ArticleThe Journal of biological chemistry2010
Repression of smooth muscle differentiation by a novel high mobility group box-containing protein, HMG2L1.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- A novel mouse model carrying a gene trap insertion into the Hmgxb4 gene locus to examine Hmgxb4 expression in vivo.Physiological reports · 2024Article
- Regulation of DNA damage and transcriptional output in the vasculature through a cytoglobin-HMGB2 axis.Redox biology · 2023Article
- HMGXB4 TargetsInternational journal of molecular sciences · 2023Article
- Article
- Purine-rich element binding protein B attenuates the coactivator function of myocardin by a novel molecular mechanism of smooth muscle gene repression.Molecular and cellular biochemistry · 2021Article
- Deficiency of the novel high mobility group protein HMGXB4 protects against systemic inflammation-induced endotoxemia in mice.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- YY1 directly interacts with myocardin to repress the triad myocardin/SRF/CArG box-mediated smooth muscle gene transcription during smooth muscle phenotypic modulation.Scientific reports · 2020Article
- Transcription factor TEAD1 is essential for vascular development by promoting vascular smooth muscle differentiation.Cell death and differentiation · 2019Article
- Possible Muscle Repair in the Human Cardiovascular System.Stem cell reviews and reports · 2017Review
- Myocardin in biology and disease.Journal of biomedical research · 2015Review
- The transcription factor TEAD1 represses smooth muscle-specific gene expression by abolishing myocardin function.The Journal of biological chemistry · 2014Article
- SOX9 and myocardin counteract each other in regulating vascular smooth muscle cell differentiation.Biochemical and biophysical research communications · 2012Article
- Transforming growth factor-β1-induced transcript 1 protein, a novel marker for smooth muscle contractile phenotype, is regulated by serum response factor/myocardin protein.The Journal of biological chemistry · 2011Article
- Signaling mechanisms that regulate smooth muscle cell differentiation.Arteriosclerosis, thrombosis, and vascular biology · 2011Review
- Vascular smooth muscle progenitor cells: building and repairing blood vessels.Circulation research · 2011Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The molecular mechanisms regulating smooth muscle-specific gene expression during smooth muscle development are poorly understood. Myocardin is an extraordinarily powerful cofactor of serum response factor (SRF) that stimulates expression of smooth muscle-specific genes. In an effort to search for proteins that regulate myocardin function, we identified a novel HMG box-containing protein HMG2L1 (high mobility group 2 like 1). We found that HMG2L1 expression is correlated with the smooth muscle cell (SMC) synthetic phenotype. Overexpression of HMG2L1 in SMCs down-regulated smooth muscle marker expression. Conversely, depletion of endogenous HMG2L1 in SMCs increases smooth muscle-specific gene expression. Furthermore, we found HMG2L1 specifically abrogates myocardin-induced activation of smooth muscle-specific genes. By GST pulldown assays, the interaction domains between HMG2L1 and myocardin were mapped to the N termini of each of the proteins. Finally, we demonstrated that HMG2L1 abrogates myocardin function through disrupting its binding to SRF and abolishing SRF-myocardin complex binding to the promoters of smooth muscle-specific genes. This study provides the first evidence of this novel HMG2L1 molecule playing an important role in attenuating smooth muscle differentiation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.