2011
DOI: 10.4161/cc.10.8.15334
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Give me a break, but not in mitosis

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Cited by 48 publications
(30 citation statements)
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“…Since ubiquitination does not occur on mitotic chromatin, 53BP1 cannot localize to sites of DNA damage during mitosis, while γH2AX remains and provides a marker of mitotic DNA damage. 12,13 In the subsequent G 1 phase, 53BP1 is recruited to the damaged regions and prevents undesired DNA end processing until lesion is repaired during the next S phase. However, the precise molecular mechanisms regulating formation of these endogenous 53BP1 nuclear bodies remain to be elucidated.…”
Section: Resultsmentioning
confidence: 99%
See 1 more Smart Citation
“…Since ubiquitination does not occur on mitotic chromatin, 53BP1 cannot localize to sites of DNA damage during mitosis, while γH2AX remains and provides a marker of mitotic DNA damage. 12,13 In the subsequent G 1 phase, 53BP1 is recruited to the damaged regions and prevents undesired DNA end processing until lesion is repaired during the next S phase. However, the precise molecular mechanisms regulating formation of these endogenous 53BP1 nuclear bodies remain to be elucidated.…”
Section: Resultsmentioning
confidence: 99%
“…Moreover, due to the lacking ubiquitination of mitotic chromatin, 53BP1 cannot bind to DNA lesions until cells exit from mitosis and enter the next G 1 . 12,13 Thus, γH2AX appears to be an essential marker of endogenous DNA lesions present in unperturbed mitosis. Previously, we have shown that Wip1 associates with the chromatin and dephosphorylates γH2AX.…”
mentioning
confidence: 99%
“…Occurrence of γH2AX signals during mitosis after DNA damage induction has been previously reported [16] [20] [21] leading to the assumption that persisting γH2AX signals may serve to facilitate DDR in the novel cell generation [22] [23]. Thus, the observed γH2AX signal increase in CHO9 metaphases treated with BLM could correspond to a DDR related H2AX 139 phosphorylation persisting through mitosis.…”
Section: Blm-exposure Increased γH2ax Signals On Metaphase Chromosomesmentioning
confidence: 94%
“…Once these cell cycle checkpoints are passed, mammalian cells go through mitosis, even in the presence of DNA damage. A still poorly understood γH2AX immunostaining has been observed in mitotic chromosomes, probably related to these checkpoint pathways [16] [20]- [22], serving to facilitate DDR activation and accelerate DNA damage repair in the novel cell generation [22] [23].…”
Section: H2ax 139 Phosphorylation Related To Dna Damage Responsementioning
confidence: 99%
“…58 Accordingly, RNF8 starts accumulating at the separated chromatids in telophase, which is a late stage of mitosis, when sister telomeres have separated. 61 …”
Section: Dsb-induced Ddr In Mitosismentioning
confidence: 99%