نتایج جستجو برای: nondystrophic myotonia

تعداد نتایج: 1472  

Journal: :Neuroscience letters 2011
Akira Tsujino Muneshige Kaibara Hideki Hayashi Hiroto Eguchi Susumu Nakayama Katsuya Sato Taku Fukuda Yohei Tateishi Susumu Shirabe Kohtaro Taniyama Atsushi Kawakami

Myotonia congenita is caused by mutation of the CLCN1 gene, which encodes the human skeletal muscle chloride channel (ClC-1). The ClC-1 protein is a dimer comprised of two identical subunits each incorporating its own separate pore. However, the precise pathophysiological mechanism underlying the abnormal ClC-1 channel gating in some mutants is not fully understood. We characterized a ClC-1 mut...

Journal: :Clinical genetics 2011
C Sun M Van Ghelue L Tranebjærg F Thyssen Ø Nilssen T Torbergsen

Myotonia is characterized by hyperexcitability of the muscle cell membrane. Myotonic disorders are divided into two main categories: non-dystrophic and dystrophic myotonias. The non-dystrophic myotonias involve solely the muscle system, whereas the dystrophic myotonias are characterized by multisystem involvement and additional muscle weakness. Each category is further subdivided into different...

Journal: :Human molecular genetics 1998
C Kubisch T Schmidt-Rose B Fontaine A H Bretag T J Jentsch

Mutations in the ClC-1 muscle chloride channel cause either recessive or dominant myotonia congenita. Using a systematic screening procedure, we have now identified four novel missense mutations in dominant (V286A, F307S) and recessive myotonia (V236L, G285E), and have analysed the effect of these and other recently described mutations (A313T, I556N) on channel properties in the Xenopus oocyte ...

Journal: :Proceedings of the Royal Society of Medicine 1935

Journal: :The Journal of clinical investigation 2008
Lawrence J Hayward Joanna S Kim Ming-Yang Lee Hongru Zhou Ji W Kim Kumudini Misra Mohammad Salajegheh Fen-fen Wu Chie Matsuda Valerie Reid Didier Cros Eric P Hoffman Jean-Marc Renaud Stephen C Cannon Robert H Brown

Hyperkalemic periodic paralysis (HyperKPP) produces myotonia and attacks of muscle weakness triggered by rest after exercise or by K+ ingestion. We introduced a missense substitution corresponding to a human familial HyperKPP mutation (Met1592Val) into the mouse gene encoding the skeletal muscle voltage-gated Na+ channel NaV1.4. Mice heterozygous for this mutation exhibited prominent myotonia a...

Journal: :Journal of neurology, neurosurgery, and psychiatry 2009
J Trip G Drost H B Ginjaar F H M Nieman A J van der Kooi M de Visser B G M van Engelen C G Faber

OBJECTIVE To redefine phenotypical characteristics for both chloride (ClCh) and sodium channelopathies (NaCh) in non-dystrophic myotonic syndromes (NDM). METHODS In a cross-sectional, nationwide study, standardised interviews and clinical bedside tests were performed in 62 genetically confirmed NDM patients, 32 ClCh and 30 NaCh. RESULTS Standardised interviews revealed that ClCh reported a ...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2006
Rahul N Kanadia Jihae Shin Yuan Yuan Stuart G Beattie Thurman M Wheeler Charles A Thornton Maurice S Swanson

RNA-mediated pathogenesis is a recently developed disease model that proposes that certain types of mutant genes produce toxic transcripts that inhibit the activities of specific proteins. This pathogenesis model was proposed first for the neuromuscular disease myotonic dystrophy (DM), which is associated with the expansion of structurally related (CTG)(n) and (CCTG)(n) microsatellites in two u...

2014
Wei Cheng Jing Tian Jean-Marc Burgunder Walter Hunziker How-Lung Eng

Myotonia congenita is a human muscle disorder caused by mutations in CLCN1, which encodes human chloride channel 1 (CLCN1). Zebrafish is becoming an increasingly useful model for human diseases, including muscle disorders. In this study, we generated transgenic zebrafish expressing, under the control of a muscle specific promoter, human CLCN1 carrying mutations that have been identified in huma...

Journal: :The Journal of Nervous and Mental Disease 1917

Journal: :European Journal of Human Genetics 2009

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