有哪些信誉好的足球投注网站a splice site mutation in laminin-α2 results in a severe muscular dystrophy and growth abnormalities in zebrafish剪切位点突变在laminin-α2结果严重的肌肉萎缩症和斑马鱼的增长异常.pdfVIP
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a splice site mutation in laminin-α2 results in a severe muscular dystrophy and growth abnormalities in zebrafish剪切位点突变在laminin-α2结果严重的肌肉萎缩症和斑马鱼的增长异常
A Splice Site Mutation in Laminin-a2 Results in a Severe
Muscular Dystrophy and Growth Abnormalities in
Zebrafish
1 1 1 2 3
Vandana A. Gupta , Genri Kawahara , Jennifer A. Myers , Aye T. Chen , Thomas E. Hall , M.
1 3 2 2,4 1 1
Chiara Manzini , Peter D. Currie , Yi Zhou , Leonard I. Zon , Louis M. Kunkel , Alan H. Beggs *
1 Genomics Program and Division of Genetics, Boston Children’s Hospital, Harvard Medical School, The Manton Center for Orphan Disease Research, Boston,
Massachusetts, United States of America, 2 Stem Cell Program and Pediatric Hematology/Oncology, Boston Children’s Hospital and Dana Farber Cancer Institute, Harvard
Stem Cell Institute, Harvard Medical School, Boston, Massachusetts, United States of America, 3 Australian Regenerative Medicine Institute, Monash University, Clayton
Campus, Victoria, Australia, 4 Howard Hughes Medical Institute, San Francisco, California, United States of America
Abstract
Congenital muscular dystrophy (CMD) is a clinically and genetically heterogeneous group of inherited muscle disorders. In
patients, muscle weakness is usually present at or shortly after birth and is progressive in nature. Merosin deficient
congenital muscular dystrophy (MDC1A) is a form of CMD caused by a defect in the laminin-a2 gene (LAMA2). Laminin-a2 is
an extracellular matrix protein that interacts with the dystrophin-dystroglycan (DGC) complex in membranes providing
stability to muscle fibers. In an N-ethyl-N-nitrosourea mutagenesis screen to develop zebrafish models of neuromuscular
diseases, we identified a mutant fish that exhibit
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