نتایج جستجو برای: dominant mutation

تعداد نتایج: 404478  

Ali Hossein Saberi, Atousa Hafizi, Gholamreza Shariati, Hamid Galehdari, Mohammad Hamid, Saeid Reza Khatami,

Introduction: Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common genetic kidney disorders with the incidence of 1 in 1,000 births. ADPKD is genetically heterogeneous with two genes identified: PKD1 (16p13.3, 46 exons) and PKD2 (4q21, 15 exons). Eighty five percent of the patients with ADPKD have at least one mutation in the PKD1 gene. Genetic studies have demonstrate...

Journal: :Annals of neurology 2005
Dena G Hernandez Coro Paisán-Ruíz Aideen McInerney-Leo Shushant Jain Andreas Meyer-Lindenberg E Whitney Evans Karen F Berman Janel Johnson Georg Auburger Alejandro A Schäffer Grisel J Lopez Robert L Nussbaum Andrew B Singleton

We have recently identified mutations in a gene leucine-rich repeat kinase-2 (LRRK2), which cause autosomal dominant Parkinson's disease. Here, we describe two families with autosomal dominant Parkinson's disease caused by a LRRK2 G2019S mutation. We present here a clinical description of patients, including 6-(18)F-fluoro-L-dopa positron emission tomography and discuss the potential implicatio...

Journal: :Biochemical and biophysical research communications 2002
Masumi Nishi Akihiro Yasue Shinichirou Nishimatu Tsutomu Nohno Takashi Yamaoka Mitsuo Itakura Keiji Moriyama Hideyo Ohuchi Sumihare Noji

Myostatin, which is a member of the TGF-beta superfamily, is a negative regulator of skeletal muscle formation. Double-muscled Piedmontese cattle have a C313Y mutation in myostatin and show increased skeletal muscle mass which resulted from an increase of myofiber number (hyperplasia) without that of myofiber size (hypertrophy). To examine whether this mutation in myostatin gene affects muscle ...

Journal: :American journal of medical genetics. Part A 2011
Niloofar Bazazzadegan Abraham M Sheffield Masoomeh Sobhani Kimia Kahrizi Nicole C Meyer Guy Van Camp Nele Hilgert Seyedeh Sedigheh Abedini Farkhondeh Habibi Ahmad Daneshi Carla Nishimura Matthew R Avenarius Mohammad Farhadi Richard J H Smith Hossein Najmabadi

Mutations in GJB2, encoding connexin 26 (Cx26), cause both autosomal dominant and autosomal recessive nonsyndromic hearing loss (ARNSHL) at the DFNA3 and DFNB1 loci, respectively. Most of the over 100 described GJB2 mutations cause ARNSHL. Only a minority has been associated with autosomal dominant hearing loss. In this study, we present two families with autosomal dominant nonsyndromic hearing...

Journal: :Archives of neurology 2007
Elodie Chabrol Cyprian Popescu Isabelle Gourfinkel-An Oriane Trouillard Christel Depienne Kristen Senechal Michel Baulac Eric LeGuern Stéphanie Baulac

BACKGROUND Mutations in the leucine-rich, glioma-inactivated 1 (LGI1) gene have been implicated in autosomal dominant lateral temporal epilepsy. OBJECTIVE To describe the clinical and genetic findings in 2 families with autosomal dominant lateral temporal epilepsy and the functional consequences of 2 novel mutations in LGI1. DESIGN Clinical, genetic, and functional investigations. SETTING...

2005
Bonita J. Biegalke Seongman Kang Jinwook Shin Boyoun Park Sungwook Lee Youngkyun Kim Kwangseog Ahn

2017
Hongyang Wang Kaiwen Wu Lan Yu Linyi Xie Wenping Xiong Dayong Wang Jing Guan Qiuju Wang

To decipher the phenotype and genotype of a Chinese family with autosomal dominant non-syndromic hearing loss (ADNSHL) and a novel dominant missense mutation in the GJB2 gene (DFNA3), mutation screening of GJB2 was performed on the propositus from a five-generation ADNSHL family through polymerase chain reaction amplification and Sanger sequencing. The candidate variation and the co-segregation...

Journal: :Muscle & nerve 2014
Saskia Lassche Sergio Lainez Bastiaan R Bloem Bart P C van de Warrenburg Jeannette Hofmeijer Henny H Lemmink Joost G J Hoenderop René J M Bindels Gea Drost

We describe the clinical phenotype of a novel de novo KNCA1 mutation, and functional characterization of the effects of the mutation on Kv1.1 channel function. HEK293 cells were transfected transiently with either wild-type or mutant channels. Representative currents were evoked after application of a series of square voltage steps from -80 mV to +50 mV in 200-ms intervals from Vh = -80 mV. Ext...

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