نتایج جستجو برای: dystrophin deletions

تعداد نتایج: 22547  

2017
Seena Vengalil Veeramani Preethish-Kumar Kiran Polavarapu Manjunath Mahadevappa Deepha Sekar Meera Purushottam Priya Treesa Thomas Saraswathi Nashi Atchayaram Nalini

BACKGROUND AND PURPOSE Studies of cases of Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) confirmed by multiplex ligation-dependent probe amplification (MLPA) have determined the clinical characteristics, genotype, and relations between the reading frame and phenotype for different countries. This is the first such study from India. METHODS A retrospective genotype-phen...

2009
Antonella Carsana Giulia Frisso Mariano Intrieri Maria Roberta Tremolaterra Giovanni Savarese Giovanni Scapagnini Gabriella Esposito Lucio Santoro Francesco Salvatore

Duchenne (DMD) and Becker muscular dystrophies (BMD) are X-linked recessive neuromuscular disorders caused by mutations in the dystrophin gene. In most cohorts, DMD/BMD are due to deletions (60-80%) and duplications (6-10%) involving one or more exons. The remaining cases are caused by different type of point mutations. We analyzed 179 unrelated male patients, 296 women belonging to 137 DMD/BMD...

Journal: :Clinical chemistry 2011
Giulio Piluso Manuela Dionisi Francesca Del Vecchio Blanco Annalaura Torella Stefania Aurino Marco Savarese Teresa Giugliano Enrico Bertini Alessandra Terracciano Mariz Vainzof Chiara Criscuolo Luisa Politano Carlo Casali Filippo Maria Santorelli Vincenzo Nigro

BACKGROUND Array-based comparative genomic hybridization (aCGH) is a reference high-throughput technology for detecting large pathogenic or polymorphic copy-number variations in the human genome; however, a number of quantitative monogenic mutations, such as smaller heterozygous deletions or duplications, are usually missed in most disease genes when proper multiplex ligation-dependent probe as...

Journal: :Clinical chemistry 2008
Lee-Jun C Wong David Dimmock Michael T Geraghty Richard Quan Uta Lichter-Konecki Jing Wang Ellen K Brundage Fernando Scaglia A Craig Chinault

BACKGROUND direct DNA sequencing is the primary clinical technique for identifying mutations in human disease, but sequencing often does not detect intragenic or whole-gene deletions. Oligonucleotide array-based comparative genomic hybridization (CGH) is currently in clinical use to detect major changes in chromosomal copy number. METHODS a custom oligonucleotide-based microarray was construc...

Journal: :Journal of molecular and cellular cardiology 1997
R D Bies M Maeda S L Roberds E Holder T Bohlmeyer J B Young K P Campbell

5'-mutations in the dystrophin gene can result in cardiomyopathy without clinically-apparent skeletal myopathy. The effect of dystrophin mutations on the assembly and stability of the dystrophin associated protein (DAP) complex in human heart are not fully understood. The molecular defect in the dystrophin complex was explored in a family with an X-linked pedigree and severe dilated cardiomyopa...

Journal: : 2023

Duchenne muscular dystrophy is a genetic orphan neuromuscular disease caused by mutation in the DMD gene encoding protein dystrophin. As result of developing and progressive muscle damage atrophy, children lose ability to walk, develop respiratory cardiac disorders. The core elements good care standards are early diagnosis, prevention treatment osteoporosis, daily physical therapy, regular reha...

2011
Sebahattin Cirak Virginia Arechavala-Gomeza Michela Guglieri Lucy Feng Silvia Torelli Karen Anthony Stephen Abbs Maria Elena Garralda John Bourke Dominic J Wells George Dickson Matthew JA Wood Steve D Wilton Volker Straub Ryszard Kole Stephen B Shrewsbury Caroline Sewry Jennifer E Morgan Kate Bushby Francesco Muntoni

BACKGROUND We report clinical safety and biochemical efficacy from a dose-ranging study of intravenously administered AVI-4658 phosphorodiamidate morpholino oligomer (PMO) in patients with Duchenne muscular dystrophy. METHOD We undertook an open-label, phase 2, dose-escalation study (0·5, 1·0, 2·0, 4·0, 10·0, and 20·0 mg/kg bodyweight) in ambulant patients with Duchenne muscular dystrophy age...

Journal: :Cell 1991
J M Ervasti K P Campbell

The stoichiometry, cellular location, glycosylation, and hydrophobic properties of the components in the dystrophin-glycoprotein complex were examined. The 156, 59, 50, 43, and 35 kd dystrophin-associated proteins each possess unique antigenic determinants, enrich quantitatively with dystrophin, and were localized to the skeletal muscle sarcolemma. The 156, 50, 43, and 35 kd dystrophin-associat...

Journal: :The Journal of biological chemistry 1991
J M Ervasti S D Kahl K P Campbell

Dystrophin was purified from rabbit skeletal muscle by alkaline dissociation of dystrophin-glycoprotein complex which was first prepared by derivatized lectin chromatography. Dystrophin-glycoprotein complex was isolated from digitonin-solubilized rabbit skeletal muscle membranes by a novel two-step method involving succinylated wheat germ agglutinin (sWGA) chromatography and DEAE-cellulose ion ...

Journal: :Scientific reports 2016
Jinhong Meng John R Counsell Mojgan Reza Steven H Laval Olivier Danos Adrian Thrasher Hanns Lochmüller Francesco Muntoni Jennifer E Morgan

Autologous stem cells that have been genetically modified to express dystrophin are a possible means of treating Duchenne Muscular Dystrophy (DMD). To maximize the therapeutic effect, dystrophin construct needs to contain as many functional motifs as possible, within the packaging capacity of the viral vector. Existing dystrophin constructs used for transduction of muscle stem cells do not cont...

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