gammaH2AX and MDC1: anchoring the DNA-damage-response machinery to broken chromosomes.

No abstract is available for this paper.

• Publication year

  2006

• Venue

  DNA Repair

• Publication date

  2006-05-10

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1016/J.DNAREP.2006.01.012PMID 16531125
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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• gamma-H2AX dephosphorylation by protein phosphatase 2A facilitates DNA double-strand break repair.

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• DNA damage response pathway uses histone modification to assemble a double-strand break-specific cohesin domain.

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• Recruitment of the INO80 complex by H2A phosphorylation links ATP-dependent chromatin remodeling with DNA double-strand break repair.

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• INO80 and gamma-H2AX interaction links ATP-dependent chromatin remodeling to DNA damage repair.

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• Postreplicative recruitment of cohesin to double-strand breaks is required for DNA repair.

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• H2AX haploinsufficiency modifies genomic stability and tumor susceptibility.

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• DNA damage-induced G2–M checkpoint activation by histone H2AX and 53BP1

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• Genomic Instability in Mice Lacking Histone H2AX

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