Reactivation of fetal splicing programs in diabetic hearts is mediated by protein kinase C Signaling

Sunil K. Verma, Vaibhav Deshmukh, Patrick Liu, Curtis A. Nutter, Rosario Espejo, Ming Lung Hung, Guey Shin Wang, Gene W. Yeo, Muge N. Kuyumcu-Martinez

Research output: Contribution to journalArticle

31 Scopus citations

Abstract

Background: Chronic PKC activation is the leading pathogenic component of diabetes in the heart. Results: PKCα/β promotes fetal splicing patterns in adult diabetic hearts via phosphorylation of the RNA-binding proteins CELF1 and Rbfox2. Conclusion: PKCα/β contributes to diabetes pathogenesis by manipulating developmentally regulated alternative splicing. Significance: Identifying downstream effectors of PKC can provide novel therapeutics for cardiac pathogenesis of diabetes.

Original languageEnglish (US)
Pages (from-to)35372-35386
Number of pages15
JournalJournal of Biological Chemistry
Volume288
Issue number49
DOIs
StatePublished - Dec 6 2013

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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    Verma, S. K., Deshmukh, V., Liu, P., Nutter, C. A., Espejo, R., Hung, M. L., Wang, G. S., Yeo, G. W., & Kuyumcu-Martinez, M. N. (2013). Reactivation of fetal splicing programs in diabetic hearts is mediated by protein kinase C Signaling. Journal of Biological Chemistry, 288(49), 35372-35386. https://doi.org/10.1074/jbc.M113.507426