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.

MYOCARDIN

Smooth muscle cells (SM) and cardiac muscle cells-specific transcriptional factor which uses the canonical single or multiple CArG boxes DNA sequence. Acts as a cofactor of serum response factor (SRF) with the potential to modulate SRF-target genes. Plays a crucial role in cardiogenesis, urinary bladder development, and differentiation of the smooth muscle cell lineage (myogenesis) (By similarity).

Cardiac muscle cell differentiation Source: BHF-UCL
Cardiac ventricle development Source: Ensembl
Cardiocyte differentiation Source: UniProtKB
Cellular component maintenance Source: Ensembl
Digestive tract development Source: Ensembl
Ductus arteriosus closure Source: Ensembl
Lung alveolus development Source: Ensembl
Negative regulation of amyloid-beta clearance Source: BHF-UCL
Negative regulation of cardiac muscle cell apoptotic process Source: Ensembl
Negative regulation of cell adhesion molecule production Source: Ensembl
Negative regulation of cell population proliferation Source: BHF-UCL
Negative regulation of cyclin-dependent protein serine/threonine kinase activity Source: BHF-UCL
Negative regulation of myotube differentiation Source: Ensembl
Negative regulation of platelet-derived growth factor receptor-beta signaling pathway Source: Ensembl
Negative regulation of skeletal muscle cell differentiation Source: BHF-UCL
Negative regulation of transcription by RNA polymerase II Source: Ensembl
Negative regulation of vascular associated smooth muscle cell migration Source: Ensembl
Negative regulation of vascular associated smooth muscle cell proliferation Source: Ensembl
Positive regulation of cardiac muscle cell differentiation Source: BHF-UCL
Positive regulation of cardiac vascular smooth muscle cell differentiation Source: BHF-UCL
Positive regulation of cell population proliferation Source: Ensembl
Positive regulation of DNA binding Source: Ensembl
Positive regulation of DNA-binding transcription factor activity Source: BHF-UCL
Positive regulation of gene expression Source: Ensembl
Positive regulation of miRNA transcription Source: Ensembl
Positive regulation of smooth muscle cell differentiation Source: BHF-UCL
Positive regulation of smooth muscle contraction Source: BHF-UCL
Positive regulation of transcription, DNA-templated Source: UniProtKB
Positive regulation of transcription by RNA polymerase II Source: BHF-UCL
Positive regulation of transcription from RNA polymerase II promoter involved in myocardial precursor cell differentiation Source: BHF-UCL
Positive regulation of transcription from RNA polymerase II promoter involved in smooth muscle cell differentiation Source: BHF-UCL
Positive regulation of transforming growth factor beta receptor signaling pathway Source: Ensembl
Regulation of cell growth by extracellular stimulus Source: Ensembl
Regulation of histone acetylation Source: UniProtKB
Regulation of myoblast differentiation Source: Ensembl
Regulation of phenotypic switching Source: Ensembl
Regulation of smooth muscle cell differentiation Source: BHF-UCL
Response to hypoxia Source: BHF-UCL
Smooth muscle cell differentiation Source: BHF-UCL
Urinary bladder development Source: UniProtKB
Uterus development Source: Ensembl
Vascular associated smooth muscle cell differentiation Source: Ensembl
Vasculogenesis Source: Ensembl
Ventricular cardiac muscle cell differentiation Source: Ensembl

Nucleus

Megabladder, congenital (MGBL):
An autosomal dominant congenital anomaly characterized by a massively dilated urinary bladder with disrupted smooth muscle in the bladder wall. MGBL is a sex-limited trait with 95% male predominance, and incomplete penetrance. Affected males frequently die in utero.

Phosphorylation regulates negatively the intrinsic myocardin transcriptional activity.