نتایج جستجو برای: scn4a

تعداد نتایج: 166  

Journal: :Iranian journal of neurology 2015
Mohammad Mehdi Heidari Mehri Khatami Shahriar Nafissi Faezeh Hesami-Zokai Afshin Khorrami

BACKGROUND Non-dystrophic myotonias are a heterogeneous set of skeletal, muscular channelopathies, which have been associated with point mutations within sodium channel α-subunit (SCN4A) gene. Because exons 22 and 24 of SCN4A gene are recognized as hot spots for this disease, the purpose of the study is to identify mutation in exons 22 and 24 of SCN4A gene in Iranian non-dystrophic myotonias pa...

2011
Ji-Yeon Han June-Bum Kim

Familial hyperkalemic periodic paralysis (HYPP) is an autosomaldominant channelopathy characterized by transient and recurrent episodes of paralysis with concomitant hyperkalemia. Mutations in the skeletal muscle voltage-gated sodium channel gene SCN4A have been reported to be responsible for this disease. Here, we report the case of a 16-year-old girl with HYPP whose mutational analysis reveal...

Journal: :Molecular medicine reports 2015
Xiao-Ying Wang Bing-Wen Ren Zeng-Hua Yong Hong-Yan Xu Qiu-Xia Fu He-Bin Yao

Mutations in CACNA1S (calcium channel, voltage‑dependent, L type, alpha 1S subunit) and SCN4A (sodium channel, voltage‑gated, type IV, alpha subunit) are associated with hypokalemic periodic paralysis (HPP). The aim of the current study was to investigate CACNA1S and SCN4A mutations in patients with HPP. Mutations in CACNA1S and SCN4A were detected in three familial hypokalemic periodic paralys...

2015
Jinxin Li Qinghai Huang Liang Ge Jing Xu Xingjuan Shi Wei Xie Xiang Liu Xiangdong Liu

Paramyotonia congenita (PC) is a rare autosomal dominant neuromuscular disorder characterized by juvenile onset and development of cold-induced myotonia after repeated activities. The disease is mostly caused by genetic mutations of the sodium channel, voltage-gated, type IV, alpha subunit (SCN4A) gene. This study intended to systematically identify the causative genetic variations of a Chinese...

Journal: :Lancet 2018
Roope Männikkö Leonie Wong David J Tester Michael G Thor Richa Sud Dimitri M Kullmann Mary G Sweeney Costin Leu Sanjay M Sisodiya David R FitzPatrick Margaret J Evans Iona J M Jeffrey Jacob Tfelt-Hansen Marta C Cohen Peter J Fleming Amie Jaye Michael A Simpson Michael J Ackerman Michael G Hanna Elijah R Behr Emma Matthews

BACKGROUND Sudden infant death syndrome (SIDS) is the leading cause of post-neonatal infant death in high-income countries. Central respiratory system dysfunction seems to contribute to these deaths. Excitation that drives contraction of skeletal respiratory muscles is controlled by the sodium channel NaV1.4, which is encoded by the gene SCN4A. Variants in NaV1.4 that directly alter skeletal mu...

Journal: :iranian journal of neurology 0
mohammad mehdi heidari department of biology, school of science, yazd university, yazd, iran mehri khatami department of biology, school of science, yazd university, yazd, iran shahriar nafissi department of neurology, school of medicine, tehran university of medical sciences, tehran, iran faezeh hesami-zokai department of biology, school of science, yazd university, yazd, iran afshin khorrami department of biology, school of science, yazd university, yazd, iran

background: non-dystrophic myotonias are a heterogeneous set of skeletal, muscular channelopathies, which have been associated with point mutations within sodium channel α-subunit (scn4a) gene. because exons 22 and 24 of scn4a gene are recognized as hot spots for this disease, the purpose of the study is to identify mutation in exons 22 and 24 of scn4a gene in iranian non-dystrophic myotonias p...

2009
Sang-Chan Lee Hyang-Sook Kim Yeong-Eun Park Young-Chul Choi Kyu-Hyun Park Dae-Seong Kim

BACKGROUND AND PURPOSE Mutations of the skeletal muscle sodium channel gene SCN4A, which is located on chromosome 17q23-25, are associated with various neuromuscular disorders that are labeled collectively as skeletal muscle sodium channelopathy. These disorders include hyperkalemic periodic paralysis (HYPP), hypokalemic periodic paralysis, paramyotonia congenita (PMC), potassium-aggravated myo...

Journal: :International journal of clinical and experimental pathology 2015
Changshui Xu Junjia Qi Yingying Shi Yan Feng Weizhou Zang Jiewen Zhang

Four generations of a Chinese family with a mild form of paramyotonia congenital was characterized in phenotype and genotype. For each member, clinical history, physical examination, laboratory tests, electrophysiological and gene analyses were recorded and carried out. A potassium loading, exercise and cold provocation were further tested to diagnose the clinical differentiation. All members s...

2014
Silvia Corrochano Roope Männikkö Peter I. Joyce Philip McGoldrick Jessica Wettstein Glenda Lassi Dipa L. Raja Rayan Gonzalo Blanco Colin Quinn Andrianos Liavas Arimantas Lionikas Neta Amior James Dick Estelle G. Healy Michelle Stewart Sarah Carter Marie Hutchinson Liz Bentley Pietro Fratta Andrea Cortese Roger Cox Steve D. M. Brown Valter Tucci Henning Wackerhage Anthony A. Amato Linda Greensmith Martin Koltzenburg Michael G. Hanna Abraham Acevedo-Arozena

Mutations in the skeletal muscle channel (SCN4A), encoding the Nav1.4 voltage-gated sodium channel, are causative of a variety of muscle channelopathies, including non-dystrophic myotonias and periodic paralysis. The effects of many of these mutations on channel function have been characterized both in vitro and in vivo. However, little is known about the consequences of SCN4A mutations downstr...

2007
June-Bum Kim Man-Ho Kim Soon Ju Lee Dae-Joong Kim Byung Churl Lee

Familial hypokalemic periodic paralysis (HOPP) is a rare autosomal-dominant disease characterized by reversible attacks of muscle weakness occurring with episodic hypokalemia. Mutations in the skeletal muscle calcium (CACNA1S) and sodium channel (SCN4A) genes have been reported to be responsible for familial HOPP. Fifty-one HOPP patients from 20 Korean families were studied to determine the rel...

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