pubmed-article:7532676 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:7532676 | lifeskim:mentions | umls-concept:C0086574 | lld:lifeskim |
pubmed-article:7532676 | lifeskim:mentions | umls-concept:C0003320 | lld:lifeskim |
pubmed-article:7532676 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:7532676 | lifeskim:mentions | umls-concept:C0729218 | lld:lifeskim |
pubmed-article:7532676 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:7532676 | pubmed:dateCreated | 1995-3-24 | lld:pubmed |
pubmed-article:7532676 | pubmed:abstractText | Stimulation of B and T cells via the antigen receptor, by phorbol ester or by phorbol ester and ionomycin, leads to nuclear translocation of the inducible transcription factor NF-kappa B, comprising the p50 and p65 rel-related polypeptides. In this report we show that c-rel is a component of the antigen receptor-induced kappa B binding proteins in both B and T cells. Whereas NF-kappa B can be induced by phorbol ester alone, optimal induction of c-rel requires stimulation by both phorbol ester and ionomycin, the dual signal that is necessary for proliferation of untransformed lymphocytes. Furthermore, c-rel induction is blocked by the immunosuppressive drug FK506 that is known to inhibit B and T cell activation. c-rel-dependent transactivation of the interleukin-2 receptor alpha chain (IL-2R alpha) promoter is augmented by coexpression of calcineurin, suggesting the involvement of a calcineurin-dependent intracellular pathway. Our results identify c-rel as a target of immunosuppressive agents and illustrate the similarity of activation pathways in both B and T cells. | lld:pubmed |
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pubmed-article:7532676 | pubmed:language | eng | lld:pubmed |
pubmed-article:7532676 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7532676 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:7532676 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:7532676 | pubmed:month | Mar | lld:pubmed |
pubmed-article:7532676 | pubmed:issn | 0022-1007 | lld:pubmed |
pubmed-article:7532676 | pubmed:author | pubmed-author:BurakoffS JSJ | lld:pubmed |
pubmed-article:7532676 | pubmed:author | pubmed-author:SenRR | lld:pubmed |
pubmed-article:7532676 | pubmed:author | pubmed-author:VenkataramanL... | lld:pubmed |
pubmed-article:7532676 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:7532676 | pubmed:day | 1 | lld:pubmed |
pubmed-article:7532676 | pubmed:volume | 181 | lld:pubmed |
pubmed-article:7532676 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:7532676 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:7532676 | pubmed:pagination | 1091-9 | lld:pubmed |
pubmed-article:7532676 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:7532676 | pubmed:year | 1995 | lld:pubmed |
pubmed-article:7532676 | pubmed:articleTitle | FK506 inhibits antigen receptor-mediated induction of c-rel in B and T lymphoid cells. | lld:pubmed |
pubmed-article:7532676 | pubmed:affiliation | Rosenstiel Research Center, Brandeis University, Waltham, Massachusetts 02254-9110. | lld:pubmed |