“…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.…”
“…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.…”
“…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
“…58 Accordingly, RNF8 starts accumulating at the separated chromatids in telophase, which is a late stage of mitosis, when sister telomeres have separated. 61 …”
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