The ATM–Chk2–Cdc25A checkpoint pathway guards against radioresistant DNA synthesis

By J. Falck, Niels Mailand, R. Syljuåsen, J. Bartek, J. Lukas. Nature, 2001

1,201 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/8bc47eb87892336e102582c00de40e687402fdf6

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In Cell Biology

1. R. Abraham

In Molecular Biology

1. Thomas Helleday
2. Ricky A. Sharma
3. R. Abraham
4. Zdenko Herceg

In Oncology

1. R. Abraham
2. D. Raulet
3. Thomas Helleday

Citations in the corpus

• DNA repair pathways as targets for cancer therapy (2008, background): “Cell-cycle checkpoints are regulated by effector kinases, such as ataxia telangiectasia mutated ( ATM ) and ATM and Rad3-related ( ATR”
• Regulation of ligands for the NKG2D activating receptor (2013, background): “ATM or ATR activation can cause cell cycle arrest, either through the action of p53 or by a p53-independent mechanism (37).”
• Toward maintaining the genome: DNA damage and replication checkpoints. (2002, background): “Cdc25A is also implicated as a downstream effector since it appears to regulate ORC complexes at initiation (59).”
• DNA double-strand break repair: from mechanistic understanding to cancer treatment. (2007, background): “It has been clear for many years that ionizing radiation directly impairs replication origin firing through ATM signaling [95,96], in a process that is facilitated by the MRN complex [97].”
• Histone acetylation by Trrap–Tip60 modulates loading of repair proteins and repair of DNA double-strand breaks (2006, background): “To test whether DNA-damage detection and signalling is affected in cells lacking Trrap, we investigated the autoactivation of ATM (as assessed by autophosphorylation of ATM at Ser 1981) and the ATM– Chk2 – Cdc25A cascade, steps that are proposed to be important in irradiation-induced DNA-damage s”
• Regulation and mechanisms of mammalian double-strand break repair (2003, background): “A hallmark of AT is RDS, which could be the result of impairing two separate, parallel signaling pathways (Falck et al., 2001, 2002).”
• Cell cycle checkpoint signaling through the ATM and ATR kinases. (2001, background): “An intriguing report now shows that the surveillance functions of the ATM–hChk2 pathway are not confined to G1 phase (Falck et al. 2001).”