نتایج جستجو برای: multiplex ligation dependentprobe amplification

تعداد نتایج: 97340  

Journal: :genetics in the 3rd millennium 0
مینا حیات نوسعید mina hayat nosaeid molecular medicine department, biotechnology research center, pasteur institute of iran, tehran, iran رضا مهدیان reza mahdian سمیه جمالی somayeh jamali مرضیه رئیسی marzieh raeisi فهیمه مریمی fahimeh mariami صادق باباشاه sadegh babashah شبنم وحیدپور

mutations in the dystrophin gene cause duchenne muscular dystrophy (dmd), the most commonly inherited neuromuscular disorder, and becker muscular dystrophy (bmd), the milder allelic form of the disease. the mutation spectrum within this gene is unusual in that deletion of one or more exons are found in ~65% of cases. since no effective treatment is so far available for these diseases, the ident...

Journal: :BMJ open 2016
Christophe Rosty Mark Clendenning Michael D Walsh Stine V Eriksen Melissa C Southey Ingrid M Winship Finlay A Macrae Alex Boussioutas Nicola K Poplawski Susan Parry Julie Arnold Joanne P Young Graham Casey Robert W Haile Steven Gallinger Loïc Le Marchand Polly A Newcomb John D Potter Melissa DeRycke Noralane M Lindor Stephen N Thibodeau John A Baron Aung Ko Win John L Hopper Mark A Jenkins Daniel D Buchanan

OBJECTIVES Immunohistochemistry for DNA mismatch repair proteins is used to screen for Lynch syndrome in individuals with colorectal carcinoma (CRC). Although solitary loss of PMS2 expression is indicative of carrying a germline mutation in PMS2, previous studies reported MLH1 mutation in some cases. We determined the prevalence of MLH1 germline mutations in a large cohort of individuals with a...

2015
Paulo Marcio Yamaguti Pollyanna Almeida Costa dos Santos Bruno Sakamoto Leal Viviane Brandão Bandeira de Mello Santana Juliana Forte Mazzeu Ana Carolina Acevedo Francisco de Assis Rocha Neves

BACKGROUND Familial hypomagnesemia with hypercalciuria and nephrocalcinosis is a rare autosomal recessive renal disease characterized by tubular disorders at the thick ascending limb of Henle's loop. It is caused by mutations in the tight junction structural proteins claudin-16 or claudin-19, which are encoded by the CLDN16 and CLDN19 genes, respectively. Patients exhibit excessive wasting of c...

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