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Gene Review

Cdh15  -  cadherin 15

Mus musculus

Synonyms: AI323380, Cadherin-14, Cadherin-15, Cdh14, M cadherin, ...
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Disease relevance of Cdh15


High impact information on Cdh15

  • The numbers of satellite cells detected in this way are significantly greater than those identified by the other three markers.We conclude that the expression of CD34, Myf5, and M-cadherin defines quiescent, committed precursors and speculate that the CD34(-ve), Myf5(-ve) minority may be involved in maintaining the lineage-committed majority [2].
  • Expression of M-cadherin, a member of the cadherin multigene family, correlates with differentiation of skeletal muscle cells [3].
  • M-cadherin mRNA is present at low levels in myoblasts and is upregulated in myotube-forming cells [3].
  • Here we report the identification and characterization of the cDNA of another member of the cadherin family, M-cadherin (M for muscle), from differentiating muscle cells [3].
  • In mouse L cells (fibroblasts), M-cadherin mRNA is undetectable [3].

Biological context of Cdh15


Anatomical context of Cdh15


Associations of Cdh15 with chemical compounds

  • Mcad positive cells in normal and denervated muscles did not incorporate bromodeoxyuridine within 24 hr after injection in vivo, indicating that Mcad is expressed on mitotically quiescent satellite cells [4].
  • Following muscle denervation no evidence was found for re-expression of M-cadherin under conditions where there was strong expression of the nicotinic acetylcholine receptor on myofibres [6].
  • (1) Analysis by laser scan microscopy revealed that the destruction of microtubules by nocodazole leads to an altered cell surface distribution of M-cadherin in differentiating myogenic cells [8].

Physical interactions of Cdh15


Co-localisations of Cdh15


Regulatory relationships of Cdh15


Other interactions of Cdh15


Analytical, diagnostic and therapeutic context of Cdh15

  • The expression of Mcad was studied by immunofluorescence in regenerating, denervated, and normal mouse muscles [4].
  • Based on its expression pattern and observations in cell culture, it has been postulated that M-cadherin may be important for the fusion of myoblasts to form myotubes, the correct localization and function of satellite cells during muscle regeneration, and the specialized architecture of adhering junctions in granule cells of cerebellar glomeruli [12].
  • The spatiotemporal distribution of M-cadherin mRNA has been determined by in situ hybridization in the mouse embryo and in adult skeletal muscle following experimental regeneration and denervation [6].
  • Using a multiplex single-cell RT-PCR assay we simultaneously monitored expression of all four MyoD family regulators of muscle determination and differentiation (MRFs) together with two candidate markers of satellite cell identity, c-met and m-cadherin [13].
  • Serial frozen sections were prepared for immunohistochemistry using specific antibodies to M-cadherin, myoD, Myogenin, myosin heavy chain, and alfa-actin molecule [14].


  1. Upregulation and redistribution of cadherins reveal specific glial and muscle cell phenotypes during wallerian degeneration and muscle denervation in the mouse. Padilla, F., Marc Mège, R., Sobel, A., Nicolet, M. J. Neurosci. Res. (1999) [Pubmed]
  2. Expression of CD34 and Myf5 defines the majority of quiescent adult skeletal muscle satellite cells. Beauchamp, J.R., Heslop, L., Yu, D.S., Tajbakhsh, S., Kelly, R.G., Wernig, A., Buckingham, M.E., Partridge, T.A., Zammit, P.S. J. Cell Biol. (2000) [Pubmed]
  3. Expression of M-cadherin, a member of the cadherin multigene family, correlates with differentiation of skeletal muscle cells. Donalies, M., Cramer, M., Ringwald, M., Starzinski-Powitz, A. Proc. Natl. Acad. Sci. U.S.A. (1991) [Pubmed]
  4. Expression pattern of M-cadherin in normal, denervated, and regenerating mouse muscles. Irintchev, A., Zeschnigk, M., Starzinski-Powitz, A., Wernig, A. Dev. Dyn. (1994) [Pubmed]
  5. Identification of imprinted loci by methylation-sensitive representational difference analysis: application to mouse distal chromosome 2. Kelsey, G., Bodle, D., Miller, H.J., Beechey, C.V., Coombes, C., Peters, J., Williamson, C.M. Genomics (1999) [Pubmed]
  6. The cell adhesion molecule M-cadherin is specifically expressed in developing and regenerating, but not denervated skeletal muscle. Moore, R., Walsh, F.S. Development (1993) [Pubmed]
  7. Localized deposition of M-cadherin in the glomeruli of the granular layer during the postnatal development of mouse cerebellum. Bahjaoui-Bouhaddi, M., Padilla, F., Nicolet, M., Cifuentes-Diaz, C., Fellmann, D., Mege, R.M. J. Comp. Neurol. (1997) [Pubmed]
  8. The M-cadherin catenin complex interacts with microtubules in skeletal muscle cells: implications for the fusion of myoblasts. Kaufmann, U., Kirsch, J., Irintchev, A., Wernig, A., Starzinski-Powitz, A. J. Cell. Sci. (1999) [Pubmed]
  9. M-cadherin activates Rac1 GTPase through the Rho-GEF trio during myoblast fusion. Charrasse, S., Comunale, F., Fortier, M., Portales-Casamar, E., Debant, A., Gauthier-Rouvière, C. Mol. Biol. Cell (2007) [Pubmed]
  10. Distinct location and prevalence of alpha-, beta-catenins and gamma-catenin/plakoglobin in developing and denervated skeletal muscle. Cifuentes-Diaz, C., Goudou, D., Mège, R.M., Velasco, E., Nicolet, M., Herrenknecht, K., Rubin, L., Rieger, F. Cell Adhes. Commun. (1998) [Pubmed]
  11. Cadherins M, 11, and 6 expression patterns suggest complementary roles in mouse neuromuscular axis development. Padilla, F., Broders, F., Nicolet, M., Mege, R.M. Mol. Cell. Neurosci. (1998) [Pubmed]
  12. The cell adhesion molecule M-cadherin is not essential for muscle development and regeneration. Hollnagel, A., Grund, C., Franke, W.W., Arnold, H.H. Mol. Cell. Biol. (2002) [Pubmed]
  13. Single-cell analysis of regulatory gene expression in quiescent and activated mouse skeletal muscle satellite cells. Cornelison, D.D., Wold, B.J. Dev. Biol. (1997) [Pubmed]
  14. Impaired expression of myogenic regulatory molecules in the pelvic floor muscles of murine embryos with anorectal malformations. Aoi, S., Shimotake, T., Tsuda, T., Deguchi, E., Iwai, N. J. Pediatr. Surg. (2005) [Pubmed]
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