2016
DOI: 10.1536/ihj.16-404
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Regulation of Cardiac Transcription Factor GATA4 by Post-Translational Modification in Cardiomyocyte Hypertrophy and Heart Failure

Abstract: SummaryHeart failure is a leading cause of cardiovascular mortality in industrialized countries. During development and deterioration of heart failure, cardiomyocytes undergo maladaptive hypertrophy, and changes in the cellular phenotype are accompanied by reinduction of the fetal gene program. Gene expression in cardiomyocytes is regulated by various nuclear transcription factors, co-activators, and co-repressors. The zinc finger protein GATA4 is one such transcription factor involved in the regulation of car… Show more

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Cited by 31 publications
(38 citation statements)
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“…The cardiac-specific transcription factor GATA4 is required for the expression of hypertrophic gene tran-scriptions such as ANF, BNP, β-MHC, and ET-1 [9,36]. The transcriptional activity of GATA4 is regulated by post-transcriptional modifications such as phosphorylation, acetylation, and sumoylation [6]. GATA4 can be directly phosphorylated at serine 105 by ERK1/2 [37].…”
Section: Discussionmentioning
confidence: 99%
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“…The cardiac-specific transcription factor GATA4 is required for the expression of hypertrophic gene tran-scriptions such as ANF, BNP, β-MHC, and ET-1 [9,36]. The transcriptional activity of GATA4 is regulated by post-transcriptional modifications such as phosphorylation, acetylation, and sumoylation [6]. GATA4 can be directly phosphorylated at serine 105 by ERK1/2 [37].…”
Section: Discussionmentioning
confidence: 99%
“…cated into the nucleus and phosphorylates GATA4, a zinc finger transcription factor that plays an essential role in pathological cardiac hypertrophy and dysfunction. When GATA4 is phosphorylated, its binding activity to DNA is activated, which up-regulates the gene transcription involved in pathological cardiac hypertrophy [6,7]. In response to hypertrophic stimuli, GATA4 forms a large complex with ERK, NFAT3, CDK9, RACK1, MEF2, and p300 [6,[8][9][10][11][12].…”
Section: Introductionmentioning
confidence: 99%
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“…Despite the fact that similar transcription factors were activated downstream of α 1 -AR and ETR, JQ1 only attenuated the α 1 -AR response. The receptor-specific attenuation of transcription factor activity may be due to distinct signalling mechanisms required for transcription factor activation, creating a differential dependence on Brd4 activity (6265). However, the greater number of transcription factors attenuated by JQ1 following α 1 -AR activation suggests that it leads to an active form of Brd4 that more readily binds to chromatin and promotes the activity of transcription factors.…”
Section: Discussionmentioning
confidence: 99%