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myocardin is an essential component of the regulatory pathway for myocardial differentiation
several transcription factors, that is SRF, myocardin, and GATA6, that induce the expression of SM-MHC in animal cap cells
Study shows that vascular endothelial growth factor A stimulates STAT3 activity via nitrosylation of myocardin to regulate the expression of vascular smooth muscle cell differentiation markers.
conditional knockout models have revealed a critical role for myocardin during cardiac chamber maturation, and a surprising function for myocardin in the regulation of cardiomyocyte proliferation, cell death, and possibly mitochondrial function.
YAP negatively regulates differentiation of Vascular smooth muscle cells (VSMCs) derived from cardiovascular progenitor cell (CVPC) by decreasing transcription of myocardin in a NKX2.5-dependent manner.
Myocardin inhibits estrogen receptor alpha-mediated proliferation of human breast cancer cells via regulating MicroRNA expression.
Key role for miR-214 in modulation of MEF2C-MYOCD-LMOD1 signaling.
Study demonstrates that myocardin indirectly down-regulates Cx43 through its repressive action on miR-206 to regulate vascular smooth muscle cell phenotypic switch.
These results have revealed the roles for atrogin-1 in the regulation of smooth muscle contractility through enhancement of myocardin ubiquitylation/degradation and its transcriptional activity.
our study reveals that Ang II downregulates miR-145 to regulate Klf4 and myocardin expression in HCASMCs under high glucose conditions. Ang II plays a critical role in the regulation of miR-145 under hyperglycemic conditions
Human expression data disclosed correlations of MYOCD with CAV1 in a majority of human tissues and in the heart, correlation with MKL2 (MRTF-B) was observed.
inhibition of GSK-3beta reduces myocardin transcriptional activity, suggesting a role for GSK-3beta in myocardin transcriptional activity and smooth muscle differentiation
STAT3 protein regulates vascular smooth muscle cell phenotypic switch by interaction with myocardin and SRF.
TMEM16A and myocardin form a positive feedback loop that is disrupted by KLF5 during Ang II-induced vascular remodeling.
TNFalpha differentially regulates myocardin expression and activity
Propose myocardin as a guardian of the contractile, noninflammatory VSMC phenotype, with loss of myocardin representing a critical permissive step in the process of phenotypic transition and inflammatory activation, at the onset of vascular disease.
it is probably that miR135b promotes proliferation, invasion and migration of osteosarcoma cells by degrading myocardin
Early cardiac marker gene myocardin levels in peripheral blood mononuclear cells reflect severity in stable coronary artery disease.
Myocardin meditates apoptosis in breast cancer through affecting maspin re-expression and epigenetic modification.
the first evidence demonstrating that TEAD1 is a novel general repressor of smooth muscle-specific gene expression through interfering with myocardin binding to SRF.
ChIP analysis established that PDGF-BB-induced repression of Myocd gene expression is most likely regulated by enhanced binding of Klf4 and Klf5 to a lesser extent, to the PRR of PrmM
The dynamic expression of Sox9 and the interaction between TSHZ3, SOX9 and MYOCD provide a mechanism that regulates the pace the myogenic program in the ureter.
P53 promotes retinoid acid-induced smooth muscle cell differentiation by targeting myocardin.
Long noncoding RNAs cardiac autophagy inhibitory factor (lncRNA CAIF) regulates autophagy through controlling p53 and myocardin.
TAZ and MyoC856 physically interact. SynergyTAZ and Myocardin (MyoC856), in regulating smooth muscle gene activation was observed in primary aortic vascular smooth muscle cells.
two MEF2 sites in the enhancer function cooperatively due to bridging of the MEF2C-bound sites by the SAP domain-containing co-activator protein myocardin
c-Myb regulates proliferation/differentiation of adventitial Sca1+ vascular smooth muscle progenitor cells by transcriptional activation of myocardin.
Knock down of the serum response factor (SRF), which mediates many of the effects of myocardin, decreased cavin-1 but increased caveolin-1 and -2 mRNAs.
Cholesterol loading of vascular smooth muscle cells converts them to a macrophage-appearing state by downregulating the miR-143/145-myocardin axis.
Our data illustrate a novel mechanism that connects MRTF-A dependent histone H3K4 methylation to HSC activation.
DKK3 induces stem cell differentiation into smooth muscle lineage via ATF6 signaling and myocardin expression.
Myocardin has a critical role in maintenance of vascular and visceral smooth muscle homeostasis during postnatal development
Foxf2 attenuated myocardin/serum response factor signaling in smooth muscle cells through direct binding to the N-terminal region of myocardin
The authors describe the of a Cre knock-in into the Myocardin locus and show that Myocardin expression marks the earliest cardiac and smooth muscle lineages.
KLF4 is a regulator of cardiac hypertrophy by modulating the expression and the activity of myocardin.
Insulin potentiates TNF-alpha in inducing NF-kappaB and SRF/SRE activities. In hyperinsulinemic states, myocardin may act as a nuclear effector of insulin, promoting cardiac hypertrophy.
Data indicate that Nkx2-5, Tbx5, Gata4, or Myocd alone did not induce the de novo expression of cardiac marker proteins in 10T1/2 non-myoblastic cells.
Expression of myocardin-A (and TERT) promotes promyogenic gene expression in mesenchymal stem cells.
Data indicate that interferon regulatory factor 8 (IRF8) inhibited smooth muscle cells (SMCs) marker gene expression through regulating serum response factor (SRF) transactivation in a myocardin-dependent manner.
a moderate inhibition (e.g., normalization) of the activated MYOCD signaling in the diseased heart may be promising from a therapeutic point of view
MYOCD DeltaExon 11 may participate in modulating smooth muscle cell phenotype, potentially acting as a dominant-negative repressor of contraction-related genes.
Data show that forced myocd-A expression in the LVFW caused abnormal ECG.
Thrombin stimulates swine smooth muscle cell differentiation from peripheral blood mononuclear cells via protease-activated receptor-1, RhoA, and myocardin.
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.
, SRF co-factor protein (cardiac and smooth muscle)
, SRF cofactor protein
, basic SAP coiled-coil transcription activator 2
, transcription factor myocardin