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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
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 (show YAP1 Antibodies) negatively regulates differentiation of Vascular smooth muscle cells (VSMCs) derived from cardiovascular progenitor cell (CVPC) by decreasing transcription of myocardin in a NKX2.5 (show NKX2-5 Antibodies)-dependent manner.
Myocardin inhibits estrogen receptor alpha (show ESR1 Antibodies)-mediated proliferation of human breast cancer cells via regulating MicroRNA expression.
Key role for miR (show MLXIP Antibodies)-214 in modulation of MEF2C (show MEF2C Antibodies)-MYOCD-LMOD1 (show LMOD1 Antibodies) signaling.
Study demonstrates that myocardin indirectly down-regulates Cx43 (show GJA1 Antibodies) through its repressive action on miR (show MLXIP Antibodies)-206 to regulate vascular smooth muscle cell phenotypic switch.
These results have revealed the roles for atrogin-1 (show FBXO32 Antibodies) in the regulation of smooth muscle contractility through enhancement of myocardin ubiquitylation/degradation and its transcriptional activity.
our study reveals that Ang II (show AGT Antibodies) downregulates miR (show MLXIP Antibodies)-145 to regulate Klf4 (show KLF4 Antibodies) and myocardin expression in HCASMCs under high glucose conditions. Ang II (show AGT Antibodies) plays a critical role in the regulation of miR (show MLXIP Antibodies)-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.
Long noncoding RNAs cardiac autophagy inhibitory factor (lncRNA CAIF) regulates autophagy through controlling p53 (show TP53 Antibodies) and myocardin.
TAZ (show TAZ Antibodies) 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 (show MEF2C Antibodies) sites in the enhancer function cooperatively due to bridging of the MEF2C (show MEF2C Antibodies)-bound sites by the SAP (show APCS Antibodies) domain-containing co-activator protein myocardin
c-Myb (show MYB Antibodies) regulates proliferation/differentiation of adventitial Sca1 (show ATXN1 Antibodies)+ 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 (show MLXIP Antibodies)-143/145-myocardin axis.
Our data illustrate a novel mechanism that connects MRTF-A (show MKL1 Antibodies) dependent histone H3K4 methylation to HSC (show FUT1 Antibodies) activation.
DKK3 (show DKK3 Antibodies) induces stem cell differentiation into smooth muscle lineage via ATF6 (show ATF6 Antibodies) signaling and myocardin expression.
TMEM16A (show ANO1 Antibodies) and myocardin form a positive feedback loop that is disrupted by KLF5 (show KLF5 Antibodies) during Ang II (show AGT Antibodies)-induced vascular remodeling.
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 (show F2 Antibodies) stimulates swine smooth muscle cell differentiation from peripheral blood mononuclear cells via protease-activated receptor-1 (show F2R Antibodies), RhoA (show RHOA Antibodies), 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