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修复蛋白对替代性DNA结构进行诱变处理的不同机制。

Distinct mechanisms of mutagenic processing of alternative DNA structures by repair proteins.

作者信息

McKinney Jennifer A, Wang Guliang, Vasquez Karen M

机构信息

Division of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin, Dell Pediatric Research Institute, Austin, TX, USA.

出版信息

Mol Cell Oncol. 2020 Apr 2;7(3):1743807. doi: 10.1080/23723556.2020.1743807. eCollection 2020.

DOI:10.1080/23723556.2020.1743807
PMID:32391433
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7199757/
Abstract

Repetitive sequences can form a variety of alternative DNA structures (non-B DNA) that can modulate transcription, replication, and repair. However, non-B DNA-forming sequences can also stimulate mutagenesis, and are enriched at mutation hotspots in human cancer genomes. Interestingly, different types of non-B DNA stimulate mutagenesis via distinct repair processing mechanisms.

摘要

重复序列可形成多种可调节转录、复制和修复的替代性DNA结构（非B型DNA）。然而，形成非B型DNA的序列也可刺激诱变作用，并且在人类癌症基因组的突变热点处富集。有趣的是，不同类型的非B型DNA通过不同的修复加工机制刺激诱变作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f579/7199757/9f1870a2f4b4/kmco-07-03-1743807-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f579/7199757/9f1870a2f4b4/kmco-07-03-1743807-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f579/7199757/9f1870a2f4b4/kmco-07-03-1743807-g001.jpg

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