Conserved modes of recruitment of ATM, ATR and DNA-PKcs to sites of DNA damage

By J. Falck, J. Coates, Stephen P. Jackson. Nature, 2005

1,349 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/c34a722957340c95ed5a6255f5b3ea328147cec6

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. Stephen P. Jackson
2. J. Bartek
3. J. Lukas
4. M. Lieber
5. S. Polo
6. M. Foiani
7. Dana Branzei
8. T. Stracker

In Molecular Biology

1. Stephen P. Jackson
2. J. Bartek
3. J. Lukas
4. S. Polo
5. P. Jeggo
6. M. Lieber
7. Andrew N. Blackford
8. L. Zou

In Oncology

1. Stephen P. Jackson
2. J. Bartek
3. J. Lukas
4. P. Jeggo
5. S. Polo
6. L. Zou
7. Alexandre Maréchal
8. M. Lieber

Citations in the corpus

• The role of double-strand break repair — insights from human genetics (2006, background): “Current evidence indicates that the MRE11–RAD50–NBS1 complex (MRN complex) is the primary DSB sensor that recruits ATM to the DS”
• Surviving the breakup: the DNA damage checkpoint. (2006, background): “Rather than using Ddc2/ATRIP, these kinases bind DNA through their interaction with the DNA-binding MRX/MRN complex (Figure 2a) (43, 101).”
• ATM Activation by Oxidative Stress (2010, background): “Following DNA damage, ATM arrives early at the DNA DSB sites, associating either with DNA that flank the break, or with the MRN complex at the break site through the C terminus of NBS1 [47, 48].”
• Chapter 1. General introduction (2015, neutral): “with speci! c factors: NBS1/Xrs2 (for ATM/Tel1), ATR-interacting protein (ATRIP)/Ddc2 in yeast (for ATR/Mec1) and Ku80 (for DNA-PK) (10).”
• Dynamics of DNA damage response proteins at DNA breaks: a focus on protein modifications. (2011, background): “MRN contributes to the recruitment and activation of the apical DDR kinase ATM (ataxia telangiectasia mutated) (Uziel et al. 2003; Falck et al. 2005; Lee and Paull 2005), while RPA recruits the ATR (ATM and rad3-related) kinase via its partner protein, ATRIP (ATR-interacting partner) (Cortez et al.”
• The Mechanism of Double-Strand DNA Break Repair by the Nonhomologous DNA End Joining Pathway (2010, background): “The MRX nuclease system and the DNAPKcs system both rely on the same conserved C-terminal tail for protein-protein interaction, also suggesting that the Artemis:DNA-PKcs complex may have evolved to replace the MRX complex for vertebrate NHEJ (46).”
• ATM, ATR, and DNA-PK: The Trinity at the Heart of the DNA Damage Response. (2017, background): “, 2006), in a process that requires ATM binding to the C terminus of NBS1 (Falck et al., 2005), a component of the MRE11-RAD50-NBS1 (MRN) complex (Carney et al.”
• The p53 protein and its molecular network: modelling a missing link between DNA damage and cell fate. (2014, background): “In these cases ATM associates with DNA break sites and the ATM attraction to unwinding DNA break ends is modulated by the C-terminus of Nbs1 [28], a part of the complex of Mre11 / Rad50 / Nbs1 proteins that actually acts as a sensor of DNA DSBs [8].”
• The MRE11 complex: starting from the ends (2011, background): “The C terminus of NBS1 contains a 24 amino acid conserved motif that interacts with AT”
• Regulation of DNA repair throughout the cell cycle (2008, background): “Activation and recruitment of these kinases to DNA lesions occurs through direct interactions with the specificity factors NBS1 (for ATM), ATRIP (for ATR) and Ku80 (for DNA-PK”
• RNF8 ubiquitylates histones at DNA double-strand breaks and promotes assembly of repair proteins. (2007, neutral): “Because NBS1 also directly binds ATM ( Falck et al., 2005; You et al., 2005), the MDC1-mediated retention of NBS1 has a crucial physiological significance for the initial”
• ATM- and cell cycle-dependent regulation of ATR in response to DNA double-strand breaks (2006, background): “Furthermore, ATM and ATR are recruited to sites of DNA damage by related mechanism”