Requirement of the MRN complex for ATM activation by DNA damage

By Tamar Uziel, Y. Lerenthal, L. Moyal, Y. Andegeko, L. Mittelman, Yosef Shiloh. EMBO Journal, 2003

1,167 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/192b3a444ceea4022bb6d5eed0fa728718f42bb2

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Citations in the corpus

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].”
DNA damage sensing by the ATM and ATR kinases. (2013, background): “rapid localization of ATM to DSBs and its activation in cells, and purified MRN complex is sufficient to directly stimulate the dimeric/oligomeric ATM kinase in the presence of dsDNA (Uziel et al. 2003; Lee and Paull 2005).”
ATM- and cell cycle-dependent regulation of ATR in response to DNA double-strand breaks (2006, background): “IR-induced Chk1 phosphorylation and RPA focus formation was therefore examined in Mre11-deficient ataxia-telangiectasia-like disorder (ATLD) cells stably transfected with an empty vector or with vectors directing the expression of full-length Mre11 or the nuclease-dead mutant Mre11-3 (ref”
ATM Activation by Oxidative Stress (2010, background): “ATM activation is inhibited in cells deficient in NBS1 or Mre11 in response to DNA DSBs [25].”
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 MRE11 complex: starting from the ends (2011, methodology): “In mammalian systems, the MRE11 nuclease activity has been implicated in the activation of ATM through several approaches and phenotypic outcomes, including effects on the stability of replication forks and the initiation of checkpoints and repair processe”
ATM, ATR, and DNA-PK: The Trinity at the Heart of the DNA Damage Response. (2017, background): “This complex can stimulate ATM kinase activity directly in vitro (Lee and Paull, 2004, 2005), and is required for optimal ATM signaling in cells (Carson et al., 2003; Uziel et al., 2003), indicating that MRN both recruits ATM to DNA lesions and stimulates ATM kinase activity once there.”
DNA damage-induced cell death: from specific DNA lesions to the DNA damage response and apoptosis. (2013, background): “In the absence of the MRN complex, the catalytic activity of ATM and Ser1981 phosphorylation is reduced [93] and”