DNA damage-induced activation of p53 by the checkpoint kinase Chk2.

By A. Hirao, Y. Kong, S. Matsuoka, A. Wakeham, J. Ruland, Hiroki Yoshida, Dou Liu, Stephen J. Elledge, T. Mak. Science, 2000

1,362 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/a98f8309364a52f898af97cfa17b32c6dd1f7f07

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Citations in the corpus

Cell cycle checkpoint signaling through the ATM and ATR kinases. (2001, background): “Hence, loss of either of two biochemically connected checkpoint kinases, ATM or Chk2, paradoxically increases the resistance of immature (CD4+CD8+) T cells to ionizing radiation (IR)-induced apoptosis (Xu and Baltimore 1996; Hirao 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).”
Regulation of p53 activity by its interaction with homeodomain-interacting protein kinase-2 (2002, background): “For example, Ser 6, Ser 9, Ser 15, Ser 20 and Ser 37 are phosphorylated in response to DNA damage, probably by protein kinases including ATM, Chk2, DNA-PK and AT”
Regulation of HDM2 activity by the ribosomal protein L11. (2003, neutral): “CANCER CELL : JUNE 2003 · VOL. 3 · COPYRIGHT 2003 CELL PRESS 577 al., 2001; Chehab et al., 2000; Goldberg et al., 2002; Hirao et al., 2000; Maya et al., 2001; Shieh et al., 2000).”
Toward maintaining the genome: DNA damage and replication checkpoints. (2002, background): “This phosphorylation by ATM likely causes p53 transcriptional activation (51), while phosphorylation of p53 at Ser 20 by Chk2 acting downstream of ATM, reduces the ability of ubiquitin ligase Mdm2 to bind p53, thus promoting its stabilization (34, 87, 90, 169).”
Ubiquitination, phosphorylation and acetylation: the molecular basis for p53 regulation. (2003, background): “Phosphorylation of Ser20 by checkpoint kinase 1 (Chk1) and Chk2 in response to ionizing radiation is important in abrogating the p53–Mdm2 interaction [6–8].”
The ATM–Chk2–Cdc25A checkpoint pathway guards against radioresistant DNA synthesis (2001, background): “In addition to Cdc25A, Chk2 also efficiently phosphorylates the p53 tumour suppressor in response to DNA damag”
DNA double-strand breaks: signaling, repair and the cancer connection (2001, background): “Notably, expression of dominant-negative CHK1 and CHK2 mutants lead to defective p53 stabilization in response to IR, and Chek2 −/− embryonic stem cells are defective in p53 stabilization after IR (ref”
Mechanisms of human DNA repair: an update. (2003, background): “…Chk1 are able to phosphorylate p53 at Ser20 (Shieh et al., 2000), giving rise to blockage of the MDM2-binding site-thus leading to release of p53 from MDM2-a protein that normally targets p53 for ubiquitin-dependent degradation (Chehab et al., 1999, 2000; Hirao et al., 2000; Unger et al., 1999).”
Regulation of the G2/M transition by p53 (2001, background): “However, these pathways are not completely independent because Chk1 and Chk2 can phosphorylate serine 20 in the amino-terminal region of p53 (Hirao et al., 2000; Shieh et al., 2000, Figure 1).”