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Evidence for a lack of DNA double-strand break repair in human cells exposed to very low x-ray doses
TLDR
Evidence is presented that foci of γ-H2AX (a phosphorylated histone), detected by immunofluorescence, are quantitatively the same as DSBs and are capable of quantifying the repair of individual D SBs, allowing the investigation of DSB repair after radiation doses as low as 1 mGy, an improvement by several orders of magnitude over current methods. Expand
ATM and DNA-PK Function Redundantly to Phosphorylate H2AX after Exposure to Ionizing Radiation
TLDR
It is shown that under most normal growth conditions, IR-induced H2AX phosphorylation can be carried out by ATM and DNA-PK in a redundant, overlapping manner. Expand
Pathways of DNA Double-Strand Break Repair during the Mammalian Cell Cycle
TLDR
It is shown here that NHEJ-defective hamster cells (CHO mutant V3 cells) have strongly reduced repair in all cell cycle phases after 1 Gy of irradiation, and HR is particularly important in late S/G2, where both pathways contribute to repair and radioresistance. Expand
ATM signaling facilitates repair of DNA double-strand breaks associated with heterochromatin.
TLDR
It is shown that < or =25% of DSBs require ATM signaling for repair, and this percentage correlates with increased chromatin but not damage complexity, which suggests that the importance of ATM signalling for DSB repair increases as the heterochromatic component of a genome expands. Expand
A pathway of double-strand break rejoining dependent upon ATM, Artemis, and proteins locating to gamma-H2AX foci.
TLDR
It is shown that ataxia telangiectasia mutated protein (ATM) and Artemis, the protein defective in patients with RS-SCID, function in a common double-strand break repair pathway that also requires H2AX, 53BP1, Nbs1, Mre11, and DNA-PK. Expand
γH2AX foci analysis for monitoring DNA double-strand break repair: Strengths, limitations and optimization
TLDR
Evidence is presented that following exposure to ionising radiation, γH2AX foci analysis can provide a sensitive monitor of DSB formation and repair and techniques to optimise the analysis are described, enabling the procedure to be optimally exploited but not misused. Expand
In vivo formation and repair of DNA double-strand breaks after computed tomography examinations.
TLDR
The data show that the in vivo induction and repair of DSBs can be assessed in individuals exposed to low radiation doses, adding a further dimension to DSB repair studies and providing the opportunity to identify repair-compromised individuals after diagnostic irradiation procedures. Expand
Factors determining DNA double‐strand break repair pathway choice in G2 phase
TLDR
It is proposed that NHEJ initially attempts to repair DSBs and, if rapid rejoining does not ensue, then resection occurs promoting repair by HR, and novel roles for ATM in regulating DSB end resection are identified. Expand
The impact of a negligent G2/M checkpoint on genomic instability and cancer induction
TLDR
The impact of a negligent G2/M checkpoint on genomic stability and cancer risk is considered and a defined threshold of 10–20 DSBs is shown. Expand
53BP1-dependent robust localized KAP-1 phosphorylation is essential for heterochromatic DNA double-strand break repair
TLDR
It is proposed that ionizing-radiation induced foci (IRIF) spatially concentrate ATM activity to promote localized alterations in regions of chromatin otherwise inhibitory to repair. Expand
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