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See Latest ArticlesWarm-blood cardioplegic arrest induces selective mitochondrial translocation of protein kinase C(epsilon) followed by interaction with 6.1 inwardly rectifying potassium channel subunit in viable myocytes overexpressing urocortin
The Journal of Thoracic and Cardiovascular Surgery, 06/25/09
Chen-Scarabelli C et al. - After iatrogenic ischemia/reperfusion injury, urocortin expression in viable cells selectively colocalized with enhanced phosphorylation and mitochondrial relocation of protein kinase C(epsilon), suggesting a cardioprotective role for endogenous urocortin. The physical interaction of activated protein kinase C(epsilon) with 6.1 inwardly rectifying potassium channel, enhanced by cardioplegic arrest, may represent a conjectural mechanism of urocortin-mediated cardioprotection.
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