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Gene Review

MYOCD  -  myocardin

Homo sapiens

Synonyms: MYCD, Myocardin
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Disease relevance of MYOCD


Psychiatry related information on MYOCD

  • Thus, SRF-MYOCD overexpression in small cerebral arteries appears to initiate independently of Abeta a pathogenic pathway mediating arterial hypercontractility and CBF dysregulation, which are associated with Alzheimer's dementia [5].

High impact information on MYOCD

  • One of the most exciting recent discoveries was the identification of the serum response factor (SRF) coactivator gene myocardin that appears to be required for expression of many SMC differentiation marker genes, and for initial differentiation of SMC during development [6].
  • Using a bioinformatics-based screen for unknown cardiac-specific genes, we identified a novel and highly potent transcription factor, named myocardin, that is expressed in cardiac and smooth muscle cells [7].
  • Activation of cardiac gene expression by myocardin, a transcriptional cofactor for serum response factor [7].
  • Expression of a dominant negative mutant of myocardin in Xenopus embryos interferes with myocardial cell differentiation [7].
  • Myocardin belongs to the SAP domain family of nuclear proteins and activates cardiac muscle promoters by associating with SRF [7].

Chemical compound and disease context of MYOCD


Biological context of MYOCD


Anatomical context of MYOCD

  • Whereas myocardin is expressed specifically in cardiac and smooth muscle cells, MRTF-A and -B are expressed in numerous embryonic and adult tissues [11].
  • Together, these data were consistent with a model wherein MKL1 transduces signals from the cytoskeleton to the nucleus in SMCs and regulates SRF-dependent SMC differentiation autonomously or in concert with myocardin [8].
  • Its ability to transactivate smooth muscle-specific genes has been firmly established in animal cells but its effect on heart muscle genes has been investigated less extensively and the consequences of ectopic myocardin expression in human cells are unknown [1].
  • OBJECTIVE: Myocardin is a coactivator of serum response factor (SRF) required for vascular smooth muscle cell (VSMC) differentiation [9].
  • Myocardin Sumoylation Transactivates Cardiogenic Genes in Pluripotent 10T1/2 Fibroblasts [12].

Associations of MYOCD with chemical compounds

  • Here, we found that myocardin's activity was strongly enhanced by SUMO-1 via modification of a lysine residue primarily located at position 445 and that the conversion of this residue to arginine (K445R) impaired myocardin transactivation [12].
  • Importantly, TRAM-34 completely blocked PDGF-BB-induced suppression of SMMHC, SMalphaA, smoothelin-B, and myocardin and inhibited PDGF-BB-stimulated migration by approximately 50% [13].
  • 5. Zipzap/p200 activated the promoter of cardiac genes and potentiated the effect of myocardin on ANF promoter activity [14].
  • We found that myocardin mRNA expression is upregulated significantly in the hypoxic pulmonary vessels and cultured cells but downregulated in PH with Sildenafil treatment [2].
  • Interestingly, inactivation of RhoA with C3-exoenzyme or treatment with ROK inhibitors strongly inhibited myocardin mRNA expression in retinoic acid-treated A404 cells or human iliac vein SMCs [4].

Physical interactions of MYOCD

  • Myocardin and myocardin-related transcription factors (MRTFs) interact with SRF and potently stimulate SRF-dependent transcription [15].

Regulatory relationships of MYOCD


Other interactions of MYOCD


Analytical, diagnostic and therapeutic context of MYOCD


  1. Activation of cardiac and smooth muscle-specific genes in primary human cells after forced expression of human myocardin. van Tuyn, J., Knaän-Shanzer, S., van de Watering, M.J., de Graaf, M., van der Laarse, A., Schalij, M.J., van der Wall, E.E., de Vries, A.A., Atsma, D.E. Cardiovasc. Res. (2005) [Pubmed]
  2. Transdifferentiation of pulmonary arteriolar endothelial cells into smooth muscle-like cells regulated by myocardin involved in hypoxia-induced pulmonary vascular remodelling. Zhu, P., Huang, L., Ge, X., Yan, F., Wu, R., Ao, Q. International journal of experimental pathology (2006) [Pubmed]
  3. Myocardin induces cardiomyocyte hypertrophy. Xing, W., Zhang, T.C., Cao, D., Wang, Z., Antos, C.L., Li, S., Wang, Y., Olson, E.N., Wang, D.Z. Circ. Res. (2006) [Pubmed]
  4. LPP expression during in vitro smooth muscle differentiation and stent-induced vascular injury. Gorenne, I., Jin, L., Yoshida, T., Sanders, J.M., Sarembock, I.J., Owens, G.K., Somlyo, A.P., Somlyo, A.V. Circ. Res. (2006) [Pubmed]
  5. Serum response factor and myocardin mediate arterial hypercontractility and cerebral blood flow dysregulation in Alzheimer's phenotype. Chow, N., Bell, R.D., Deane, R., Streb, J.W., Chen, J., Brooks, A., Van Nostrand, W., Miano, J.M., Zlokovic, B.V. Proc. Natl. Acad. Sci. U.S.A. (2007) [Pubmed]
  6. Molecular regulation of vascular smooth muscle cell differentiation in development and disease. Owens, G.K., Kumar, M.S., Wamhoff, B.R. Physiol. Rev. (2004) [Pubmed]
  7. Activation of cardiac gene expression by myocardin, a transcriptional cofactor for serum response factor. Wang, D., Chang, P.S., Wang, Z., Sutherland, L., Richardson, J.A., Small, E., Krieg, P.A., Olson, E.N. Cell (2001) [Pubmed]
  8. Megakaryoblastic leukemia factor-1 transduces cytoskeletal signals and induces smooth muscle cell differentiation from undifferentiated embryonic stem cells. Du, K.L., Chen, M., Li, J., Lepore, J.J., Mericko, P., Parmacek, M.S. J. Biol. Chem. (2004) [Pubmed]
  9. HERP1 inhibits myocardin-induced vascular smooth muscle cell differentiation by interfering with SRF binding to CArG box. Doi, H., Iso, T., Yamazaki, M., Akiyama, H., Kanai, H., Sato, H., Kawai-Kowase, K., Tanaka, T., Maeno, T., Okamoto, E., Arai, M., Kedes, L., Kurabayashi, M. Arterioscler. Thromb. Vasc. Biol. (2005) [Pubmed]
  10. Myocardin is a critical serum response factor cofactor in the transcriptional program regulating smooth muscle cell differentiation. Du, K.L., Ip, H.S., Li, J., Chen, M., Dandre, F., Yu, W., Lu, M.M., Owens, G.K., Parmacek, M.S. Mol. Cell. Biol. (2003) [Pubmed]
  11. Potentiation of serum response factor activity by a family of myocardin-related transcription factors. Wang, D.Z., Li, S., Hockemeyer, D., Sutherland, L., Wang, Z., Schratt, G., Richardson, J.A., Nordheim, A., Olson, E.N. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  12. Myocardin Sumoylation Transactivates Cardiogenic Genes in Pluripotent 10T1/2 Fibroblasts. Wang, J., Li, A., Wang, Z., Feng, X., Olson, E.N., Schwartz, R.J. Mol. Cell. Biol. (2007) [Pubmed]
  13. Upregulation of intermediate-conductance Ca2+-activated K+ channel (IKCa1) mediates phenotypic modulation of coronary smooth muscle. Tharp, D.L., Wamhoff, B.R., Turk, J.R., Bowles, D.K. Am. J. Physiol. Heart Circ. Physiol. (2006) [Pubmed]
  14. Zipzap/p200 is a novel zinc finger protein contributing to cardiac gene regulation. Zhang, X., Azhar, G., Zhong, Y., Wei, J.Y. Biochem. Biophys. Res. Commun. (2006) [Pubmed]
  15. Control of smooth muscle development by the myocardin family of transcriptional coactivators. Wang, D.Z., Olson, E.N. Curr. Opin. Genet. Dev. (2004) [Pubmed]
  16. Myocardin/MKL family of SRF coactivators: key regulators of immediate early and muscle specific gene expression. Cen, B., Selvaraj, A., Prywes, R. J. Cell. Biochem. (2004) [Pubmed]
  17. Coactivation of MEF2 by the SAP domain proteins myocardin and MASTR. Creemers, E.E., Sutherland, L.B., Oh, J., Barbosa, A.C., Olson, E.N. Mol. Cell (2006) [Pubmed]
  18. Bone morphogenetic protein-induced MSX1 and MSX2 inhibit myocardin-dependent smooth muscle gene transcription. Hayashi, K., Nakamura, S., Nishida, W., Sobue, K. Mol. Cell. Biol. (2006) [Pubmed]
  19. Fine-tuning in Ca2+ homeostasis underlies progression of cardiomyopathy in myocytes derived from genetically modified embryonic stem cells. Grey, C., Méry, A., Pucéat, M. Hum. Mol. Genet. (2005) [Pubmed]
  20. Jagged1-selective Notch Signaling Induces Smooth Muscle Differentiation via a RBP-J{kappa}-dependent Pathway. Doi, H., Iso, T., Sato, H., Yamazaki, M., Matsui, H., Tanaka, T., Manabe, I., Arai, M., Nagai, R., Kurabayashi, M. J. Biol. Chem. (2006) [Pubmed]
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