Research LettersNew possibilities for prenatal diagnosis of muscular dystrophies: forced myogenesis with an adenoviral MyoD-vector
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Cited by (13)
Transcription factor rational design improves directed differentiation of human mesenchymal stem cells into skeletal myocytes
2011, Molecular TherapyCitation Excerpt :These findings complement studies on the enhanced contribution of fibroblasts14,15 and mesoangioblasts of patients affected by inclusion-body myositis8 to skeletal muscle cell formation upon ectopic MyoD expression. MyoD-mediated myogenic conversion of nonmuscle cells is also used for the molecular diagnosis of muscular dystrophies, in particular DMD, as a way of bypassing the constraints associated with limited human muscle availability.16,17,18,19,20 For the same reason, MyoD-forced myogenesis is applied in the testing of exon skipping therapy for DMD.21
Dystrophinopathy carrier determination and detection of protein deficiencies in muscular dystrophy using lentiviral MyoD-forced myogenesis
2007, Neuromuscular DisordersCitation Excerpt :Overexpression of MyoD in non-muscle cells produces fused multi-nucleated myotubes with well-defined sarcomeric structure, morphologically indistinguishable from their muscle-derived counterparts. Studies by Sancho and Roest have highlighted the potential of MyoD-forced myogenesis for prenatal diagnosis of Duchenne muscular dystrophy (DMD) by either direct immunohistochemical detection of dystrophin [8], or as a source of muscle-specific cDNA for use in a protein truncation test [9,10]. In the latter case, identification of a nonsense mutation resulting in a premature stop codon was then used for prenatal diagnosis of Duchenne muscular dystrophy in a subsequent pregnancy.
Adenoviral mediated MyoD gene transfer into fibroblasts: Myogenic disease diagnosis
2006, Brain and DevelopmentMyoD-induced reprogramming of human fibroblasts and urinary stem cells in vitro: protocols and their applications
2023, Frontiers in PhysiologyLack of Myostatin Reduces MyoD Induced Myogenic Potential of Primary Muscle Fibroblasts
2014, Journal of Cellular Biochemistry