pubmed-article:15870282 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:15870282 | lifeskim:mentions | umls-concept:C0111208 | lld:lifeskim |
pubmed-article:15870282 | lifeskim:mentions | umls-concept:C0567416 | lld:lifeskim |
pubmed-article:15870282 | lifeskim:mentions | umls-concept:C0600388 | lld:lifeskim |
pubmed-article:15870282 | lifeskim:mentions | umls-concept:C0751984 | lld:lifeskim |
pubmed-article:15870282 | lifeskim:mentions | umls-concept:C1426113 | lld:lifeskim |
pubmed-article:15870282 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:15870282 | pubmed:issue | 10 | lld:pubmed |
pubmed-article:15870282 | pubmed:dateCreated | 2005-5-4 | lld:pubmed |
pubmed-article:15870282 | pubmed:abstractText | The mitogen-activated protein kinase extracellular signal-regulated kinase (ERK) is activated following engagement of the T-cell receptor and is required for interleukin 2 (IL-2) production and T-cell proliferation. This activation is enhanced by stimulation of the coreceptor CD28 and inhibited by the coreceptor CTLA-4. We show that the small G protein Rap1 is regulated in the opposite manner; it is inhibited by CD28 and activated by CTLA-4. Together, CD3 and CTLA-4 activate Rap1 in a sustained manner. To delineate T-cell function in the absence of Rap1 activity, we generated transgenic mice expressing Rap1GAP1, a Rap1-specific GTPase-activating protein. Transgenic mice showed lymphadenopathy, and transgenic T cells displayed increased ERK activation, proliferation, and IL-2 production. More significantly, the inhibitory effect of CTLA-4 on T-cell function in Rap1GAP1-transgenic T cells was reduced. We demonstrate that CTLA-4 activates Rap1, and we propose that intracellular signals from CTLA-4 antagonize CD28, at least in part, at the level of Rap1. | lld:pubmed |
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pubmed-article:15870282 | pubmed:language | eng | lld:pubmed |
pubmed-article:15870282 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15870282 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:15870282 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15870282 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15870282 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:15870282 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:15870282 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:15870282 | pubmed:month | May | lld:pubmed |
pubmed-article:15870282 | pubmed:issn | 0270-7306 | lld:pubmed |
pubmed-article:15870282 | pubmed:author | pubmed-author:CareyKendall... | lld:pubmed |
pubmed-article:15870282 | pubmed:author | pubmed-author:StorkPhilip... | lld:pubmed |
pubmed-article:15870282 | pubmed:author | pubmed-author:WetzelScott... | lld:pubmed |
pubmed-article:15870282 | pubmed:author | pubmed-author:ParkerDavid... | lld:pubmed |
pubmed-article:15870282 | pubmed:author | pubmed-author:DillonTara... | lld:pubmed |
pubmed-article:15870282 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:15870282 | pubmed:volume | 25 | lld:pubmed |
pubmed-article:15870282 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:15870282 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:15870282 | pubmed:pagination | 4117-28 | lld:pubmed |
pubmed-article:15870282 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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