Ataxia telangiectasia-mutated phosphorylates Chk2 in vivo and in vitro.

By S. Matsuoka, G. Rotman, Akira Ogawa, Yosef Shiloh, K. Tamai, Stephen J. Elledge. Proceedings of the National Academy of Sciences of the United States of America, 2000

896 citations recorded by the source corpus.

Subfields: Cancer Research, Cell Biology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/7f392f3ba36d7628c2e12bc161f99fc6df6a392b

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Citations in the corpus

• The ATM-Chk2 and ATR-Chk1 pathways in DNA damage signaling and cancer. (2010, background): “ATM and Chk2 are activated potently by radiation and genotoxins that induce DSBs, but only weakly, if at all, by agents that block DNA replication without inducing damage (Matsuoka et al., 2000).”
• Cellular response to oxidative stress: Signaling for suicide and survival * (2002, background): “Chk2, another kinase capable of phosphorylating serine-20 of p53 (Hirao et al., 2000), is directly phosphorylated by ATM following IR and by ATR (ATM and Rad3-related) following UVC treatment (Matsuoka et al., 2000; reviewed in Shiloh, 2001).”
• Low-penetrance susceptibility to breast cancer due to CHEK2*1100delC in noncarriers of BRCA1 or BRCA2 mutations (2002, background): “In mammalian cells, CHEK2 is activated, through phosphorylation by AT”
• BRCA1 and BRCA2: 1994 and beyond (2004, background): “CHK2 encodes the human homologue of the yeast checkpoint kinases Cds1 and Rad53 (Ref”
• DNA damage-induced cell death: from specific DNA lesions to the DNA damage response and apoptosis. (2013, background): “after the formation of DSBs at Thr68 [114], while ATR phosphorylates Chk1 (checkpoint kinase-1) at Ser345 upon stalled DNA rep-”
• Regulation of the G2/M transition by p53 (2001, background): “Atm and Atr can phosphorylate and activate the serine kinases Chk1 and Chk2 (Chaturvedi et al., 1999; Liu et al., 2000; Matsuoka et al., 2000, Figure 1).”
• Mechanisms of human DNA repair: an update. (2003, background): “Upon activation of their intrinsic kinase activity, ATM and/or ATR phosphorylate Chk1 and Chk2, which in turn phosphorylate p53 and CDc25, thus provoking cell cycle arrest.”