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Myocardin, Myocd
This gene encodes a nuclear protein, which is expressed in heart, aorta, and in smooth muscle cell-containing tissues. It functions as a transcriptional co-activator of serum response factor (SRF) and modulates expression of cardiac and smooth muscle-specific SRF-target genes, and thus may play a crucial role in cardiogenesis and differentiation of the smooth muscle cell lineage. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.[provided by RefSeq, Sep 2009] (from NCBI)
Top mentioned proteins: serum response factor, Actin, MUC4, V1a, CAN
Papers on Myocardin
Targeted exome sequencing profiles genetic alterations in leiomyosarcoma.
Singer et al., New York City, United States. In Genes Chromosomes Cancer, Feb 2016
FISH analysis showed amplification of the myocardin (MYOCD) gene in 5 of 25 (20%) cases analyzed.
Myocardin-related Transcription Factor Regulates Nox4 Protein Expression: LINKING CYTOSKELETAL ORGANIZATION TO REDOX STATE.
Kapus et al., Copenhagen, Denmark. In J Biol Chem, Feb 2016
Myocardin-related transcription factor (MRTF), a Rho/actin polymerization-controlled coactivator of serum response factor, drives myofibroblast transition from various precursors.
Myocardin-related transcription factors are required for cardiac development and function.
Bassel-Duby et al., Dallas, United States. In Dev Biol, Nov 2015
Myocardin-Related Transcription Factors A and B (MRTF-A and MRTF-B) are highly homologous proteins that function as powerful coactivators of serum response factor (SRF), a ubiquitously expressed transcription factor essential for cardiac development.
Requirement of miR-9-dependent regulation of Myocd in PASMCs phenotypic modulation and proliferation induced by hepatopulmonary syndrome rat serum.
Lu et al., Chongqing, China. In J Cell Mol Med, Oct 2015
Myocardin, a robust transcriptional coactivator of serum response factor, plays a critical role in the vascular smooth muscle cell phenotypic switch.
Endothelial depletion of murine SRF/MRTF provokes intracerebral hemorrhagic stroke.
Nordheim et al., Tübingen, Germany. In Proc Natl Acad Sci U S A, Sep 2015
Cerebral microbleeds and larger hemorrhages developed upon postnatal and adult depletion of either SRF or its cofactors Myocardin Related Transcription Factor (MRTF-A/-B), revealing essential requirements of ongoing SRF/MRTF activity for maintenance of cerebral small vessel integrity.
Myocardin in biology and disease.
Miano, Rochester, United States. In J Biomed Res, 2015
Myocardin (MYOCD) is a potent transcriptional coactivator that functions primarily in cardiac muscle and smooth muscle through direct contacts with serum response factor (SRF) over cis elements known as CArG boxes found near a number of genes encoding for contractile, ion channel, cytoskeletal, and calcium handling proteins.
Myocardin Family Members Drive Formation of Caveolae.
Swärd et al., Lund, Sweden. In Plos One, 2014
Myocardin (MYOCD) and its relative MRTF-A (MKL1) are transcriptional coactivators that control genes which promote smooth muscle differentiation.
miR-27 and miR-125 Distinctly Regulate Muscle-Enriched Transcription Factors in Cardiac and Skeletal Myocytes.
Franco et al., Jaén, Spain. In Biomed Res Int, 2014
Overexpression of miR-27 leads to impair expression of Mstn and Myocd in HL1 atrial cardiomyocytes but not in Sol8 skeletal muscle myoblasts, while overexpression of miR-125 resulted in selective upregulation of Mef2d in HL1 atrial cardiomyocytes and downregulation in Sol8 cells.
A MicroRNA-Transcription Factor Blueprint for Early Atrial Arrhythmogenic Remodeling.
Mikhailov et al., A Coruña, Spain. In Biomed Res Int, 2014
MicroRNA (miRNA) transcriptome and expression of candidate transcription factors (TFs) with potential roles in arrhythmogenesis, such as Pitx2, Tbx5, and myocardin (Myocd), were analyzed by microarray, qRT-PCR, and Western blotting in left atrial (LA) samples from pigs with transitory AF established by right atrial tachypacing.
Myocardin and smooth muscle differentiation.
Zheng, Calgary, Canada. In Arch Biochem Biophys, 2014
Myocardin (MYOCD), a co-transcriptional activator of serum response factor (SRF), stimulates the expression of smooth muscle (SM) genes and inhibits the cell cycle.
Blood-borne circadian signal stimulates daily oscillations in actin dynamics and SRF activity.
Schibler et al., Genève, Switzerland. In Cell, 2013
Our data suggest that in mouse liver SRF is regulated via dramatic diurnal changes of actin dynamics, leading to the rhythmic translocation of the SRF coactivator Myocardin-related transcription factor-B (MRTF-B) into the nucleus.
Atorvastatin inhibits myocardin expression in vascular smooth muscle cells.
Zheng et al., Calgary, Canada. In Hypertension, 2012
Data shsow that atorvastatin (ATV) inhibits myocardin gene expression in vivo and in vitro, suggesting a novel mechanism for ATV inhibition of vascular contraction.
Yap1 protein regulates vascular smooth muscle cell phenotypic switch by interaction with myocardin.
Chen et al., Ann Arbor, United States. In J Biol Chem, 2012
down-regulation of Yap1 promotes VSMC contractile phenotype by both up-regulating myocardin expression
Cooperation of myocardin and Smad2 in inducing differentiation of mesenchymal stem cells into smooth muscle cells.
Zhang et al., Tianjin, China. In Iubmb Life, 2012
site-direct mutation analysis of SM22alpha promoter demonstrated that myocardin and Smad2 coactivated SM22alpha promoter mainly depending on CArG box and less on smad binding elements sites
Urokinase receptor associates with myocardin to control vascular smooth muscle cells phenotype in vascular disease.
Dumler et al., Hannover, Germany. In Arterioscler Thromb Vasc Biol, 2012
Nuclear uPAR associates with myocardin, which is then recruited from the promoters of serum response factor target genes and undergoes proteasomal degradation. This mechanism contributes to adverse vascular remodeling after injury in vivo.
Transforming growth factor-β1-induced transcript 1 protein, a novel marker for smooth muscle contractile phenotype, is regulated by serum response factor/myocardin protein.
Zhou et al., Albany, United States. In J Biol Chem, 2012
Transforming growth factor-beta1-induced transcript 1 protein, a novel marker for smooth muscle contractile phenotype, is regulated by serum response factor/myocardin protein.
The imbalance of vascular molecules in Alzheimer's disease.
Bell, Rochester, United States. In J Alzheimers Dis, 2011
In particular, the vascular-specific transcription factors MEOX2, MYOCD, and SRF, genetic risk factor APOE4, transport proteins LRP1 and RAGE, and circulating molecules such as sLRP1, homocysteine, and albumin are discussed.
A regulatory pathway involving Notch1/beta-catenin/Isl1 determines cardiac progenitor cell fate.
Srivastava et al., San Francisco, United States. In Nat Cell Biol, 2009
Notch1 positively, and beta-catenin negatively, regulated expression of the cardiac transcription factors, Isl1, Myocd and Smyd1.
SRF and myocardin regulate LRP-mediated amyloid-beta clearance in brain vascular cells.
Zlokovic et al., Rochester, United States. In Nat Cell Biol, 2009
We suggest that SRF and MYOCD function as a transcriptional switch, controlling Abeta cerebrovascular clearance and progression of AD.
Role of the blood-brain barrier in the pathogenesis of Alzheimer's disease.
Zlokovic et al., Rochester, United States. In Curr Alzheimer Res, 2007
In addition, we have identified two vascularly restricted genes, GAX (growth arrest-specific homeobox), which controls LRP1 expression in brain capillaries and brain angiogenesis, and MYOCD (myocardin), which controls contractility of cerebral arterial smooth muscle cells and influences cerebral blood flow.
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