ArticleMolecular and cellular biology1996
Recruitment of the tinman homolog Nkx-2.5 by serum response factor activates cardiac alpha-actin gene transcription.
Article in Molecular and cellular biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
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82 citing papers in PubMed, 274 citations in OpenAlex.
- Effect of resistance exercise contraction mode and protein supplementation on members of the STARS signalling pathway.The Journal of physiology · 2013Trial
- Is the Cis-Element CACCC-Box a Master Regulatory Element during Cardiovascular Disease? A Bioinformatics Approach from the Perspective of the Krüppel-like Family of Transcription Factors.Life (Basel, Switzerland) · 2024Article
- Mutant SRF and YAP1 remodel the chromatin to entice cardiac myocyte nuclear division.The journal of cardiovascular aging · 2022Article
- SRF: a seriously responsible factor in cardiac development and disease.Journal of biomedical science · 2022Review
- Second heart field-specific expression of Nkx2-5 requires promoter proximal interaction with Srf.Mechanisms of development · 2020Article
- Novel mutations of the SRF gene in Chinese sporadic conotruncal heart defect patients.BMC medical genetics · 2020Article
- GRAF3 serves as a blood volume-sensitive rheostat to control smooth muscle contractility and blood pressure.Small GTPases · 2020Article
- Druggable targets in the Rho pathway and their promise for therapeutic control of blood pressure.Pharmacology & therapeutics · 2019Review
- Heart morphogenesis gene regulatory networks revealed by temporal expression analysis.Development (Cambridge, England) · 2017Article
- Generation of Nkx2-5/CreER transgenic mice for inducible Cre expression in developing hearts.Genesis (New York, N.Y. : 2000) · 2017Article
- SIRT1 deacetylates the cardiac transcription factor Nkx2.5 and inhibits its transcriptional activity.Scientific reports · 2016Article
- Identification and expression of SRF targeted by miR-133a during early development of Paralichthys olivaceus.Fish physiology and biochemistry · 2015Article
- Signaling Pathways and Gene Regulatory Networks in Cardiomyocyte Differentiation.Tissue engineering. Part B, Reviews · 2015Review
- Regulation of Connective Tissue Growth Factor and Cardiac Fibrosis by an SRF/MicroRNA-133a Axis.PloS one · 2015Article
- The functional diversity of essential genes required for mammalian cardiac development.Genesis (New York, N.Y. : 2000) · 2014Review
- Co-activation of nuclear factor-κB and myocardin/serum response factor conveys the hypertrophy signal of high insulin levels in cardiac myoblasts.The Journal of biological chemistry · 2014Article
- Inositol polyphosphate multikinase is a coactivator for serum response factor-dependent induction of immediate early genes.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Lrrc10 is a novel cardiac-specific target gene of Nkx2-5 and GATA4.Journal of molecular and cellular cardiology · 2013Article
- Evolutionary conservation of Nkx2.5 autoregulation in the second heart field.Developmental biology · 2013Article
- An intragenic SRF-dependent regulatory motif directs cardiac-specific microRNA-1-1/133a-2 expression.PloS one · 2013Article
22 more citing papers are in PubMed but not listed here.
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2 authors at 1 institution in 1 country.
Funding
Abstract
We recently showed that the cardiogenic homeodomain factor Nkx-2.5 served as a positive acting accessory factor for serum response factor (SRF) and that together they provided strong transcriptional activation of the cardiac alpha-actin promoter, depending upon intact serum response elements (SREs) (C. Y. Chen, J. Croissant, M. Majesky, S. Topouz, T. McQuinn, M. J. Frankovsky, and R. J. Schwartz, Dev. Genet. 19:119-130, 1996). As shown here, Nkx-2.5 and SRF collaborated to activate the endogenous murine cardiac alpha-actin gene in 10T1/2 fibroblasts by a mechanism in which SRF recruited Nkx-2.5 to the alpha-actin promoter. Activation of a truncated promoter consisting of the proximal alpha-actin SRE1 occurred even when Nkx-2.5 DNA-binding activity was blocked by a point mutation in the third helix of its homeodomain. Investigation of protein-protein interactions showed that Nkx-2.5 was bound to SRF in the absence of DNA in soluble protein complexes retrieved from cardiac myocyte nuclei but could also be detected in coassociated binding complexes on the proximal SRE1. Recruitment of Nkx-2.5 to an SRE depended upon SRF DNA-binding activity and was blocked by the dominant negative SRFpm1 mutant, which allowed for dimerization of SRF monomers but prevented DNA binding. Interactive regions shared by Nkx-2.5 and SRF were mapped to N-terminal/helix I and helix II/helix III regions of the Nkx-2.5 homeodomain and to the N-terminal extension of the MADS box. Our study suggests that physical association between Nkx-2.5 and SRF is one way that cardiac specified genes are activated in cardiac cell lineages.
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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.