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Expression of a Dominant Negative CELF Protein In Vivo Leads to Altered Muscle Organization, Fiber Size, and Subtype

By Dara S. Berger, Michelle Moyer, Gregory M. Kliment, Erik van Lunteren and Andrea N. Ladd
Topics: Research Article
Publisher: Public Library of Science
OAI identifier: oai:pubmedcentral.nih.gov:3082560
Provided by: PubMed Central

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  1. (2005). A dynamic balance between activation and repression regulates pre-mRNA alternative splicing during heart development.
  2. (2003). A functional deadenylation assay identifies human CUG-BP as a deadenylation factor.
  3. (2003). A muscleblind knockout model for myotonic dystrophy.
  4. (2008). A postnatal switch of CELF and MBNL1 proteins reprograms alternative splicing in the developing heart.
  5. (2001). Aberrant regulation of insulin receptor alternative splicing is associated with insulin resistance in myotonic dystrophy.
  6. (1995). Activation of the myogenin promoter during mouse embryogenesis in the absence of positive autoregulation.
  7. (1997). Altered phosphorylation and intracellular distribution of a (CUG)n triplet repeat RNAbinding protein in patients with myotonic dystrophy and in myotonin protein kinase knockout mice.
  8. (2008). Alternative isoform regulation in human tissue transcriptomes.
  9. (1992). An unstable triplet repeat in a gene related to myotonic muscular dystrophy.
  10. (2005). Cardiac-specific repression of CELF activity disrupts alternative splicing and causes cardiomyopathy.
  11. (2009). CELF-mediated alternative splicing is required for cardiac function during early, but not later, postnatal life.
  12. (2008). Deep surveying of alternative splicing complexity in the human transcriptome by high-throughput sequencing.
  13. (1998). Disruption of splicing regulated by a CUG-binding protein in myotonic dystrophy.
  14. (2002). Dynamic antagonism between ETR-3 and PTB regulates cell type-specific alternative splicing.
  15. (1998). EDEN and EDEN-BP, a cis element and an associated factor that mediate sequence-specific mRNA deadenylation in xenopus embryos.
  16. (2004). EDEN-BP-dependent post-transcriptional regulation of gene expression in Xenopus somitic segmentation.
  17. (2007). Elevation of RNA-binding protein CUGBP1 is an early event in an inducible heart-specific mouse model of myotonic dystrophy.
  18. (1999). Etr-1, a homologue of a protein linked to myotonic dystrophy, is essential for muscle development in caenorhabditis elegans.
  19. (2008). Expanded CTG repeats within the DMPK 3’ UTR causes severe skeletal muscle wasting in an inducible mouse model for myotonic dystrophy.
  20. (2006). Failure of MBNL1-dependent post-natal splicing transitions in myotonic dystrophy.
  21. (2010). Heartspecific overexpression of CUGBP1 reproduces functional and molecular abnormalities of myotonic dystrophy type 1.
  22. (2007). Inactivation of CUG-BP1/CELF1 causes growth, viability, and spermatogenesis defects in mice.
  23. (2007). Increased steady-state levels of CUGBP1 in myotonic dystrophy 1 are due to PKC-mediated hyperphosphorylation.
  24. (2007). Ladd A
  25. (2002). Loss of the muscle-specific chloride channel in type 1 myotonic dystrophy lead to misregulated alternative splicing.
  26. (1992). Mapping of myogenin transcription during embryogenesis using transgenes linked to the myogenin control region.
  27. (2001). Mice transgenic for the human myotonic dystrophy region with expanded CTG repeats display muscular and brain abnormalities.
  28. (2010). MicroRNAs coordinate an alternative splicingnetwork duringmouse postnatalheart development.GenesDev.
  29. (2006). Misregulation of alternative splicing causes pathogenesis in myotonic dystrophy.
  30. (2001). Molecular basis for impaired muscle differentiation in myotonic dystrophy.
  31. (1992). Molecular basis of myotonic dystrophy - expansion of a trinucleotide (CTG) repeat at the 3’ end of a transcript encoding a protein kinase family member.
  32. (1994). Muscle histopathology in myotonic dystrophy in relation to age and muscular weakness.
  33. (1992). Myotonic dystrophy mutation - an unstable CTG repeat in the 3’ untranslated region of the gene.
  34. (2004). Overexpression of CUG triplet repeat-binding protein, CUGBP1, in mice inhibits myogenesis.
  35. (2007). Physical continuity of the perimysium from myofibers to tendons: Involvement in lateral force transmission in skeletal muscle.
  36. (2001). RNA CUG repeats sequester CUGBP1 and alter protein levels and activity of CUGBP1.
  37. (2001). The CELF family of RNA binding proteins is implicated in cell-specific and developmentally regulated alternative splicing.
  38. (2005). Transgenic mice expressing CUG-BP1 reproduce splicing mis-regulation observed in myotonic dystrophy.