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Phosphorylation of histone H2AX and activation of Mre11, Rad50, and Nbs1 in response to replication-dependent DNA double-strand breaks induced by mammalian DNA topoisomerase I cleavage complexes. (Q44378806)

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scientific article published on 25 March 2003

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English	Phosphorylation of histone H2AX and activation of Mre11, Rad50, and Nbs1 in response to replication-dependent DNA double-strand breaks induced by mammalian DNA topoisomerase I cleavage complexes.	scientific article published on 25 March 2003

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1 November 2019

Phosphorylation of histone H2AX and activation of Mre11, Rad50, and Nbs1 in response to replication-dependent DNA double-strand breaks induced by mammalian DNA topoisomerase I cleavage complexes (English)

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phosphorylation

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Yves Pommier

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Takahisa Furuta

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Haruyuki Takemura

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Zhi-Yong Liao

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Christophe Redon

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Olga A Sedelnikova

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Duane R Pilch

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Emmy P Rogakou

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Arkady Celeste

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Hua Tang Chen

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Andre Nussenzweig

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Mirit I Aladjem

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William M Bonner

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25 March 2003

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20303-20312

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1 November 2019

Rearrangements of chromatin structure in newly repaired regions of deoxyribonucleic acid in human cells treated with sodium butyrate or hydroxyurea

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Chromosomal stability and the DNA double-stranded break connection

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When repair meets chromatin. First in series on chromatin dynamics

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Evolutionary conservation of histone macroH2A subtypes and domains

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Phylogenetic analysis of the core histones H2A, H2B, H3, and H4

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Histone H2A variants H2AX and H2AZ

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DNA Double-stranded Breaks Induce Histone H2AX Phosphorylation on Serine 139

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Megabase chromatin domains involved in DNA double-strand breaks in vivo

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Response to RAG-mediated VDJ cleavage by NBS1 and gamma-H2AX

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AID is required to initiate Nbs1/γ-H2AX focus formation and mutations at sites of class switching

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Initiation of DNA fragmentation during apoptosis induces phosphorylation of H2AX histone at serine 139

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DNA repair: spot(light)s on chromatin.

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

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Increased ionizing radiation sensitivity and genomic instability in the absence of histone H2AX

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Genomic instability in mice lacking histone H2AX

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Single-strand interruptions in replicating chromosomes cause double-strand breaks

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Topoisomerase I-mediated DNA damage

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Benzo[a]pyrene diol epoxide adducts in DNA are potent suppressors of a normal topoisomerase I cleavage site and powerful inducers of other topoisomerase I cleavages

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Different effects on human topoisomerase I by minor groove and intercalated deoxyguanosine adducts derived from two polycyclic aromatic hydrocarbon diol epoxides at or near a normal cleavage site

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Cellular roles of dna topoisomerases: a molecular perspective

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A Model for the Mechanism of Human Topoisomerase I

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Overexpression of a kinase-inactive ATR protein causes sensitivity to DNA-damaging agents and defects in cell cycle checkpoints

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ATM phosphorylates histone H2AX in response to DNA double-strand breaks

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NBS1 localizes to gamma-H2AX foci through interaction with the FHA/BRCT domain

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