کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10823532 | 1061882 | 2009 | 16 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Novel DNA mismatch-repair activity involving YB-1 in human mitochondria
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کلمات کلیدی
antimycin AEMSAMitoplastY-box binding protein 1WCECOXIVYB-1MMRMSIMitochondrial DNA - DNA میتوکندریاMALDI–TOF - MALDI-TOFsiRNA - siRNAelectromobility shift assay - آزمایش الکتریکی حرکتیsmall interfering ribonucleic acid - اسید ریبونوکلئیک دخالت کندMicrosatellite instability - بی ثباتی ریزماهواره ایmismatch repair - تعمیر ناسازگاریmtDNA - دیانای میتوکندریاییwhole cell extract - عصاره کل سلولMatrix-assisted laser desorption/ionization–time of flight - مدت زمان جذب / زمان یونیزاسیون لیزر ماتریس کمک می کندMitochondria - میتوکندریاCaP - کلاه لبه دارChloramphenicol - کلرامفنیکل
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Maintenance of the mitochondrial genome (mtDNA) is essential for proper cellular function. The accumulation of damage and mutations in the mtDNA leads to diseases, cancer, and aging. Mammalian mitochondria have proficient base excision repair, but the existence of other DNA repair pathways is still unclear. Deficiencies in DNA mismatch repair (MMR), which corrects base mismatches and small loops, are associated with DNA microsatellite instability, accumulation of mutations, and cancer. MMR proteins have been identified in yeast and coral mitochondria; however, MMR proteins and function have not yet been detected in human mitochondria. Here we show that human mitochondria have a robust mismatch-repair activity, which is distinct from nuclear MMR. Key nuclear MMR factors were not detected in mitochondria, and similar mismatch-binding activity was observed in mitochondrial extracts from cells lacking MSH2, suggesting distinctive pathways for nuclear and mitochondrial MMR. We identified the repair factor YB-1 as a key candidate for a mitochondrial mismatch-binding protein. This protein localizes to mitochondria in human cells, and contributes significantly to the mismatch-binding and mismatch-repair activity detected in HeLa mitochondrial extracts, which are significantly decreased when the intracellular levels of YB-1 are diminished. Moreover, YB-1 depletion in cells increases mitochondrial DNA mutagenesis. Our results show that human mitochondria contain a functional MMR repair pathway in which YB-1 participates, likely in the mismatch-binding and recognition steps.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: DNA Repair - Volume 8, Issue 6, 4 June 2009, Pages 704-719
Journal: DNA Repair - Volume 8, Issue 6, 4 June 2009, Pages 704-719
نویسندگان
Nadja C. de Souza-Pinto, Penelope A. Mason, Kazunari Hashiguchi, Lior Weissman, Jingyan Tian, David Guay, Michel Lebel, Tinna V. Stevnsner, Lene Juel Rasmussen, Vilhelm A. Bohr,