ArticleProceedings of the National Academy of Sciences of the United States of America2011
Serine 105 phosphorylation of transcription factor GATA4 is necessary for stress-induced cardiac hypertrophy in vivo.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 99 citations in OpenAlex.
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- Osimertinib induces reversible cardiac dysfunction through the GATA4-MYLK3-MYL2 axis.European heart journal · 2026Article
- Transcriptional regulation in heart development, disease and regeneration: reassessing the fetal gene hypothesis.Nature reviews. Cardiology · 2026Review
- The role of collagen triple helix repeat containing 1 (CTHRC1) in cancer development and progression.Expert opinion on therapeutic targets · 2024Review
- Sibjotang Protects against Cardiac Hypertrophy In Vitro and In Vivo.Life (Basel, Switzerland) · 2023Article
- Monoamine oxidase A-dependent ROS formation modulates human cardiomyocyte differentiation through AKT and WNT activation.Basic research in cardiology · 2023Article
- Differential Response of Transcription Factors to Activated Kinases in Steroidogenic and Non-Steroidogenic Cells.International journal of molecular sciences · 2022Article
- Antenatal Glucocorticoid Administration Promotes Cardiac Structure and Energy Metabolism Maturation in Preterm Fetuses.International journal of molecular sciences · 2022Review
- Towards Understanding the Gene-Specific Roles of GATA Factors in Heart Development: Does GATA4 Lead the Way?International journal of molecular sciences · 2022Review
- Cardiomyocyte stromal interaction molecule 1 is a key regulator of CaPhysiological reports · 2022Article
- Multimerization of the GATA4 transcription factor regulates transcriptional activity and cardiomyocyte hypertrophic response.International journal of biological sciences · 2022Article
- Transcription Factors Involved in the Development and Prognosis of Cardiac Remodeling.Frontiers in pharmacology · 2022Review
- Integrated Quantitative Phosphoproteomics and Cell-based Functional Screening Reveals Specific Pathological Cardiac Hypertrophy-related Phosphorylation Sites.Molecules and cells · 2021Article
- Proteomic analysis identifies key differences in the cardiac interactomes of dystrophin and micro-dystrophin.Human molecular genetics · 2021Article
- Review
- Microfibrillar-Associated Protein 4 Regulates Stress-Induced Cardiac Remodeling.Circulation research · 2021Article
- Toward a New Paradigm for Targeted Natriuretic Peptide Enhancement in Heart Failure.Frontiers in physiology · 2021Review
- ERK signalling: a master regulator of cell behaviour, life and fate.Nature reviews. Molecular cell biology · 2020Review
- Phosphorylation of GATA4 at serine 105 is required for left ventricular remodelling process in angiotensin II-induced hypertension in rats.Basic & clinical pharmacology & toxicology · 2020Article
- GATA4-targeted compound exhibits cardioprotective actions against doxorubicin-induced toxicity in vitro and in vivo: establishment of a chronic cardiotoxicity model using human iPSC-derived cardiomyocytes.Archives of toxicology · 2020Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Cardiac hypertrophy is an adaptive growth process that occurs in response to stress stimulation or injury wherein multiple signal transduction pathways are induced, culminating in transcription factor activation and the reprogramming of gene expression. GATA4 is a critical transcription factor in the heart that is known to induce/regulate the hypertrophic program, in part, by receiving signals from MAPKs. Here we generated knock-in mice in which a known MAPK phosphorylation site at serine 105 (S105) in Gata4 that augments activity was mutated to alanine. Homozygous Gata4-S105A mutant mice were viable as adults, although they showed a compromised stress response of the myocardium. For example, cardiac hypertrophy in response to phenylephrine agonist infusion for 2 wk was largely blunted in Gata4-S105A mice, as was the hypertrophic response to pressure overload at 1 and 2 wk of applied stimulation. Gata4-S105A mice were also more susceptible to heart failure and cardiac dilation after 2 wk of pressure overload. With respect to the upstream pathway, hearts from Gata4-S105A mice did not efficiently hypertrophy following direct ERK1/2 activation using an activated MEK1 transgene in vivo. Mechanistically, GATA4 mutant protein from these hearts failed to show enhanced DNA binding in response to hypertrophic stimulation. Moreover, hearts from Gata4-S105A mice had significant changes in the expression of hypertrophy-inducible, fetal, and remodeling-related genes.
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