Title : Angiotensin II increases expression of alpha1C subunit of L-type calcium channel through a reactive oxygen species and cAMP response element-binding protein-dependent pathway in HL-1 myocytes.

Pub. Date : 2007 May 25

PMID : 17463319






3 Functional Relationships(s)
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1 Ang II (1 micromol/L, 2 hours) induced serine 133 phosphorylation of CREB and binding of CREB to CRE and increased LCC alpha1C subunit gene promoter activity through a protein kinase C/NADPH oxidase/reactive oxygen species pathway, which was blocked by the Ang II type 1 receptor blocker losartan and the antioxidant simvastatin. Simvastatin cAMP responsive element binding protein 1 Rattus norvegicus
2 In the rat model, Ang II infusion increased LCC alpha1C subunit expression and serine 133 phosphorylation of CREB, which were attenuated by oral losartan and simvastatin. Simvastatin cAMP responsive element binding protein 1 Rattus norvegicus
3 In summary, Ang II induced LCC alpha1C subunit expression via a protein kinase C-, reactive oxygen species-, and CREB-dependent pathway and was blocked by losartan and simvastatin. Simvastatin cAMP responsive element binding protein 1 Rattus norvegicus