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Open AccessJournal ArticleDOI

The Histone Mark H3K36me3 Regulates Human DNA Mismatch Repair through Its Interaction with MutSα

TLDR
It is shown that an epigenetic histone mark, H3K36me3, is required in vivo to recruit the mismatch recognition protein hMutSα onto chromatin through direct interactions with the hMSH6 PWWP domain.
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This article is published in Cell.The article was published on 2013-04-25 and is currently open access. It has received 504 citations till now. The article focuses on the topics: DNA mismatch repair & Histone code.

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Journal ArticleDOI

Mechanisms of DNA damage, repair, and mutagenesis.

TL;DR: This introductory review will delineate mechanisms of DNA damage and the counteracting repair/tolerance pathways to provide insights into the molecular basis of genotoxicity in cells that lays the foundation for subsequent articles in this issue.
Journal ArticleDOI

Writing, erasing and reading histone lysine methylations

TL;DR: A more detailed understanding of histone lysine methylation is necessary for elucidating complex biological processes and, ultimately, for developing and improving disease treatments.
References
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Journal ArticleDOI

Mapping the hallmarks of lung adenocarcinoma with massively parallel sequencing

TL;DR: Exome and genome sequences and whole-genome sequence analysis revealed frequent structural rearrangements, including in-frame exonic alterations within EGFR and SIK2 kinases, which are attractive targets for biological characterization and therapeutic targeting of lung adenocarcinoma.
Journal ArticleDOI

Mismatch repair in replication fidelity, genetic recombination, and cancer biology.

TL;DR: Homologs of bacterial MutS and MutL, which play key roles in mismatch recognition and initiation of repair, have been identified in yeast and mammalian cells and results in a large increase in spontaneous mutability.
Journal Article

Methylation of the hMLH1 Promoter Correlates with Lack of Expression of hMLH1 in Sporadic Colon Tumors and Mismatch Repair-defective Human Tumor Cell Lines

TL;DR: Analysis of sporadic colorectal tumors for the expression of hMLH1 by immunohistochemistry indicates that DNA methylation is likely to be a common mode of mismatch repair gene inactivation in sporadic tumors.
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