نتایج جستجو برای: scn1a mutations

تعداد نتایج: 173129  

Journal: :PLoS Genetics 2009
Christel Depienne Delphine Bouteiller Boris Keren Emmanuel Cheuret Karine Poirier Oriane Trouillard Baya Benyahia Chloé Quelin Wassila Carpentier Sophie Julia Alexandra Afenjar Agnès Gautier François Rivier Sophie Meyer Patrick Berquin Marie Hélias Isabelle Py Serge Rivera Nadia Bahi-Buisson Isabelle Gourfinkel-An Cécile Cazeneuve Merle Ruberg Alexis Brice Rima Nabbout Eric LeGuern

Dravet syndrome (DS) is a genetically determined epileptic encephalopathy mainly caused by de novo mutations in the SCN1A gene. Since 2003, we have performed molecular analyses in a large series of patients with DS, 27% of whom were negative for mutations or rearrangements in SCN1A. In order to identify new genes responsible for the disorder in the SCN1A-negative patients, 41 probands were scre...

Journal: :Brain : a journal of neurology 2007
Louise A Harkin Jacinta M McMahon Xenia Iona Leanne Dibbens James T Pelekanos Sameer M Zuberi Lynette G Sadleir Eva Andermann Deepak Gill Kevin Farrell Mary Connolly Thorsten Stanley Michael Harbord Frederick Andermann Jing Wang Sat Dev Batish Jeffrey G Jones William K Seltzer Alison Gardner Grant Sutherland Samuel F Berkovic John C Mulley Ingrid E Scheffer

The relationship between severe myoclonic epilepsy of infancy (SMEI or Dravet syndrome) and the related syndrome SMEI-borderland (SMEB) with mutations in the sodium channel alpha 1 subunit gene SCN1A is well established. To explore the phenotypic variability associated with SCN1A mutations, 188 patients with a range of epileptic encephalopathies were examined for SCN1A sequence variations by de...

Journal: :Archives of neurology 2008
Claudio Zucca Francesca Redaelli Roberta Epifanio Nicoletta Zanotta Antonino Romeo Monica Lodi Pierangelo Veggiotti Giovanni Airoldi Chris Panzeri Romina Romaniello Gianni De Polo Paolo Bonanni Simonetta Cardinali Cinzia Baschirotto Loreto Martorell Renato Borgatti Nereo Bresolin Maria Teresa Bassi

BACKGROUND Sodium channel alpha 1 subunit gene, SCN1A, is the gene encoding the neuronal voltage-gated sodium channel alpha 1 subunit (Na(v)1.1) and is mutated in different forms of epilepsy. Mutations in this gene were observed in more than 70% of patients with severe myoclonic epilepsy of infancy (SMEI) and were also found in different types of infantile epileptic encephalopathy. OBJECTIVE ...

Journal: :Neurology 2006
J C Mulley P Nelson S Guerrero L Dibbens X Iona J M McMahon L Harkin J Schouten S Yu S F Berkovic I E Scheffer

We examined cases of severe myoclonic epilepsy of infancy (SMEI) for exon deletions or duplications within the sodium channel SCN1A gene by multiplex ligation-dependent probe amplification. Two of 13 patients (15%) who fulfilled the strict clinical definition of SMEI but without SCN1A coding or splicing mutations had exonic deletions of SCN1A.

2018
Min Jung Cho Soon Sung Kwon Ara Ko Seung-Tae Lee Young Mock Lee Heung Dong Kim Hee Jung Chung Se Hee Kim Joon Soo Lee Dae-Sung Kim Hoon-Chul Kang

BACKGROUND AND PURPOSE The aim of this study was to determine the effectiveness of stiripentol (STP) add-on therapy to valproate and clobazam in patients with Dravet syndrome (DS) according to the presence of mutations in the sodium channel alpha-1 subunit gene (SCN1A). METHODS We performed direct sequencing to analyze SCN1A mutations in 32 patients with clinically confirmed with DS, and clas...

2013
Kazuhiro Yamakawa

Dravet syndrome is caused by mutations of the SCN1A gene that encodes voltage-gated sodium channel alpha-1 subunit. SCN1A-knock-in mouse with a disease-relevant nonsense mutation that we generated reproduced the disease phenotypes. Both homozygous and heterozygous knock-in mice developed epileptic seizures within the fi rst postnatal month. Our immunohistochemical studies showed that in wild-ty...

Journal: :The New England journal of medicine 2010
Lata Vadlamudi Leanne M Dibbens Kate M Lawrence Xenia Iona Jacinta M McMahon Wayne Murrell Alan Mackay-Sim Ingrid E Scheffer Samuel F Berkovic

De novo mutations are a cause of sporadic disease, but little is known about the developmental timing of such mutations. We studied concordant and discordant monozygous twins with de novo mutations in the sodium channel α1 subunit gene (SCN1A) causing Dravet's syndrome, a severe epileptic encephalopathy. On the basis of our findings and the literature on mosaic cases, we conclude that de novo m...

Journal: :Human molecular genetics 2007
Melinda S Martin Bin Tang Ligia A Papale Frank H Yu William A Catterall Andrew Escayg

The mammalian genome contains four voltage-gated sodium channel genes that are primarily expressed in the central nervous system: SCN1A, SCN2A, SCN3A and SCN8A. Mutations in SCN1A and SCN2A are responsible for several dominant idiopathic epilepsy disorders, including generalized epilepsy with febrile seizures plus (GEFS+) and severe myoclonic epilepsy of infancy (SMEI). Mutations in SCN8A are a...

Journal: :The Journal of clinical investigation 2005
Miriam H Meisler Jennifer A Kearney

Since the first mutations of the neuronal sodium channel SCN1A were identified 5 years ago, more than 150 mutations have been described in patients with epilepsy. Many are sporadic mutations and cause loss of function, which demonstrates haploinsufficiency of SCN1A. Mutations resulting in persistent sodium current are also common. Coding variants of SCN2A, SCN8A, and SCN9A have also been identi...

Journal: :Seizure 2010
Mei-Juan Yu Yi-Wu Shi Mei-Mei Gao Wei-Yi Deng Xiao-Rong Liu Li Chen Yue-Sheng Long Yong-Hong Yi Wei-Ping Liao

Till now truncation mutations of voltage-gated sodium channel alpha subunit type I (SCN1A) gene were mostly found in severe myoclonic epilepsy of infancy (SMEI) patients. In this research we first identified two novel de novo truncation mutations (S662X and M145fx148) in two patients whose phenotypes were quite milder compared with SMEI patients. One patient was diagnosed as generalized epileps...

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