H2AX haploinsufficiency modifies genomic stability and tumor susceptibility.
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ABSTRACT:
SUBMITTER: Celeste A
PROVIDER: S-EPMC4737479 | biostudies-literature | 2003 Aug
REPOSITORIES: biostudies-literature
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H2AX haploinsufficiency modifies genomic stability and tumor susceptibility.
Celeste Arkady A Difilippantonio Simone S Difilippantonio Michael J MJ Fernandez-Capetillo Oscar O Pilch Duane R DR Sedelnikova Olga A OA Eckhaus Michael M Ried Thomas T Bonner William M WM Nussenzweig André A
Cell 20030801 3
Histone H2AX becomes phosphorylated in chromatin domains flanking sites of DNA double-strand breakage associated with gamma-irradiation, meiotic recombination, DNA replication, and antigen receptor rearrangements. Here, we show that loss of a single H2AX allele compromises genomic integrity and enhances the susceptibility to cancer in the absence of p53. In comparison with heterozygotes, tumors arise earlier in the H2AX homozygous null background, and H2AX(-/-) p53(-/-) lymphomas harbor an incre ...[more]
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