Identification of εPKC targets during cardiac ischemic injury

dc.creatorBudas, Grant
dc.creatorCosta Junior, Helio Miranda
dc.creatorFerreira, Julio Cesar Batista
dc.creatorFerreira, André Teixeira da Silva
dc.creatorPerales, Jonas
dc.creatorKrieger, José Eduardo
dc.creatorMochly-Rosen, Daria
dc.creatorSchechtman, Deborah
dc.date2017-05-02T12:56:37Z
dc.date2017-05-02T12:56:37Z
dc.date2012
dc.date.accessioned2023-09-26T20:11:55Z
dc.date.available2023-09-26T20:11:55Z
dc.identifierBUDAS, Grant; et al. Identification of εPKC targets during cardiac ischemic injury. Circ J., v. 76, n.6, p.1476–1485, 2012.
dc.identifier1346-9843
dc.identifierhttps://www.arca.fiocruz.br/handle/icict/18706
dc.identifier1347-4820
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8851118
dc.descriptionBackground—Activation of ε protein kinase C (εPKC) protects hearts from ischemic injury. However, some of the mechanism(s) of εPKC mediated cardioprotection are still unclear. Identification of εPKC targets may aid to elucidate εPKC–mediated cardioprotective mechanisms. Previous studies, using a combination of εPKC transgenic mice and difference in gel electrophoresis (DIGE), identified a number of proteins involved in glucose metabolism, whose expression was modified by εPKC. These studies, were accompanied by metabolomic analysis, and suggested that increased glucose oxidation may be responsible for the cardioprotective effect of εPKC. However, whether these εPKC-mediated alterations were due to differences in protein expression or phosphorylation was not determined.
dc.formatapplication/pdf
dc.languageeng
dc.publisherNational Institute of Health
dc.rightsopen access
dc.subjectMitocôndrias
dc.subjectProteína Quinase C
dc.subjectIsquemia
dc.subjectFosforilação
dc.subjectεPKC
dc.subjectischemia
dc.subjectphosphorylation
dc.subjectmitochondria
dc.subjectMitocôndrias
dc.subjectProteína Quinase C
dc.subjectIsquemia
dc.subjectFosforilação
dc.titleIdentification of εPKC targets during cardiac ischemic injury
dc.typeArticle


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