ArticleThe Journal of cell biology2013
Dysbindin is a potent inducer of RhoA-SRF-mediated cardiomyocyte hypertrophy.
Article in The Journal of cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Elevated levels of Letm1 drives mitochondrial dysfunction and cardiomyocyte stress-mediated apoptosis in cultured cardiomyocytes.Cell communication and signaling : CCS · 2025Article
- RICH1 is a novel key suppressor of isoproterenol‑ or angiotensin II‑induced cardiomyocyte hypertrophy.Molecular medicine reports · 2024Article
- Fibin regulates cardiomyocyte hypertrophy and causes protein-aggregate-associated cardiomyopathyFrontiers in molecular biosciences · 2023Article
- SRF: a seriously responsible factor in cardiac development and disease.Journal of biomedical science · 2022Review
- Isobaric Tags for Relative and Absolute Quantitation Identification of Blood Proteins Relevant to Paroxetine Response in Patients With Major Depressive Disorder.Frontiers in psychiatry · 2022Article
- SH3-Binding Glutamic Acid Rich-Deficiency Augments Apoptosis in Neonatal Rat Cardiomyocytes.International journal of molecular sciences · 2021Article
- RhoA: a dubious molecule in cardiac pathophysiology.Journal of biomedical science · 2021Review
- Article
- The E3 ubiquitin ligase HectD3 attenuates cardiac hypertrophy and inflammation in mice.Communications biology · 2020Article
- Effect of atorvastatin on cardiomyocyte hypertrophy through suppressing MURC induced by volume overload and cyclic stretch.Journal of cellular and molecular medicine · 2019Article
- Desmosomes: Essential contributors to an integrated intercellular junction network.F1000Research · 2019Review
- HDAC6 Regulates the MRTF-A/SRF Axis and Vascular Smooth Muscle Cell Plasticity.JACC. Basic to translational science · 2018Article
- TRIM24 protein promotes and TRIM32 protein inhibits cardiomyocyte hypertrophy via regulation of dysbindin protein levels.The Journal of biological chemistry · 2017Article
- MicroRNA miR-301a is a novel cardiac regulator of Cofilin-2.PloS one · 2017Article
- Sumoylation-independent activation of Calcineurin-NFAT-signaling via SUMO2 mediates cardiomyocyte hypertrophy.Scientific reports · 2016Article
- Myozap Deficiency Promotes Adverse Cardiac Remodeling via Differential Regulation of Mitogen-activated Protein Kinase/Serum-response Factor and β-Catenin/GSK-3β Protein Signaling.The Journal of biological chemistry · 2016Article
- RhoA activity increased in myocardium of arrhythmogenic cardiomyopathy patients and affected connexin 43 protein expression in HL-1 cells.International journal of clinical and experimental medicine · 2015Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysbindin is an established schizophrenia susceptibility gene thoroughly studied in the context of the brain. We have previously shown through a yeast two-hybrid screen that it is also a cardiac binding partner of the intercalated disc protein Myozap. Because Dysbindin is highly expressed in the heart, we aimed here at deciphering its cardiac function. Using a serum response factor (SRF) response element reporter-driven luciferase assay, we identified a robust activation of SRF signaling by Dysbindin overexpression that was associated with significant up-regulation of SRF gene targets, such as Acta1 and Actc1. Concurrently, we identified RhoA as a novel binding partner of Dysbindin. Further phenotypic and mechanistic characterization revealed that Dysbindin induced cardiac hypertrophy via RhoA-SRF and MEK1-ERK1 signaling pathways. In conclusion, we show a novel cardiac role of Dysbindin in the activation of RhoA-SRF and MEK1-ERK1 signaling pathways and in the induction of cardiac hypertrophy. Future in vivo studies should examine the significance of Dysbindin in cardiomyopathy.
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