A critical role for histone H2AX in recruitment of repair factors to nuclear foci after DNA damage.

By T. Paull, E. Rogakou, Vikky Yamazaki, C. Kirchgessner, M. Gellert, W. Bonner. Current Biology, 2000

2,252 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/124630f902cee0943fe368549e62a67f35dd693d

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Citations in the corpus

ROS and the DNA damage response in cancer (2018, background): “Phosphorylated H2AX (γH2AX) helps to recruit multiple components of the DDR to the site of DNA DSBs to initiate DNA DSB repair [58,59].”
Cell cycle checkpoint signaling through the ATM and ATR kinases. (2001, background): “These ATM-containing complexes are colocalized with the phosphorylated form of histone H2AX, which suggests that they are generated in close proximity to DNA dsbs (Downs et al. 2000; Paull et al. 2000).”
MDC1 is a mediator of the mammalian DNA damage checkpoint (2003, background): “Many DNA damage-signalling proteins are recruited to sites of damag”
Histone H2AX phosphorylation is dispensable for the initial recognition of DNA breaks (2003, background): “DNA damage sensors, including proteins belonging to the phosphatidylinositol-3-OH kinase (PI(3)K)like family (ATM, DNA-PK (DNA-dependent protein kinase) and ATR (ATM- and Rad3-related)) are rapidly loaded onto the break.”
ATM and DNA-PK Function Redundantly to Phosphorylate H2AX after Exposure to Ionizing Radiation (2004, methodology): “protein kinase (DNA-PK)-defective tumor line M059J (18).”
Role of RAD52 Epistasis Group Genes in Homologous Recombination and Double-Strand Break Repair (2002, methodology): “Preirradiation exposure of cells to the fungal metabolite wortmannin, which inhibits phosphatidylinositol 3-kinases, prevented the formation of -H2AX and Rad50 foci, suggesting that -H2AX is required to recruit Rad50 to sites of damage (279).”
Regulation of nucleosome dynamics by histone modifications (2013, neutral): “Set1 Stable binding and infrequent dissociation n p g r e V i e W recruits the DNA repair machinery to double-strand breaks 56 .”
γH2AX foci analysis for monitoring DNA double-strand break repair: Strengths, limitations and optimization (2010, background): “γH2AX foci analysis is one such assay that exploits an early step in the damage response, namely the phosphorylation of H2AX, a variant form of the histone, H2A.(2,3) Since phosphorylated H2AX, designated γH2AX, expands a large distance (Mbp) from the DSB site and since specific γH2AX antibodies are”
A role for Saccharomyces cerevisiae histone H2A in DNA repair (2000, background): “Recent work in mammalian cells has shown that the DNA-damage-dependent phosphorylation of the human H2AX SQE motif is greatly impaired by the PIKK family inhibitor wortmanni”
RNF8 transduces the DNA-damage signal via histone ubiquitylation and checkpoint protein assembly. (2007, background): “It is generally accepted that the phosphorylation of histone variant H2AX is the initial signal upon DNA lesion detection. g-H2AX is required for the sustained localization of a number of DNA-damage mediator/repair factors at chromatin regions at or near the sites of DNA damage (Paull et al., 2000).”
The JNK signal transduction pathway. (2007, neutral): “Previous studies have suggested that H2AX phosphorylation by members of the PIKK group of kinases is a consequence of apoptosis [41,42]; however, the recent study by Lu and colleagues indicates that JNK-mediated H2AX phosphorylation may be essential for DNA fragmentation in UV-stimulated cells [39].”