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Maged1, a new regulator of skeletal myogenic differentiation and muscle regeneration

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Abstract
Background: In normal adult skeletal muscle, cell turnover is very slow. However, after an acute lesion or in chronic pathological conditions, such as primary myopathies, muscle stem cells, called satellite cells, are induced to proliferate, then withdraw definitively from the cell cycle and fuse to reconstitute functional myofibers. Results: We show that Maged1 is expressed at very low levels in normal adult muscle but is strongly induced after injury, during the early phase of myoblast differentiation. By comparing in vitro differentiation of myoblasts derived from wild-type or Maged1 knockout mice, we observed that Maged1 deficiency results in reduced levels of p21(CIP1/WAF1), defective cell cycle exit and impaired myotube maturation. In vivo, this defect results in delayed regeneration of injured muscle. Conclusions: These data demonstrate for the first time that Maged1 is an important factor required for proper skeletal myoblast differentiation and muscle healing.
Keywords
CELL-CYCLE ARREST, GENE-EXPRESSION, DNA-BINDING, RETINOBLASTOMA PROTEIN, NEUROTROPHIN RECEPTOR, NECDIN INTERACTS, CDK INHIBITORS, FAMILY PROTEIN, IN-VIVO, MYOD

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Chicago
Nguyen, Tuan HN, Mathieu Bertrand, Christiane Sterpin, Younes Achouri, and Olivier RY De Backer. 2010. “Maged1, a New Regulator of Skeletal Myogenic Differentiation and Muscle Regeneration.” Bmc Cell Biology 11.
APA
Nguyen, T. H., Bertrand, M., Sterpin, C., Achouri, Y., & De Backer, O. R. (2010). Maged1, a new regulator of skeletal myogenic differentiation and muscle regeneration. BMC CELL BIOLOGY, 11.
Vancouver
1.
Nguyen TH, Bertrand M, Sterpin C, Achouri Y, De Backer OR. Maged1, a new regulator of skeletal myogenic differentiation and muscle regeneration. BMC CELL BIOLOGY. 2010;11.
MLA
Nguyen, Tuan HN, Mathieu Bertrand, Christiane Sterpin, et al. “Maged1, a New Regulator of Skeletal Myogenic Differentiation and Muscle Regeneration.” BMC CELL BIOLOGY 11 (2010): n. pag. Print.
@article{3025286,
  abstract     = {Background: In normal adult skeletal muscle, cell turnover is very slow. However, after an acute lesion or in chronic pathological conditions, such as primary myopathies, muscle stem cells, called satellite cells, are induced to proliferate, then withdraw definitively from the cell cycle and fuse to reconstitute functional myofibers.
Results: We show that Maged1 is expressed at very low levels in normal adult muscle but is strongly induced after injury, during the early phase of myoblast differentiation. By comparing in vitro differentiation of myoblasts derived from wild-type or Maged1 knockout mice, we observed that Maged1 deficiency results in reduced levels of p21(CIP1/WAF1), defective cell cycle exit and impaired myotube maturation. In vivo, this defect results in delayed regeneration of injured muscle.
Conclusions: These data demonstrate for the first time that Maged1 is an important factor required for proper skeletal myoblast differentiation and muscle healing.},
  articleno    = {57},
  author       = {Nguyen, Tuan HN and Bertrand, Mathieu and Sterpin, Christiane and Achouri, Younes and De Backer, Olivier RY},
  issn         = {1471-2121},
  journal      = {BMC CELL BIOLOGY},
  keyword      = {CELL-CYCLE ARREST,GENE-EXPRESSION,DNA-BINDING,RETINOBLASTOMA PROTEIN,NEUROTROPHIN RECEPTOR,NECDIN INTERACTS,CDK INHIBITORS,FAMILY PROTEIN,IN-VIVO,MYOD},
  language     = {eng},
  pages        = {9},
  title        = {Maged1, a new regulator of skeletal myogenic differentiation and muscle regeneration},
  url          = {http://dx.doi.org/10.1186/1471-2121-11-57},
  volume       = {11},
  year         = {2010},
}

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