نتایج جستجو برای: exon deletion

تعداد نتایج: 99871  

Journal: :Human molecular genetics 1997
J O Winberg N Hammami-Hauasli O Nilssen I Anton-Lamprecht S L Naylor K Kerbacher M Zimmermann P Krajci T Gedde-Dahl L Bruckner-Tuderman

Dystrophic epidermolysis bullosa (EBD) is a clinically heterogeneous skin disorder, characterized by abnormal anchoring fibrils (AF) and loss of dermal-epidermal adherence. EBD has been linked to the COL7A1 gene at chromosome 3p21 which encodes collagen VII, the major component of the AF. Here we investigated two unrelated EBD families with different clinical phenotypes and novel combinations o...

2016
Kushal Shrestha Smita Shrestha Saroj Khatiwada Bishnu Acharya Sulochana Manandhar Rohit Kumar

Duchenne muscular dystrophy (DMD) is X-linked recessive neuromuscular disorders caused due to mutation in dystrophin gene, leading to progressive muscle weakness. This study was done to identify mutation in dystrophin gene in Nepalese patients with DMD using Multiplex Ligation Dependent Probe Amplification (MLPA) assay in Nepal. Twenty one patients from different regions of Nepal, who were clin...

Journal: :American journal of human genetics 2004
Annemieke Aartsma-Rus Anneke A M Janson Wendy E Kaman Mattie Bremmer-Bout Gert-Jan B van Ommen Johan T den Dunnen Judith C T van Deutekom

Dystrophin deficiency, which leads to severe and progressive muscle degeneration in patients with Duchenne muscular dystrophy (DMD), is caused by frameshifting mutations in the dystrophin gene. A relatively new therapeutic strategy is based on antisense oligonucleotides (AONs) that induce the specific skipping of a single exon, such that the reading frame is restored. This allows the synthesis ...

2013
Dennis Lal Eva M. Reinthaler Janine Altmüller Mohammad R. Toliat Holger Thiele Peter Nürnberg Holger Lerche Andreas Hahn Rikke S. Møller Hiltrud Muhle Thomas Sander Fritz Zimprich Bernd A. Neubauer

Partial deletions of the gene encoding the neuronal splicing regulator RBFOX1 have been reported in a range of neurodevelopmental diseases, including idiopathic generalized epilepsy. The RBFOX1 protein and its homologues (RBFOX2 and RBFOX3) regulate alternative splicing of many neuronal transcripts involved in the homeostatic control of neuronal excitability. In this study, we explored if struc...

Journal: :Case reports in genetics 2016
Theodoros Georgiou Gavriella Mavrikiou Angelos Alexandrou Elena Spanou-Aristidou Isavella Savva Theodoros Christodoulides Maria Krasia Violetta Christophidou-Anastasiadou Carolina Sismani Anthi Drousiotou George A Tanteles

Fabry disease is an X-linked lysosomal storage disorder resulting from a deficiency of the hydrolytic enzyme α-galactosidase A (α-Gal-A). It is characterized by progressive lysosomal accumulation of globotriaosylceramide (Gb3) and multisystem pathology, affecting the skin, nervous and cerebrovascular systems, kidneys, and heart. Heterozygous females typically exhibit milder symptoms and a later...

Journal: :Journal of medical genetics 2002
W Hofmann B Wappenschmidt S Berhane R Schmutzler S Scherneck

The breast and ovarian cancer susceptibility gene BRCA1 contains an unusually high density (41.5%) of Alu elements. The homology between these repetitive Alu sequences can promote ectopic or homotopic homologous recombination. Ectopic homologous recombination, such as that reported in the BRCA1 gene, leads to large genomic rearrangements, which subsequently may cause disease phenotypes. In the ...

2001
Margreet G E M Ausems Klara ten Berg Lodewijk A Sandkuijl Marian A Kroos Alfons F J Bardoel Katerina N Roumelioti Arnold J J Reuser Richard Sinke Cisca Wijmenga

EDITOR—Glycogen storage disease type II (GSD II) is an autosomal recessive lysosomal storage disorder caused by deficiency of acid á-glucosidase. The enzyme deficiency results in intralysosomal accumulation of glycogen in skeletal muscle and in other tissues. There are early and late onset phenotypes which diVer with respect to age at onset, extent of organ involvement, and clinical course of t...

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