhibitor but increased levels of p21, decreased levels of cyclin D2, and constitutive activation of several cyclin-dependent kinases in activated T cells. These data suggest that FADD is involved in the regulation of cell cycle machinery in T lymphocytes.
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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/Arabidopsis Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Ccnd2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclin D2,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclins,
http://linkedlifedata.com/resource/pubmed/chemical/Fad7 protein, Arabidopsis,
http://linkedlifedata.com/resource/pubmed/chemical/Fatty Acid Desaturases,
http://linkedlifedata.com/resource/pubmed/chemical/Microfilament Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Muscle Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell,
http://linkedlifedata.com/resource/pubmed/chemical/Tagln protein, mouse
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0021-9258
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
10
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pubmed:volume |
276
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
29815-8
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:11390402-Animals,
pubmed-meshheading:11390402-Apoptosis,
pubmed-meshheading:11390402-Arabidopsis Proteins,
pubmed-meshheading:11390402-Blastocyst,
pubmed-meshheading:11390402-Blotting, Western,
pubmed-meshheading:11390402-CD4-Positive T-Lymphocytes,
pubmed-meshheading:11390402-CD8-Positive T-Lymphocytes,
pubmed-meshheading:11390402-Cell Cycle,
pubmed-meshheading:11390402-Cell Death,
pubmed-meshheading:11390402-Cell Division,
pubmed-meshheading:11390402-Cyclin D2,
pubmed-meshheading:11390402-Cyclins,
pubmed-meshheading:11390402-Down-Regulation,
pubmed-meshheading:11390402-Fatty Acid Desaturases,
pubmed-meshheading:11390402-Flow Cytometry,
pubmed-meshheading:11390402-Lymphocyte Activation,
pubmed-meshheading:11390402-Mice,
pubmed-meshheading:11390402-Microfilament Proteins,
pubmed-meshheading:11390402-Muscle Proteins,
pubmed-meshheading:11390402-Receptors, Antigen, T-Cell,
pubmed-meshheading:11390402-T-Lymphocytes,
pubmed-meshheading:11390402-Time Factors
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pubmed:year |
2001
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pubmed:articleTitle |
FADD-deficient T cells exhibit a disaccord in regulation of the cell cycle machinery.
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pubmed:affiliation |
Department of Molecular and Cell Biology, Division of Immunology and Cancer Research Laboratory, University of California at Berkeley, California 94720, 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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