نتایج جستجو برای: جهش 35delg

تعداد نتایج: 3257  

Journal: :Journal of medical genetics 2001
L Van Laer P Coucke R F Mueller G Caethoven K Flothmann S D Prasad G P Chamberlin M Houseman G R Taylor C M Van de Heyning E Fransen J Rowland R A Cucci R J Smith G Van Camp

Fifty to eighty percent of autosomal recessive congenital severe to profound hearing impairment result from mutations in a single gene, GJB2, that encodes the protein connexin 26. One mutation of this gene, the 35delG allele, is particularly common in white populations. We report evidence that the high frequency of this allelic variant is the result of a founder effect rather than a mutational ...

Journal: :Physiological research 2013
D Groh P Seeman M Jilek J Popelář Z Kabelka J Syka

The most frequent hereditary hearing loss is caused by mutations in the GJB2 gene coding for the gap junction beta 2 protein Connexin 26 (Cx26). In contrast to many studies performed in patients with bi-allelic mutations, audiometric studies on heterozygotes are sparse and often contradictory. To evaluate hearing function in heterozygous carriers of the GJB2 c.35delG mutation, audiometry over t...

پایان نامه :وزارت علوم، تحقیقات و فناوری - دانشگاه علم و فرهنگ - دانشکده علوم پایه 1394

ناشنوایی یک اختلال ناهمگن حسی¬- عصبی می¬باشد که حدود 1 در هر 1000 تولد را در بر¬می-گیرد. به دو دسته سندرومی و غیر¬سندرومی تقسیم می¬شود و80% ناشنوایی غیرسندرومی به صورت آتوزوم مغلوب می¬باشد. میزان ازدواج خویشاوندی در کشور حدود 36/6 درصد می¬باشد که این مسئله می¬تواند بستر مناسبی را برای بروز بیماریهای آتوزوم مغلوب همچون ناشنوایی ایجاد کند. هدف از این مطالعه تشخیص مولکولی ناشنوایی آتوزوم مغلوب در ...

Journal: :Hearing research 2004
Vânia Belintani Piatto Eny Maria Goloni Bertollo Edi Lúcia Sartorato José Victor Maniglia

Mutations in the GJB2 gene are the most common cause of sensorineural non-syndromic deafness in different populations. One specific mutation, 35delG, has accounted for the majority of the mutations detected in the GJB2 gene in many countries. The aim of this study was to determine the prevalence of GJB2 mutations and the del(GJB6-D13S1830) mutation in non-syndromic deaf Brazilians. The 33 unrel...

Journal: :Journal of prenatal medicine 2013
Manuela Coco Fabrizio Salvinelli Fabio Greco Maurizio Trivelli Laura D'Emidio Alvaro Mesoraca Claudio Giorlandino Raffaella Raffio Claudio Coco

OBJECTIVE to determinate the role of heterozygosis of M34T mutation of GJB2 gene in non syndromic congenital deafness. METHODS retrospective study between March 2010 and June 2013. Molecular screening for 35delG and M34T mutations of the GJB2 gene was offered to all women undergoing to second trimester genetic amniocentesis. Patients were excluded from the study group if one of the following ...

آبسواران, ابوالفضل, اسماعیلی, محسن, جبارپور بنیادی, مرتضی, لطفلیزاده, نادر, یونس پور, رضا,

Background and Objective: Profound hearing loss is one of the most prevalent congenital disorders affecting about 1 in 1000 newborns. Autosomal recessive non-syndromic hearing loss (ARNSHL) is the predominant form of the severe inherited childhood deafness. This type of hearing loss in one-half of the cases is caused by mutations in GJB2 (connexin 26) and GJB6 (connexin 30) genes located at DFN...

Background: Hearing impairment as a heterogeneous disorder is the most common sensory defect that occur 1 in 1000. Mutations in GJB2 (CX26) gene at DFNB1 locus on 13q12 are responsible for autosomal recessive non-syndromic hearing loss (ARNSHL) in many populations. This study investigates the GJB2 gene mutations in deaf patients refereed to the deaf center of Tabriz. Methods: In the present ...

Journal: :American journal of human genetics 2005
Rikkert L Snoeckx Patrick L M Huygen Delphine Feldmann Sandrine Marlin Françoise Denoyelle Jaroslaw Waligora Malgorzata Mueller-Malesinska Agneszka Pollak Rafal Ploski Alessandra Murgia Eva Orzan Pierangela Castorina Umberto Ambrosetti Ewa Nowakowska-Szyrwinska Jerzy Bal Wojciech Wiszniewski Andreas R Janecke Doris Nekahm-Heis Pavel Seeman Olga Bendova Margaret A Kenna Anna Frangulov Heidi L Rehm Mustafa Tekin Armagan Incesulu Hans-Henrik M Dahl Desirée du Sart Lucy Jenkins Deirdre Lucas Maria Bitner-Glindzicz Karen B Avraham Zippora Brownstein Ignacio del Castillo Felipe Moreno Nikolaus Blin Markus Pfister Istvan Sziklai Timea Toth Philip M Kelley Edward S Cohn Lionel Van Maldergem Pascale Hilbert Anne-Françoise Roux Michel Mondain Lies H Hoefsloot Cor W R J Cremers Tuija Löppönen Heikki Löppönen Agnete Parving Karen Gronskov Iris Schrijver Joseph Roberson Francesca Gualandi Alessandro Martini Geneviéve Lina-Granade Nathalie Pallares-Ruiz Céu Correia Graça Fialho Kim Cryns Nele Hilgert Paul Van de Heyning Carla J Nishimura Richard J H Smith Guy Van Camp

Hearing impairment (HI) affects 1 in 650 newborns, which makes it the most common congenital sensory impairment. Despite extraordinary genetic heterogeneity, mutations in one gene, GJB2, which encodes the connexin 26 protein and is involved in inner ear homeostasis, are found in up to 50% of patients with autosomal recessive nonsyndromic hearing loss. Because of the high frequency of GJB2 mutat...

باقری, مرتضی, عبدی‌راد, عیسی, فرهودی, فریناز,

Background and Objective: Mutations in GJB2 gene is the most common cause of autosomal recessive non-syndromic hearing loss in many populations. The aim of this study was to determine the frequency of 35delG, 167delT, M34T, 235delC mutations in West Azarbaijan population. Materials and Methods: 129 patients from 96 families were studied. Mutations were detected using ASO-PCR and PCR-RFLP method...

2012
Nina Danilenko Elena Merkulava Marina Siniauskaya Olga Olejnik Anastasia Levaya-Smaliak Alena Kushniarevich Andrey Shymkevich Oleg Davydenko

The genetic nature of sensorineural hearing loss (SNHL) has so far been studied for many ethnic groups in various parts of the world. The single-nucleotide guanine deletion (35delG) of the GJB2 gene coding for connexin 26 was shown to be the main genetic cause of autosomal recessive deafness among Europeans. Here we present the results of the first study of GJB2 and three mitochondrial mutation...

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