ATM- and cell cycle-dependent regulation of ATR in response to DNA double-strand breaks

By A. Jazayeri, J. Falck, C. Lukas, J. Bartek, G. Smith, J. Lukas, Stephen P. Jackson. Nature Cell Biology, 2006

1,154 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/df117b02bcfcc2fafeaea4cbf0bff06eb862407f

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Citations in the corpus

DNA damage sensing by the ATM and ATR kinases. (2013, background): “4) (Adams et al. 2006; Jazayeri et al. 2006; Myers and Cortez 2006; Sartori et al. 2007; Peng et al. 2012; Tomimatsu et al. 2012).”
DNA helicases Sgs1 and BLM promote DNA double-strand break resection. (2008, methodology): “…for 1 h to induce DSB formation (Camptothecin was used because resection is needed for repair of Camptothecininduced DSBs and because such DSBs occur in S phase, when CDK levels are sufficient to allow efficient resection to occur) (Pommier et al. 2003; Jazayeri et al. 2006; Sartori et al. 2007).”
Encoding and Decoding Cellular Information through Signaling Dynamics (2013, neutral): “For example, when the levels of the phosphorylated kinase ATM (ATM-P) were measured at high frequency during the first hour after DNAdamage, the conclusion was that ATM is rapidly phosphorylated and reaches a maximal level within 5 min after damage, followed by a slow decrease (Jazayeri et al., 2006”
Cooperation of breast cancer proteins PALB2 and piccolo BRCA2 in stimulating homologous recombination (2010, neutral): “11 ) are required for processing the DSB to generate the replication protein A (RPA)–coated single-stranded DNA (ssDNA) that is needed for recruitment of ATM and Rad3-related (ATR) kinase and subsequent phosphorylation and activation of CHK1 (ref”
53BP1 inhibits homologous recombination in Brca1-deficient cells by blocking resection of DNA breaks (2010, positive): “Rescue of Brca1 Mutant Cells by 53BP1 Deletion Is Dependent on ATM ATM kinase activity is required for nucleolytic processing of DSBs to generate RPA-coated ssDNA (Jazayeri et al., 2006).”
p53-deficient cells rely on ATM- and ATR-mediated checkpoint signaling through the p38MAPK/MK2 pathway for survival after DNA damage. (2007, result): “Thislatterfinding is consistent with a recent study by Jazayeri et al. (2006) , which showed that both ATM and Mre11 are recruited to DNA double-strand breaks, converting them into RPA-coated single-strand DNA, which then recruits ATR.”
Surviving the breakup: the DNA damage checkpoint. (2006, background): “Recent data in human cells suggest that ATM triggers DSB resection and the consequent RPA loading and leads directly to ATR activation (28, 64).”
Dynamics of DNA damage response proteins at DNA breaks: a focus on protein modifications. (2011, background): “…of the cell cycle stage, focus formation by others—including CtIP, RPA, ATRIP–ATR, BRCA1, and RAD51—takes place effectively only in association with ssDNA formation by DNA end resection in S/G2 cells (Lisby et al. 2004; Bekker-Jensen et al. 2006; Jazayeri et al. 2006; Sartori et al. 2007).”