ATM Activation by DNA Double-Strand Breaks Through the Mre11-Rad50-Nbs1 Complex

By Ji‐Hoon Lee, T. Paull. Science, 2005

1,479 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/1e09715880b634e68dc6e4e0a897589de99f7471

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. B. Kaina
2. Jacob C. Harrison
3. J. Haber
4. Alberto Ciccia
5. Ivan Dikic
6. W. Roos
7. Stephen J. Elledge

In Molecular Biology

1. B. Kaina
2. W. Roos
3. Tony Pawson
4. Ivan Dikic
5. Alberto Ciccia
6. Y. L. Deribe
7. J. Smith
8. Jacob C. Harrison

In Oncology

1. B. Kaina
2. W. Roos
3. Tony Pawson
4. Alberto Ciccia
5. J. Smith
6. Jacob C. Harrison
7. J. Haber
8. Ivan Dikic

Citations in the corpus

• The p53 protein and its molecular network: modelling a missing link between DNA damage and cell fate. (2014, background): “The activation signal is however not biologically specified; it is assumed to be produced by changes in chromatin after DNA damage [24, 27], amplified by MRN complex (sensor of DNA DSBs) [54], or this signal may be actually the MRN complex itself and its interaction with ATM [55].”
• DNA damage-induced cell death: from specific DNA lesions to the DNA damage response and apoptosis. (2013, background): “tion was also shown to occur by interaction of ATM with the MRN complex and single-stranded DNA [94].”
• Post-translational modifications in signal integration (2010, background): “The inactive ATM dimer is recruited to DSBs by the Mre11–Rad50–Nbs1 (MRN) comple”
• Surviving the breakup: the DNA damage checkpoint. (2006, background): “These findings have led to a model in which DSB binding by MRN activates Rad50 ATPase activity, resulting in a conformational change in the MRN complex that then triggers activation of ATM (73, 162).”
• Mechanism and regulation of class switch recombination. (2008, background): “Mre11-Rad50-Nbs1—Accumulating evidence indicates that this complex of three proteins (MRN complex) travels along the DNA duplex scanning for DNA breaks and that MRN binds DSBs within seconds of their formation (129, 130).”
• The DNA Damage Response: Making it safe to play with knives (2010, background): “NBS1 associates with ATM via its C-terminal region, which promotes the recruitment of ATM to DSBs, where ATM is activated by the MRN complex by yet to be defined mechanisms, possibly involving the formation of ssDNA oligos during end resection (Figure 1A) (Jazayeri et al., 2008; Kanaar and Wyman, 20”
• The ATM-Chk2 and ATR-Chk1 pathways in DNA damage signaling and cancer. (2010, background): “ATMmonomers are then recruited to DSBs via interactions with the MRN sensor complex (Lee and Paull, 2007), stimulating full activation and providing a platform that enables ATM to act locally on multiple substrates at the site of damage.”