ArticlePloS one2011
Expression of sumoylation deficient Nkx2.5 mutant in Nkx2.5 haploinsufficient mice leads to congenital heart defects.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Zebrafish in Cardiovascular Disease Research: from Model to Application.International journal of biological sciences · 2026Review
- Downregulation of SENP1 impairs nuclear condensation of MEF2C and deteriorates ischemic cardiomyopathy.Clinical and translational medicine · 2025Article
- Sumoylation-deficient phosphoglycerate mutase 2 impairs myogenic differentiation.Frontiers in cell and developmental biology · 2022Article
- Role of Posttranslational Modifications of Proteins in Cardiovascular Disease.Oxidative medicine and cellular longevity · 2022Review
- The Function of SUMOylation and Its Critical Roles in Cardiovascular Diseases and Potential Clinical Implications.International journal of molecular sciences · 2021Review
- SUMO proteins in the cardiovascular system: friend or foe?Journal of biomedical science · 2020Review
- Contribution of Increased Expression of Yin Yang 2 to Development of Cardiomyopathy.Frontiers in molecular biosciences · 2020Article
- A deficiency in SUMOylation activity disrupts multiple pathways leading to neural tube and heart defects in Xenopus embryos.BMC genomics · 2019Article
- Developing Practical Therapeutic Strategies that Target Protein SUMOylation.Current drug targets · 2019Review
- Neddylation mediates ventricular chamber maturation through repression of Hippo signaling.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Ubiquitin and Ubiquitin-like proteins in cardiac disease and protection.Current drug targets · 2018Review
- The CSRP2BP histone acetyltransferase drives smooth muscle gene expression.Nucleic acids research · 2017Article
- SIRT1 deacetylates the cardiac transcription factor Nkx2.5 and inhibits its transcriptional activity.Scientific reports · 2016Article
- SUMO proteomics to decipher the SUMO-modified proteome regulated by various diseases.Proteomics · 2015Review
- Class I HDAC inhibition stimulates cardiac protein SUMOylation through a post-translational mechanism.Cellular signalling · 2014Article
- SUMOylation: a novel protein quality control modifier in the heart.Circulation research · 2014Article
- Functional decorations: post-translational modifications and heart disease delineated by targeted proteomics.Genome medicine · 2013Review
- Enhanced desumoylation in murine hearts by overexpressed SENP2 leads to congenital heart defects and cardiac dysfunction.Journal of molecular and cellular cardiology · 2012Article
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7 authors.
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Abstract
Nkx2.5 is a cardiac specific homeobox gene critical for normal heart development. We previously identified Nkx2.5 as a target of sumoylation, a posttranslational modification implicated in a variety of cellular activities. Sumoylation enhanced Nkx2.5 activity via covalent attachment to the lysine residue 51, the primary SUMO acceptor site. However, how sumoylation regulates the activity of Nkx2.5 in vivo remains unknown. We generated transgenic mice overexpressing sumoylation deficient mutant K51R (conversion of lysine 51 to arginine) specifically in mouse hearts under the control of cardiac α-myosin heavy chain (α-MHC) promoter (K51R-Tg). Expression of the Nkx2.5 mutant transgene in the wild type murine hearts did not result in any overt cardiac phenotype. However, in the presence of Nkx2.5 haploinsufficiency, cardiomyocyte-specific expression of the Nkx2.5 K51R mutant led to congenital heart diseases (CHDs), accompanied with decreased cardiomyocyte proliferation. Also, a number of human CHDs-associated Nkx2.5 mutants exhibited aberrant sumoylation. Our work demonstrates that altered sumoylation status may underlie the development of human CHDs associated with Nkx2.5 mutants.
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