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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
MeSH Review


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Disease relevance of Myoblasts

  • We have tested the ability of a recombinant adenovirus, containing a 6.3 kilobase pair Becker-like dystrophin complementary DNA driven by the Rous sarcoma virus promoter to direct the expression of a 'minidystrophin' in infected 293 cells and C2 myoblasts, and in the mdx mouse, after intramuscular injection [1].
  • The fate of injected myoblasts was assessed by coinfecting the cells with two retroviral vectors, one encoding hGH and the other encoding beta-galactosidase from Escherichia coli [2].
  • Myositis autoantigen expression is also markedly increased in several cancers known to be associated with autoimmune myositis, but not in their related normal tissues, demonstrating that tumor cells and undifferentiated myoblasts are antigenically similar [3].
  • At or near the time of prefusion, it becomes concentrated between adjacent aligned myoblasts and localized on membrane "blebs". H36 is present on both skeletal and cardiac cells but absent from a variety of cells that include fibroblasts, neuronal cells, and smooth muscle [4].
  • Three distinct types of adhesive behavior are seen in short term (1 h) assays, typified by secondary murine fibroblasts, adherent only on fibronectin; secondary murine myoblasts, adherent on fibronectin, laminin, and the E8 fragment; and Rugli human glioblastoma cells, adherent on fibronectin, laminin, E8, and E1-4 [5].

Psychiatry related information on Myoblasts


High impact information on Myoblasts

  • Expression of ubo is induced by Hedgehog (Hh) signaling in prospective slow muscle precursors, and its activity alone is sufficient to direct slow-twitch fiber-specific development by naive myoblasts [7].
  • Accordingly, a dominant-negative ARF6 disrupts myoblast fusion in Drosophila embryos and in mammalian myoblasts in culture, mimicking the fusion defects caused by loss of Loner [8].
  • IL-4 acts as a myoblast recruitment factor during mammalian muscle growth [9].
  • Pavlath and coworkers demonstrate a novel role for Interleukin-4 (IL-4) in regulating the fusion of myoblasts with differentiated myotubes [10].
  • Loner and ARF6, which also control the proper membrane localization of another small GTPase, Rac, are key components of a cellular apparatus required for myoblast fusion and muscle development [8].

Chemical compound and disease context of Myoblasts


Biological context of Myoblasts


Anatomical context of Myoblasts

  • Protein synthetic patterns of DMSO-inhibited cells are almost indistinguishable from those of untreated myoblasts and distinct from differentiated myotubes [21].
  • 5-azacytidine treatment of mouse C3H10T1/2 embryonic fibroblasts converts them to myoblasts at a frequency suggesting alteration of one or only a few closely linked regulatory loci [22].
  • During differentiation of embryonic chick skeletal muscle in culture, elaboration of acetylcholine receptor (AChR) and acetylcholinesterase occurs shortly after myoblast fusion [23].
  • IL-4 is expressed by a subset of muscle cells in fusing muscle cultures and requires the IL-4alpha receptor subunit on myoblasts to promote fusion and growth [9].
  • We show here that DMAHP expression in myoblasts, muscle and myocardium is reduced by the DM mutation is cis, and the magnitude of this effect depends on the extent of CTG repeat expansion [24].

Associations of Myoblasts with chemical compounds

  • Competitive interference of endogenous SET domain-dsPTPase interactions by forced expression of Sbf1 induced oncogenic transformation of NIH 3T3 fibroblasts and impaired the in vitro differentiation of C2 myoblast cells [25].
  • Replicating chicken embryo myoblasts were treated with a monoclonal antibody, CSAT, which recognizes and blocks the function of the beta subunit of integrin [26].
  • Myogenin is absent in undifferentiated cells, peaks, and then declines following a stimulus to differentiate, and is overexpressed in myoblasts selected with 5-bromodeoxyuridine for the overproduction of factors that regulate the decision to differentiate [27].
  • Control of myoblast fusion by a guanine nucleotide exchange factor, loner, and its effector ARF6 [8].
  • After a 1 hr pulse of dense amino acids and 3H-lysine, nucleosomes were isolated from chick myoblast organ cultures, and the histones were cross-linked to octamers [28].

Gene context of Myoblasts

  • Over-expression of MLP in C2 myoblasts potentiates myogenic differentiation and reduces its sensitivity to TGF beta [29].
  • The paired box transcription factor Pax7 was isolated by representational difference analysis as a gene specifically expressed in cultured satellite cell-derived myoblasts [30].
  • Finally, the biological activity of Jagged was tested using a cell culture assay in which Jagged activates rat Notch1 expressed in myoblasts and prevents muscle cell differentiation [31].
  • Replacement of the missing protein, dystrophin, using myoblast transfer in humans or viral/liposomal delivery in the mouse DMD model is inefficient and short-lived [32].
  • We report here the identification and characterization of a new gene, sem-5 (sem, sex muscle abnormal), that acts both in vulval induction and in sex myoblast migration [33].

Analytical, diagnostic and therapeutic context of Myoblasts


  1. Efficient adenovirus-mediated transfer of a human minidystrophin gene to skeletal muscle of mdx mice. Ragot, T., Vincent, N., Chafey, P., Vigne, E., Gilgenkrantz, H., Couton, D., Cartaud, J., Briand, P., Kaplan, J.C., Perricaudet, M. Nature (1993) [Pubmed]
  2. Systemic delivery of human growth hormone by injection of genetically engineered myoblasts. Dhawan, J., Pan, L.C., Pavlath, G.K., Travis, M.A., Lanctot, A.M., Blau, H.M. Science (1991) [Pubmed]
  3. Enhanced autoantigen expression in regenerating muscle cells in idiopathic inflammatory myopathy. Casciola-Rosen, L., Nagaraju, K., Plotz, P., Wang, K., Levine, S., Gabrielson, E., Corse, A., Rosen, A. J. Exp. Med. (2005) [Pubmed]
  4. Expression of a developmentally regulated antigen on the surface of skeletal and cardiac muscle cells. Kaufman, S.J., Foster, R.F., Haye, K.R., Faiman, L.E. J. Cell Biol. (1985) [Pubmed]
  5. Two distinct cell-binding domains in laminin can independently promote nonneuronal cell adhesion and spreading. Goodman, S.L., Deutzmann, R., von der Mark, K. J. Cell Biol. (1987) [Pubmed]
  6. Nitric oxide synthase gene therapy for erectile dysfunction: comparison of plasmid, adenovirus, and adenovirus-transduced myoblast vectors. Tirney, S., Mattes, C.E., Yoshimura, N., Yokayama, T., Ozawa, H., Tzeng, E., Birder, L.A., Kanai, A.J., Huard, J., de Groat, W.C., Chancellor, M.B. Molecular urology. (2001) [Pubmed]
  7. The B-cell maturation factor Blimp-1 specifies vertebrate slow-twitch muscle fiber identity in response to Hedgehog signaling. Baxendale, S., Davison, C., Muxworthy, C., Wolff, C., Ingham, P.W., Roy, S. Nat. Genet. (2004) [Pubmed]
  8. Control of myoblast fusion by a guanine nucleotide exchange factor, loner, and its effector ARF6. Chen, E.H., Pryce, B.A., Tzeng, J.A., Gonzalez, G.A., Olson, E.N. Cell (2003) [Pubmed]
  9. IL-4 acts as a myoblast recruitment factor during mammalian muscle growth. Horsley, V., Jansen, K.M., Mills, S.T., Pavlath, G.K. Cell (2003) [Pubmed]
  10. Fusion with the fused: a new role for interleukin-4 in the building of muscle. Chargé, S., Rudnicki, M.A. Cell (2003) [Pubmed]
  11. Adaptive myogenesis under hypoxia. Yun, Z., Lin, Q., Giaccia, A.J. Mol. Cell. Biol. (2005) [Pubmed]
  12. Specific induction of cell motility on laminin by alpha 7 integrin. Echtermeyer, F., Schöber, S., Pöschl, E., von der Mark, H., von der Mark, K. J. Biol. Chem. (1996) [Pubmed]
  13. Cell-surface changes during in vitro differentiation of pluripotent embryonal carcinoma cells. Muramatsu, H., Hamada, H., Noguchi, S., Kamada, Y., Muramatsu, T. Dev. Biol. (1985) [Pubmed]
  14. Pilot study of myoblast transfer in the treatment of Becker muscular dystrophy. Neumeyer, A.M., Cros, D., McKenna-Yasek, D., Zawadzka, A., Hoffman, E.P., Pegoraro, E., Hunter, R.G., Munsat, T.L., Brown, R.H. Neurology (1998) [Pubmed]
  15. Turnover of beta 1- and beta 2-adrenergic receptors after down-regulation or irreversible blockade. Neve, K.A., Molinoff, P.B. Mol. Pharmacol. (1986) [Pubmed]
  16. The synthesis and distribution of desmin and vimentin during myogenesis in vitro. Gard, D.L., Lazarides, E. Cell (1980) [Pubmed]
  17. Dynamics of demethylation and activation of the alpha-actin gene in myoblasts. Paroush, Z., Keshet, I., Yisraeli, J., Cedar, H. Cell (1990) [Pubmed]
  18. Human muscle neural cell adhesion molecule (N-CAM): identification of a muscle-specific sequence in the extracellular domain. Dickson, G., Gower, H.J., Barton, C.H., Prentice, H.M., Elsom, V.L., Moore, S.E., Cox, R.D., Quinn, C., Putt, W., Walsh, F.S. Cell (1987) [Pubmed]
  19. Tissue-specific splicing in vivo of the beta-tropomyosin gene: dependence on an RNA secondary structure. Libri, D., Piseri, A., Fiszman, M.Y. Science (1991) [Pubmed]
  20. Prevention of islet allograft rejection with engineered myoblasts expressing FasL in mice. Lau, H.T., Yu, M., Fontana, A., Stoeckert, C.J. Science (1996) [Pubmed]
  21. Manipulation of myogenesis in vitro: reversible inhibition by DMSO. Blau, H.M., Epstein, C.J. Cell (1979) [Pubmed]
  22. Expression of a single transfected cDNA converts fibroblasts to myoblasts. Davis, R.L., Weintraub, H., Lassar, A.B. Cell (1987) [Pubmed]
  23. Appearance and disappearance of acetycholine receptor during differentiation of chick skeletal muscle in vitro. Prives, J., Silman, I., Amsterdam, A. Cell (1976) [Pubmed]
  24. Expansion of the myotonic dystrophy CTG repeat reduces expression of the flanking DMAHP gene. Thornton, C.A., Wymer, J.P., Simmons, Z., McClain, C., Moxley, R.T. Nat. Genet. (1997) [Pubmed]
  25. Association of SET domain and myotubularin-related proteins modulates growth control. Cui, X., De Vivo, I., Slany, R., Miyamoto, A., Firestein, R., Cleary, M.L. Nat. Genet. (1998) [Pubmed]
  26. Occupation of the extracellular matrix receptor, integrin, is a control point for myogenic differentiation. Menko, A.S., Boettiger, D. Cell (1987) [Pubmed]
  27. Myogenin, a factor regulating myogenesis, has a domain homologous to MyoD. Wright, W.E., Sassoon, D.A., Lin, V.K. Cell (1989) [Pubmed]
  28. Conservative assembly and segregation of nucleosomal histones. Leffak, I.M., Grainger, R., Weintraub, H. Cell (1977) [Pubmed]
  29. Muscle LIM protein, a novel essential regulator of myogenesis, promotes myogenic differentiation. Arber, S., Halder, G., Caroni, P. Cell (1994) [Pubmed]
  30. Pax7 is required for the specification of myogenic satellite cells. Seale, P., Sabourin, L.A., Girgis-Gabardo, A., Mansouri, A., Gruss, P., Rudnicki, M.A. Cell (2000) [Pubmed]
  31. Jagged: a mammalian ligand that activates Notch1. Lindsell, C.E., Shawber, C.J., Boulter, J., Weinmaster, G. Cell (1995) [Pubmed]
  32. Amelioration of the dystrophic phenotype of mdx mice using a truncated utrophin transgene. Tinsley, J.M., Potter, A.C., Phelps, S.R., Fisher, R., Trickett, J.I., Davies, K.E. Nature (1996) [Pubmed]
  33. C. elegans cell-signalling gene sem-5 encodes a protein with SH2 and SH3 domains. Clark, S.G., Stern, M.J., Horvitz, H.R. Nature (1992) [Pubmed]
  34. Gene targeting in normal somatic cells: inactivation of the interferon-gamma receptor in myoblasts. Arbonés, M.L., Austin, H.A., Capon, D.J., Greenburg, G. Nat. Genet. (1994) [Pubmed]
  35. Interaction and functional collaboration of p300/CBP and bHLH proteins in muscle and B-cell differentiation. Eckner, R., Yao, T.P., Oldread, E., Livingston, D.M. Genes Dev. (1996) [Pubmed]
  36. Successful histocompatible myoblast transplantation in dystrophin-deficient mdx mouse despite the production of antibodies against dystrophin. Vilquin, J.T., Wagner, E., Kinoshita, I., Roy, R., Tremblay, J.P. J. Cell Biol. (1995) [Pubmed]
  37. Expression of nuclear lamin A and muscle-specific proteins in differentiating muscle cells in ovo and in vitro. Lourim, D., Lin, J.J. J. Cell Biol. (1989) [Pubmed]
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