| pubmed-article:8816505 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8816505 | lifeskim:mentions | umls-concept:C0087140 | lld:lifeskim |
| pubmed-article:8816505 | lifeskim:mentions | umls-concept:C0006776 | lld:lifeskim |
| pubmed-article:8816505 | lifeskim:mentions | umls-concept:C0217843 | lld:lifeskim |
| pubmed-article:8816505 | lifeskim:mentions | umls-concept:C0086860 | lld:lifeskim |
| pubmed-article:8816505 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:8816505 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
| pubmed-article:8816505 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
| pubmed-article:8816505 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:8816505 | pubmed:dateCreated | 1996-11-15 | lld:pubmed |
| pubmed-article:8816505 | pubmed:abstractText | Endothelin-1 (ET-1) triggers poorly understood nuclear signaling cascades that control gene expression, cell growth, and differentiation. To better understand how ET-1 regulates gene expression, we asked whether voltage-insensitive Ca2+ channels and Ca2+/calmodulin-dependent protein kinases (CaMKs) propagate signals from ET-1 receptors to the c-fos promoter in mesangial cells. Ca2+ influx through voltage-insensitive Ca2+ channels, one of the earliest postreceptor events in ET-1 signaling, mediated induction of c-fos mRNA and activation of the c-fos promoter by ET-1. A CaMK inhibitor (KN-93) blocked activation of the c-fos promoter by ET-1. Ectopic expression of CaMKII potentiated stimulation by ET-1, providing further evidence that CaMKs contribute to c-fos promoter activation by ET-1. The c-fos serum response element was necessary but not sufficient for CaMKII to activate the c-fos promoter. Activation of the c-fos promoter by ET-1 and CaMKII also required the FAP cis element, an AP-1-like sequence adjacent to the serum response element. Thus, voltage-insensitive Ca2+ channels and CaMKs apparently propagate ET-1 signals to the c-fos promoter that require multiple, interdependent cis elements. Moreover, these experiments suggest an important role for voltage-insensitive Ca2+ channels in nuclear signal transduction in nonexcitable cells. | lld:pubmed |
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| pubmed-article:8816505 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8816505 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8816505 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:8816505 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:8816505 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8816505 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:8816505 | pubmed:issn | 0270-7306 | lld:pubmed |
| pubmed-article:8816505 | pubmed:author | pubmed-author:WangYY | lld:pubmed |
| pubmed-article:8816505 | pubmed:author | pubmed-author:SimonsonM SMS | lld:pubmed |
| pubmed-article:8816505 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8816505 | pubmed:volume | 16 | lld:pubmed |
| pubmed-article:8816505 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8816505 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8816505 | pubmed:pagination | 5915-23 | lld:pubmed |
| pubmed-article:8816505 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
