نتایج جستجو برای: dystrophin deletions

تعداد نتایج: 22547  

Journal: :genetics in the 3rd millennium 0
محمد تقی اکبری mohammad taghi akbari no.98, akbari medical genetics laboratory, taleghani street, tehran, iranآزمایشگاه ژنتیک پزشکی دکتر اکبری، خیابان طالقانی، شماره 98، تهران، ایران./ تلفن: 8896868 شهره زارع کاریزی shohreh zare karizi akbari medical genetics laboratory, tehran, iran1- آزمایشگاه ژنتیک پزشکی دکتر اکبری، تهران، ایران شهریار نفیسی shahriai nafisi department of neurology, tehran university of medical science, tehran, iranبخش مغز و اعصاب، دانشگاه علوم پزشکی تهران، تهران، ایران زهرا بهمنی zahra bahmani akbari medical genetics laboratory, tehran, iran1- آزمایشگاه ژنتیک پزشکی دکتر اکبری، تهران، ایران

duchene and becker muscular dystrophy (dmd and bmd) are x-linked conditions that result from a defect in the dystrophin gene located on xp21. dmd is the most frequent neuromuscular disease in humans (1/3500 male newborns). in approximately 65% of dmd and bmd patients, deletions in the dystrophin gene have been identified as the molecular determinant. population-based variations in frequency and...

Journal: :Arquivos de neuro-psiquiatria 2007
Aline Andrade Freund Rosana Herminia Scola Raquel Cristina Arndt Paulo José Lorenzoni Claudia Kamoy Kay Lineu Cesar Werneck

Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) are caused by mutations in the dystrophin gene. We studied 106 patients with a diagnosis of probable DMD/BMD by analyzing 20 exons of the dystrophin gene in their blood and, in some of the cases, by immunohistochemical assays for dystrophin in muscle biopsies. In 71.7% of the patients, deletions were found in at least one of ...

Journal: :acta medica iranica 0
fardeen ali malayeri department of neurogenetics, iranian center of neurological research, imam khomeini hospital , tehran university of medical sciences, tehran, iran. and department of clinical biochemistry, isfahan pharmaceutical sciences research center, school of pharmacy and pharmaceutical sciences, isfahan university of medical sciences, isfahan, iran. mojtaba panjehpour department of clinical biochemistry, isfahan pharmaceutical sciences research center, school of pharmacy and pharmaceutical sciences, isfahan university of medical sciences, isfahan, iran. ahmad movahedian department of clinical biochemistry, isfahan pharmaceutical sciences research center, school of pharmacy and pharmaceutical sciences, isfahan university of medical sciences, isfahan, iran. majid ghaffarpour iranian center of neurological research, imam khomeini hospital, tehran university of medical sciences, tehran, iran. gholam reza zamani department of neurology, children medical center, school of medicine, tehran university of medical sciences, tehran, iran. hajifaraj tabrizi department of medical genetics, school of medicine, tehran university of medical sciences, tehran, iran.

this study determines the value of linkage analysis using six rflp markers for carrier detection and prenatal diagnosis in familial dmd/bmd cases and their family members for the first time in the iranian population. we studied the dystrophin gene in 33 unrelated patients with clinical diagnosis of dmd or bmd. subsequently, we determined the rate of heterozygosity for six intragenic rflp marker...

Journal: :iranian journal of child neurology 0
mohammad barzegar 1. pediatric health research center, tabriz university of medical sciences, tabriz, iran. 2. division of pediatric neurology, tabriz children’s hospital, tabriz university of medical sciences, tabriz, iran parinaz habibi 1. pediatric health research center, tabriz university of medical sciences, tabriz, iran. mortaza mortaza bonyady 3. center of excellence for biodiversity, department of molecular medical genetics, faculty of natural sciences university of tabriz, tabriz, iran vahideh topchizadeh 4. physical medicine & rehabilitation research center, tabriz university of medical sciences, tabriz, iran shadi shiva* 1. pediatric health research center, tabriz university of medical sciences, tabriz, iran. 2. division of pediatric neurology, tabriz children’s hospital, tabriz university of medical sciences, tabriz, iran

how to cite this article: barzegar m, habibi p, bonyady m, topchizadeh v, shiva sh. exon deletion pattern in duchene muscular dystrophy in north west of iran. iran j child neurol. 2015 winter; 9(1): 42-48. abstract objective duchene and becker muscular dystrophy (dmd/ bmd) are x-linked disorders that both are the result of heterogeneous mutations in the dystrophin gene. the frequency and distri...

Journal: :cell journal 0

introduction: duchene/ becker (dmd/bmd) muscular dystrophy is the most frequent neuromuscular disease in children which is inherited as an x-linked recessive trait. the disease is caused by partial deletion in dystrophin gene. we developed a rapid and robust method for direct identification of female carriers of deletions and duplications in the dystrophin gene, in order to prevent the affected...

Journal: :Journal of medical genetics 1993
L V Nicholson M A Johnson K M Bushby D Gardner-Medwin A Curtis I B Ginjaar J T den Dunnen J L Welch T J Butler E Bakker

This report is the second part of a trilogy from a multidisciplinary study which was undertaken to record the relationships between clinical severity and dystrophin gene and protein expression. The aim in part 2 was to correlate the effect of gene deletions on protein expression in individual patients with well defined clinical phenotypes. Among the DMD patients, most of the deletions/duplicati...

Journal: :Brain : a journal of neurology 2011
Karen Anthony Sebahattin Cirak Silvia Torelli Giorgio Tasca Lucy Feng Virginia Arechavala-Gomeza Annarita Armaroli Michela Guglieri Chiara S Straathof Jan J Verschuuren Annemieke Aartsma-Rus Paula Helderman-van den Enden Katherine Bushby Volker Straub Caroline Sewry Alessandra Ferlini Enzo Ricci Jennifer E Morgan Francesco Muntoni

Duchenne muscular dystrophy is caused by mutations in the DMD gene that disrupt the open reading frame and prevent the full translation of its protein product, dystrophin. Restoration of the open reading frame and dystrophin production can be achieved by exon skipping using antisense oligonucleotides targeted to splicing elements. This approach aims to transform the Duchenne muscular dystrophy ...

Journal: :The Journal of Cell Biology 1996
J A Rafael G A Cox K Corrado D Jung K P Campbell J S Chamberlain

Dystrophin plays an important role in skeletal muscle by linking the cytoskeleton and the extracellular matrix. The amino terminus of dystrophin binds to actin and possibly other components of the subsarcolemmal cytoskeleton, while the carboxy terminus associates with a group of integral and peripheral membrane proteins and glycoproteins that are collectively known as the dystrophin-associated ...

Journal: :genetics in the 3rd millennium 0
مینا حیات نو سعید mina hayat nosaeid molecular medicine department, biotechnology research center, pasteur institute of iran صادق فلاح محمد sadegh fallah mohammad kawsar genetics research center, tehran, iran رامک حیدری ramak heidari iran muscular dystrophy association tehran, iran سمانه فتحی آذر samaneh fathi azar 1- molecular medicine department, biotechnology research center, pasteur institute, tehran, ir سمیه جمالی somayeh jamali 1- molecular medicine department, biotechnology research center, pasteur institute, tehran, ir رضا مهدیان reza mahdian 1- molecular medicine department, biotechnology research center, pasteur institute, tehran, iran مرضیه رئیسی

duchenne muscular dystrophy (dmd) and becker muscular dystrophy (bmd) can be caused by deletions, duplications or point mutations in the dmd gene that encodes dystrophin. partial gene duplications account for up to 5-10 % of dmd and up to 5- 19% of bmd cases. cases with gene duplication in dmd/bmd are determined by quantitative methods such as maph, sothern blotting and q-pcr that are laborious...

Journal: :Rinsho shinkeigaku = Clinical neurology 2009
Ryszard Kole Arthur M Krieg

Duchenne muscular dystrophy (DMD) is caused mostly by internal deletions in the gene for dystrophin, a protein essential for maintaining muscle cell membrane integrity. These deletions abrogate the reading frame and the lack of dystrophin results in progressive muscle deterioration. DMD patients experience progressive loss of ambulation, followed by a need for assisted ventilation, and eventual...

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