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注意:仅列出部分参考文献,下载原文获取全部文献信息。Heart-specific overexpression of CUGBP1 reproduces functional and molecular abnormalities of myotonic dystrophy type 1
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CELF-mediated alternative splicing is required for cardiac function during early, but not later, postnatal life
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Expanded CTG repeats within the DMPK 3′ UTR causes severe skeletal muscle wasting in an inducible mouse model for myotonic dystrophy
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A postnatal switch of CELF and MBNL proteins reprograms alternative splicing in the developing heart
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Increased steady-state in levels of CUGBP1 in myotonic dystrophy 1 are due to PKC-mediated hyperphosphorylation
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Elevation of RNA-binding protein CUGBP1 is an early event in an inducible heart-specific mouse model of myotonic dystrophy
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Failure of MBNL1-dependent post-natal splicing transitions in myotonic dystrophy
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Dynamic balance between activation and repression regulates pre-mRNA alternative splicing during heart development
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Cardiac tissue-specific repression of CELF activity disrupts alternative splicing and causes cardiomyopathy
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Transgenic mice expressing CUG-BP1 reproduce splicing mis-regulation observed in myotonic dystrophy
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Overexpression of CUG triplet repeat-binding protein, CUGBP1, in mice inhibits myogenesis
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Loss of the muscle-specific chloride channel in type 1 myotonic dystrophy due to misregulated alternative splicing
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RNA CUG repeats sequester CUGBP1 and alter protein levels and activity of CUGBP1
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The CELF family of RNA binding proteins is implicated in cell-specific and developmentally regulated alternative splicing
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