Connexin-26 Is a Key Factor Mediating Gemcitabine Bystander Effect
نویسندگان
چکیده
منابع مشابه
The p.Cys169Tyr variant of connexin 26 is not a polymorphism
Mutations in the GJB2 gene, which encodes the gap junction protein connexin 26 (Cx26), are the primary cause of hereditary prelingual hearing impairment. Here, the p.Cys169Tyr missense mutation of Cx26 (Cx26C169Y), previously classified as a polymorphism, has been identified as causative of severe hearing loss in two Qatari families. We have analyzed the effect of this mutation using a combinat...
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متن کاملMutations in the gene for connexin 26 (GJB2) that cause hearing loss have a dominant negative effect on connexin 30.
Mutations in the gene (GJB2) encoding connexin 26 (cx26) have been linked to sensorineural hearing loss either alone or as part of a syndrome. Here we compare the properties of four cx26 mutants derived from point mutations associated with dominantly inherited hearing loss, either non-syndromic (W44S, R75W) or with various skin disorders (G59A, D66H, R75W). Since cx26 and cx30 are co-localized ...
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OBJECTIVE The objective of our study was to explore a possible molecular mechanism by which ultraviolet (UV) biophotons could elicit bystander responses in reporter cells and resolve the problem of seemingly mutually exclusive mechanisms of a physical UV signal & a soluble factor-mediated bystander signal. METHODS The human colon carcinoma cell line, HCT116 p53 +/+, was directly irradiated wi...
متن کاملA genotype-phenotype correlation for GJB2 (connexin 26) deafness.
INTRODUCTION Mutations in GJB2 are the most common cause of non-syndromic autosomal recessive hearing impairment, ranging from mild to profound. Mutation analysis of this gene is widely available as a genetic diagnostic test. OBJECTIVE To assess a possible genotype-phenotype correlation for GJB2. DESIGN Retrospective analysis of audiometric data from people with hearing impairment, segregat...
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ژورنال
عنوان ژورنال: Molecular Cancer Therapeutics
سال: 2011
ISSN: 1535-7163,1538-8514
DOI: 10.1158/1535-7163.mct-10-0693