H2AX: the histone guardian of the genome.
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TLDR
A model in which chromatin restructuring mediated by H2AX phosphorylation serves to concentrate DNA repair/signaling factors and/or tether DNA ends together, which could explain the pleotropic phenotypes observed in its absence is suggested.About:
This article is published in DNA Repair.The article was published on 2004-08-01 and is currently open access. It has received 986 citations till now. The article focuses on the topics: Histone code & Histone.read more
Citations
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Journal ArticleDOI
A census of human RNA-binding proteins.
TL;DR: This work presents a census of 1,542 manually curated RBPs that are analysed for their interactions with different classes of RNA, their evolutionary conservation, their abundance and their tissue-specific expression, a critical step towards the comprehensive characterization of proteins involved in human RNA metabolism.
Journal ArticleDOI
γH2AX and cancer
William M. Bonner,Christophe E. Redon,Jennifer S. Dickey,Asako J. Nakamura,Olga A. Sedelnikova,Stéphanie Solier,Yves Pommier +6 more
TL;DR: In this paper, the authors used histone H2AX phosphorylation on a serine four residues from the carboxyl terminus (producing gammaH2AX) as a sensitive marker for DNA double-strand breaks (DSBs).
Journal ArticleDOI
RNF8 Ubiquitylates Histones at DNA Double-Strand Breaks and Promotes Assembly of Repair Proteins
Niels Mailand,Simon Bekker-Jensen,Helene Faustrup,Fredrik Melander,Jiri Bartek,Claudia Lukas,Jiri Lukas +6 more
TL;DR: It is suggested that MDC1-mediated and RNF8-executed histone ubiquitylation protects genome integrity by licensing the DSB-flanking chromatin to concentrate repair factors near the DNA lesions.
Journal ArticleDOI
MDC1 Directly Binds Phosphorylated Histone H2AX to Regulate Cellular Responses to DNA Double-Strand Breaks
Manuel Stucki,Julie A. Clapperton,Duaa H. Mohammad,Michael B. Yaffe,Stephen J. Smerdon,Stephen P. Jackson +5 more
TL;DR: It is shown that MDC1/NFBD1-gammaH2AX complex formation regulates H2AX phosphorylation and is required for normal radioresistance and efficient accumulation of DNA-damage-response proteins on damaged chromatin.
Book ChapterDOI
The ATM-Chk2 and ATR-Chk1 pathways in DNA damage signaling and cancer.
TL;DR: Current understanding of the organization and functions of the ATM-Chk2 and ATR- Chk1 pathways are reviewed and the prospects for targeting DNA damage signaling processes for therapeutic purposes are reviewed.
References
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Journal ArticleDOI
Crystal structure of the nucleosome core particle at 2.8 Å resolution
TL;DR: The X-ray crystal structure of the nucleosome core particle of chromatin shows in atomic detail how the histone protein octamer is assembled and how 146 base pairs of DNA are organized into a superhelix around it.
Journal ArticleDOI
DNA Double-stranded Breaks Induce Histone H2AX Phosphorylation on Serine 139
TL;DR: In this paper, a histone H2AX species that has been phosphorylated specifically at serine 139 was found to be a major component of DNA double-stranded break.
Journal ArticleDOI
DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation
TL;DR: It is shown that ATM is held inactive in unirradiated cells as a dimer or higher-order multimer, with the kinase domain bound to a region surrounding serine 1981 that is contained within the previously described ‘FAT’ domain.
Journal ArticleDOI
Class Switch Recombination and Hypermutation Require Activation-Induced Cytidine Deaminase (AID), a Potential RNA Editing Enzyme
Masamichi Muramatsu,Kazuo Kinoshita,Sidonia Fagarasan,Shuichi Yamada,Yoichi Shinkai,Tasuku Honjo +5 more
TL;DR: Results suggest that AID may be involved in regulation or catalysis of the DNA modification step of both class switching and somatic hypermutation in CH12F3-2 B lymphoma.
Journal ArticleDOI
The DNA damage response: putting checkpoints in perspective
TL;DR: The inability to repair DNA damage properly in mammals leads to various disorders and enhanced rates of tumour development, and this work has shown that direct activation of DNA repair networks is needed to correct this problem.
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Genomic instability in mice lacking histone H2AX.
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