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Duchenne muscular dystrophy (DMD) is a severely debilitating and lethal disease affecting approximately 1in 3,500 male births. In a seminal discovery, the Rudnicki lab discovered that deficits in muscle stem cell asymmetric divisions is a part of the underlying mechanism that results in the progressive wasting of skeletal muscles found in DMD. Dystrophin protein, the DMD disease gene, is primarily expressed in skeletal and cardiac muscle. DMD-deficient satellite cells exhibit a 10-fold reduction in the number of asymmetric satellite stem cell divisions that dramatically decreases the generation of myogenic progenitors needed for efficient muscle regeneration. The balance between self-renewal and differentiation of muscle progenitors is regulated by DMD during embryonic and/or fetal myogenic differentiation. TO BE CONT’D
Michael Rudnicki
Université de Lyon 1
Life Sciences
Education
University of Ottawa
Globalink Research Award
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