| pubmed-article:8657160 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8657160 | lifeskim:mentions | umls-concept:C0085828 | lld:lifeskim |
| pubmed-article:8657160 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:8657160 | lifeskim:mentions | umls-concept:C1167128 | lld:lifeskim |
| pubmed-article:8657160 | lifeskim:mentions | umls-concept:C0022173 | lld:lifeskim |
| pubmed-article:8657160 | lifeskim:mentions | umls-concept:C0033640 | lld:lifeskim |
| pubmed-article:8657160 | lifeskim:mentions | umls-concept:C1948023 | lld:lifeskim |
| pubmed-article:8657160 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:8657160 | pubmed:dateCreated | 1996-7-29 | lld:pubmed |
| pubmed-article:8657160 | pubmed:abstractText | T-lymphocyte stimulation requires activation of several protein kinases, including the major phorbol ester receptor protein kinase C (PKC), ultimately leading to induction of lymphokines, such as interleukin-2 (IL-2). The revelant PKC isoforms which are involved in the activation cascades of nuclear transcription factors involved in IL-2 production have not yet been clearly defined. We have examined the potential role of two representative PKC isoforms in the induction of the IL-2 gene, i.e., PKC-alpha and PKC-theta, the latter being expressed predominantly in hematopoietic cell lines, particularly T cells. Similar to that of PKC-alpha, PKC-theta overexpression in murine EL4 thymoma cells caused a significant increase in phorbol 12-myristate 13-acetate (PMA)-induced transcriptional activation of full-length IL-2-chloramphenicol acetyltransferase (CAT) and NF-AT-CAT but not of NF-IL2A-CAT or NF-kappaB promoter-CAT reporter gene constructs. Importantly, the critical AP-1 enhancer element was differentially modulated by these two distinct PKC isoenzymes, since only PKC-theta but not PKC-alpha overexpression resulted in an approximately 2.8-fold increase in AP-1-collagenase promoter CAT expression in comparison with the vector control. Deletion of the AP-1 enhancer site in the collagenase promoter rendered it unresponsive to PKC-theta. Expression of a constitutively active mutant PKC-theta A148E (but not PKC-alpha A25E) was sufficient to induce activation of AP-1 transcription factor complex in the absence of PMA stimulation. Conversely, a catalytically inactive PKC-theta K409R (but not PKC-alpha K368R) mutant abrogated endogenous PMA-mediated activation of AP-1 transcriptional complex. Dominant negative mutant Ha-RasS17N completely inhibited the PKC-O A148E-induced signal, PKC-O. Expression of a constitutively active mutant PKC-O A148E (but not PKC-alpha A25E) was sufficient to induce activation of AP-1 transcription factor complex in the absence of PMA stimulation. Conversely, a catalytically inactive PKC-O K409R (but not PKC-alpha K368R) mutant abrogated endogenous PMA-mediated activation of AP-1 transcriptional complex. Dominant negative mutant Ha-enRasS17N completely inhibited in the PKC-O A148E-induced signal, identifying PKC-theta as a specific constituent upstream of or parallel to Ras in the signaling cascade leading to AP transcriptional activation. | lld:pubmed |
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| pubmed-article:8657160 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8657160 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8657160 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:8657160 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:8657160 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8657160 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:8657160 | pubmed:issn | 0270-7306 | lld:pubmed |
| pubmed-article:8657160 | pubmed:author | pubmed-author:BauerBB | lld:pubmed |
| pubmed-article:8657160 | pubmed:author | pubmed-author:GrunickeHH | lld:pubmed |
| pubmed-article:8657160 | pubmed:author | pubmed-author:AltmanAA | lld:pubmed |
| pubmed-article:8657160 | pubmed:author | pubmed-author:UtermannGG | lld:pubmed |
| pubmed-article:8657160 | pubmed:author | pubmed-author:WachterHH | lld:pubmed |
| pubmed-article:8657160 | pubmed:author | pubmed-author:UberallFF | lld:pubmed |
| pubmed-article:8657160 | pubmed:author | pubmed-author:BaierGG | lld:pubmed |
| pubmed-article:8657160 | pubmed:author | pubmed-author:Baier-Bitterl... | lld:pubmed |
| pubmed-article:8657160 | pubmed:author | pubmed-author:FresserFF | lld:pubmed |
| pubmed-article:8657160 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8657160 | pubmed:volume | 16 | lld:pubmed |
| pubmed-article:8657160 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8657160 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8657160 | pubmed:pagination | 1842-50 | lld:pubmed |
| pubmed-article:8657160 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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