کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2147642 | 1548420 | 2006 | 17 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Non-B DNA structure-induced genetic instability
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کلمات کلیدی
SSBTFOsFEN-1PKD1Z-DNARPAActivation-induced cytidine deaminaseMMRMBRDSBsNER - DOWNH-DNA - H DNATriplex-forming oligonucleotides - الیگونوکلئوتید های تشکیل دهنده سه گانهGenetic instability - بی ثباتی ژنتیکیDNA repair - ترمیم DNAnucleotide excision repair - تعمیر مجدد نوکلئوتیدیmismatch repair - تعمیر ناسازگاریreplication protein A - تلقیح پروتئین ADNA secondary structure - ساختار ثانویه DNAdouble-strand breaks - شکست دو ردیفFlap endonuclease-1 - فلاپ آندوسکوئاز-1major breakpoint region - منطقه توقف بزرگSingle-stranded DNA binding protein - پروتئین متصل به یک رشته DNACruciform - کریو شکلAID - کمک
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Repetitive DNA sequences are abundant in eukaryotic genomes, and many of these sequences have the potential to adopt non-B DNA conformations. Genes harboring non-B DNA structure-forming sequences increase the risk of genetic instability and thus are associated with human diseases. In this review, we discuss putative mechanisms responsible for genetic instability events occurring at these non-B DNA structures, with a focus on hairpins, left-handed Z-DNA, and intramolecular triplexes or H-DNA. Slippage and misalignment are the most common events leading to DNA structure-induced mutagenesis. However, a number of other mechanisms of genetic instability have been proposed based on the finding that these structures not only induce expansions and deletions, but can also induce DNA strand breaks and rearrangements. The available data implicate a variety of proteins, such as mismatch repair proteins, nucleotide excision repair proteins, topoisomerases, and structure specific-nucleases in the processing of these mutagenic DNA structures. The potential mechanisms of genetic instability induced by these structures and their contribution to human diseases are discussed.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis - Volume 598, Issues 1â2, 25 June 2006, Pages 103-119
Journal: Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis - Volume 598, Issues 1â2, 25 June 2006, Pages 103-119
نویسندگان
Guliang Wang, Karen M. Vasquez,