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

By O. Fernández-Capetillo, Hua-Tang Chen, Arkady Celeste, Irene M. Ward, P. Romanienko, Julio C Morales, K. Naka, Zhenfang Xia, R. Camerini‐Otero, N. Motoyama and 4 more. Nature Cell Biology, 2002

698 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/5a1a2efe84380dd3e057150679831052d375c9f4

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Citations in the corpus

• 53BP1 inhibits homologous recombination in Brca1-deficient cells by blocking resection of DNA breaks (2010, neutral): “The only known functions of 53BP1 are in transducing a subset of ATM dependent cell cycle checkpoints (DiTullio et al., 2002; Fernandez-Capetillo et al., 2002; Lee et al., 2009; Wang et al., 2002) and facilitating the joining of distal DSBs formed at dysfunctional telomeres and during lymphocyte ant”
• DNA damage sensing by the ATM and ATR kinases. (2013, background): “Whereas H2AX phosphorylation is not critical for phosphorylation of ATM substrates such as Chk2 and p53 (Fernandez-Capetillo et al. 2002; Kang et al. 2005), it is required for accumulation of numerous DNA repair proteins and chromatin-remodeling complexes around DSBs. Cumulative evidence suggests…”
• The γ‐H2A.X: Is it just a surrogate marker of double‐strand breaks or much more? (2008, background): “X manifest a G2/M checkpoint defect close to that observed in ATM cells after exposure to low, but not high, doses of IR [Fernandez-Capetillo et al., 2002].”
• Histone H2AX phosphorylation is dispensable for the initial recognition of DNA breaks (2003, background): “Although the physiological function of IRIF remains unclear, the sequestration of thousands of factors in the vicinity of a DSB might be particularly important for facilitating the repair of persistent lesions and for amplifying the damage-induced checkpoint signa”
• RNF8 transduces the DNA-damage signal via histone ubiquitylation and checkpoint protein assembly. (2007, background): “Specifically, a number of DNA-damage response proteins, including BRCA1 and MDC1 (Fernandez-Capetillo et al., 2002; Goldberg et al., 2003; Lou et al., 2003a, 2003b; Stewart et al., 2003), harbor BRCT domains that mediate binding to their respective partners in a phosphorylation-dependent manner (Yu ”
• Checking on DNA damage in S phase (2004, background): “Interestingly, cells that are derived from H2AX −/− mice show severe G2-checkpoint defects after low (but not high) doses of I”
• The role of double-strand break repair — insights from human genetics (2006, background): “The accumulation of these proteins at a DSB enhances, but is not essential for, checkpoint arres”
• Pathways of apoptotic and non-apoptotic death in tumour cells (2004, positive): “53BP1-deficient cells also show a G2-checkpoint defec”
• γ-H2AX in recognition and signaling of DNA double-strand breaks in the context of chromatin (2008, methodology): “It has been, therefore, suggested that g-H2AX is involved in the amplification step required for optimal checkpoint response at relatively low levels of DNA damage (30,98,99).”