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

doi:10.1074/jbc.M113.507426

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

Biochemistry & Molecular Biology

Research output: Contribution to journal › Article › peer-review

51 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 language	English (US)
Pages (from-to)	35372-35386
Number of pages	15
Journal	Journal of Biological Chemistry
Volume	288
Issue number	49
DOIs	https://doi.org/10.1074/jbc.M113.507426
State	Published - Dec 6 2013

ASJC Scopus subject areas

Biochemistry
Molecular Biology
Cell Biology

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title = "Reactivation of fetal splicing programs in diabetic hearts is mediated by protein kinase C Signaling",

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.",

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

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doi = "10.1074/jbc.M113.507426",

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T1 - Reactivation of fetal splicing programs in diabetic hearts is mediated by protein kinase C Signaling

AU - Verma, Sunil K.

AU - Deshmukh, Vaibhav

AU - Liu, Patrick

AU - Nutter, Curtis A.

AU - Espejo, Rosario

AU - Hung, Ming Lung

AU - Wang, Guey Shin

AU - Yeo, Gene W.

AU - Kuyumcu-Martinez, Muge N.

PY - 2013/12/6

Y1 - 2013/12/6

N2 - 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.

AB - 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.

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

Abstract

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