نتایج جستجو برای: congenital myopathy

تعداد نتایج: 131548  

Journal: :Human molecular genetics 2014
Andrea A Domenighetti Pao-Hsien Chu Tongbin Wu Farah Sheikh David S Gokhin Ling T Guo Ziyou Cui Angela K Peter Danos C Christodoulou Michael G Parfenov Joshua M Gorham Daniel Y Li Indroneal Banerjee Xianyin Lai Frank A Witzmann Christine E Seidman Jonathan G Seidman Aldrin V Gomes G Diane Shelton Richard L Lieber Ju Chen

Recent human genetic studies have provided evidences that sporadic or inherited missense mutations in four-and-a-half LIM domain protein 1 (FHL1), resulting in alterations in FHL1 protein expression, are associated with rare congenital myopathies, including reducing body myopathy and Emery-Dreifuss muscular dystrophy. However, it remains to be clarified whether mutations in FHL1 cause skeletal ...

2017
Ruple S Laughlin Zhiyv Niu Eric Wieben Margherita Milone

BACKGROUND Congenital myopathies due to ryanodine receptor (RYR1) mutations are increasingly identified and correlate with a wide range of phenotypes, most commonly that of malignant hyperthermia susceptibility and central cores on muscle biopsy with rare reports of distal muscle weakness, but in the setting of early onset global weakness. METHODS We report a case of a patient presenting with...

Journal: :Current rheumatology reports 2000
P Cherin R K Gherardi

A most unusual inflammatory myopathy, called macrophagic myofasciitis, first described by the Groupe d'Etudes et Recherche sur les Maladies Musculaires Acquises et Dysimmunitaires (GERMMAD), a specific branch of the Association Française contre les Myopathies was recorded with an increasing frequency from 1993 in the main French myopathologic centers. In October 1999, 65 macrophagic myofasciiti...

Journal: :Human mutation 2014
Minttu Marttila Vilma-Lotta Lehtokari Steven Marston Tuula A Nyman Christine Barnerias Alan H Beggs Enrico Bertini Ozge Ceyhan-Birsoy Pascal Cintas Marion Gerard Brigitte Gilbert-Dussardier Jacob S Hogue Cheryl Longman Bruno Eymard Moshe Frydman Peter B Kang Lars Klinge Hanna Kolski Hans Lochmüller Laurent Magy Véronique Manel Michèle Mayer Eugenio Mercuri Kathryn N North Sylviane Peudenier-Robert Helena Pihko Frank J Probst Ricardo Reisin Willie Stewart Ana Lia Taratuto Marianne de Visser Ekkehard Wilichowski John Winer Kristen Nowak Nigel G Laing Tom L Winder Nicole Monnier Nigel F Clarke Katarina Pelin Mikaela Grönholm Carina Wallgren-Pettersson

Mutations affecting skeletal muscle isoforms of the tropomyosin genes may cause nemaline myopathy, cap myopathy, core-rod myopathy, congenital fiber-type disproportion, distal arthrogryposes, and Escobar syndrome. We correlate the clinical picture of these diseases with novel (19) and previously reported (31) mutations of the TPM2 and TPM3 genes. Included are altogether 93 families: 53 with TPM...

2013
Minobu Shichiji Valérie Biancalana Michel Fardeau Jean-Yves Hogrel Makiko Osawa Jocelyn Laporte Norma Beatriz Romero

The X-linked myotubular myopathy (XLMTM) also called X-linked centronuclear myopathy is a rare congenital myopathy due to mutations in the MTM 1 gene encoding myotubularin. The disease gives rise to a severe muscle weakness in males at birth. The main muscle morphological characteristics (significant number of small muscle fibers with centralized nuclei and type 1 fiber predominance) are usuall...

Journal: :Journal of the neurological sciences 1995
P F van der Ven P H Jap H J ter Laak I Nonaka P G Barth R C Sengers A M Stadhouders F C Ramaekers

We have studied the expression and distribution patterns of the intermediate filament proteins desmin and vimentin, the sarcomere components titin, nebulin and myosin, the basement membrane constituents collagen type IV and laminin, and the reticular layer component collagen type VI in skeletal muscle of patients with "classic" congenital myopathies (CM), using indirect immunofluorescence assay...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2014
Vasyl Nesin Graham Wiley Maria Kousi E-Ching Ong Thomas Lehmann David J Nicholl Mohnish Suri Nortina Shahrizaila Nicholas Katsanis Patrick M Gaffney Klaas J Wierenga Leonidas Tsiokas

Signaling through the store-operated Ca(2+) release-activated Ca(2+) (CRAC) channel regulates critical cellular functions, including gene expression, cell growth and differentiation, and Ca(2+) homeostasis. Loss-of-function mutations in the CRAC channel pore-forming protein ORAI1 or the Ca(2+) sensing protein stromal interaction molecule 1 (STIM1) result in severe immune dysfunction and nonprog...

Journal: :American journal of physiology. Cell physiology 2009
David S Gokhin Marie-Louise Bang Jianlin Zhang Ju Chen Richard L Lieber

Nebulin (NEB) is a large, rod-like protein believed to dictate actin thin filament length in skeletal muscle. NEB gene defects are associated with congenital nemaline myopathy. The functional role of NEB was investigated in gastrocnemius muscles from neonatal wild-type (WT) and NEB knockout (NEB-KO) mice, whose thin filaments have uniformly shorter lengths compared with WT mice. Isometric stres...

Journal: :The Journal of clinical investigation 2014
Ankit Garg Jason O'Rourke Chengzu Long Jonathan Doering Gianina Ravenscroft Svetlana Bezprozvannaya Benjamin R Nelson Nadine Beetz Lin Li She Chen Nigel G Laing Robert W Grange Rhonda Bassel-Duby Eric N Olson

Nemaline myopathy (NM) is a congenital myopathy that can result in lethal muscle dysfunction and is thought to be a disease of the sarcomere thin filament. Recently, several proteins of unknown function have been implicated in NM, but the mechanistic basis of their contribution to disease remains unresolved. Here, we demonstrated that loss of a muscle-specific protein, kelch-like family member ...

2016
Delphine Trochet Bernard Prudhon Arnaud Jollet Stéphanie Lorain Marc Bitoun

Dynamin 2 (DNM2) is a large GTPase, ubiquitously expressed, involved in membrane trafficking and regulation of actin and microtubule cytoskeletons. DNM2 mutations cause autosomal dominant centronuclear myopathy which is a rare congenital myopathy characterized by skeletal muscle weakness and histopathological features including nuclear centralization in absence of regeneration. No curative trea...

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