Literature DB >> 15623702

Truncated ClC-1 mRNA in myotonic dystrophy exerts a dominant-negative effect on the Cl current.

Jim Berg1, Hong Jiang, Charles A Thornton, Stephen C Cannon.   

Abstract

BACKGROUND: Muscle fiber degeneration and myotonic discharges are the hallmarks of myotonic dystrophy (DM). The molecular basis for the myotonia was recently tied to abnormal splicing of the chloride channel (ClC-1) pre-mRNA, often resulting in UAG premature termination, which leads to decreased channel protein and therefore a reduced resting chloride conductance.
METHODS: The authors assessed the functional properties of two commonly occurring DM mRNA splice variants by expression in oocytes.
RESULTS: Neither splice variant coded for a functional Cl- channel. Co-injection of alternative splice variants with wild-type ClC-1 cRNA reduced the current density and accelerated channel closure upon repolarization of the membrane.
CONCLUSIONS: These data show that the aberrantly spliced chloride channel message exerts a dominant negative effect that may contribute to the development of myotonia.

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Year:  2004        PMID: 15623702     DOI: 10.1212/01.wnl.0000148482.40683.88

Source DB:  PubMed          Journal:  Neurology        ISSN: 0028-3878            Impact factor:   9.910


  14 in total

1.  Muscle weakness in myotonic dystrophy associated with misregulated splicing and altered gating of Ca(V)1.1 calcium channel.

Authors:  Zhen Zhi Tang; Viktor Yarotskyy; Lan Wei; Krzysztof Sobczak; Masayuki Nakamori; Katy Eichinger; Richard T Moxley; Robert T Dirksen; Charles A Thornton
Journal:  Hum Mol Genet       Date:  2011-12-02       Impact factor: 6.150

2.  Ribonuclear foci at the neuromuscular junction in myotonic dystrophy type 1.

Authors:  T M Wheeler; M C Krym; C A Thornton
Journal:  Neuromuscul Disord       Date:  2007-02-15       Impact factor: 4.296

3.  Muscle chloride channel dysfunction in two mouse models of myotonic dystrophy.

Authors:  John D Lueck; Ami Mankodi; Maurice S Swanson; Charles A Thornton; Robert T Dirksen
Journal:  J Gen Physiol       Date:  2006-12-11       Impact factor: 4.086

4.  Targeted splice sequencing reveals RNA toxicity and therapeutic response in myotonic dystrophy.

Authors:  Matthew K Tanner; Zhenzhi Tang; Charles A Thornton
Journal:  Nucleic Acids Res       Date:  2021-02-26       Impact factor: 16.971

Review 5.  Recent advances in myotonic dystrophy type 2.

Authors:  Christina M Ulane; Sarah Teed; Jacinda Sampson
Journal:  Curr Neurol Neurosci Rep       Date:  2014-02       Impact factor: 5.081

6.  Huntington disease skeletal muscle is hyperexcitable owing to chloride and potassium channel dysfunction.

Authors:  Christopher W Waters; Grigor Varuzhanyan; Robert J Talmadge; Andrew A Voss
Journal:  Proc Natl Acad Sci U S A       Date:  2013-05-13       Impact factor: 11.205

7.  Correction of ClC-1 splicing eliminates chloride channelopathy and myotonia in mouse models of myotonic dystrophy.

Authors:  Thurman M Wheeler; John D Lueck; Maurice S Swanson; Robert T Dirksen; Charles A Thornton
Journal:  J Clin Invest       Date:  2007-12       Impact factor: 14.808

8.  Identification of Plant-derived Alkaloids with Therapeutic Potential for Myotonic Dystrophy Type I.

Authors:  Ruben Herrendorff; Maria Teresa Faleschini; Adeline Stiefvater; Beat Erne; Tatiana Wiktorowicz; Frances Kern; Matthias Hamburger; Olivier Potterat; Jochen Kinter; Michael Sinnreich
Journal:  J Biol Chem       Date:  2016-06-13       Impact factor: 5.157

9.  Molecular Effects of the CTG Repeats in Mutant Dystrophia Myotonica Protein Kinase Gene.

Authors:  Beatriz Llamusí; Ruben Artero
Journal:  Curr Genomics       Date:  2008-12       Impact factor: 2.236

10.  MBNL and CELF proteins regulate alternative splicing of the skeletal muscle chloride channel CLCN1.

Authors:  Yoshihiro Kino; Chika Washizu; Yoko Oma; Hayato Onishi; Yuriko Nezu; Noboru Sasagawa; Nobuyuki Nukina; Shoichi Ishiura
Journal:  Nucleic Acids Res       Date:  2009-08-31       Impact factor: 16.971

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