ATM and related protein kinases: safeguarding genome integrity

By Yosef Shiloh. Nature Reviews. Cancer, 2003

2,765 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/ffb1db2289aded77bc3a5d124ec8c894adc882a8

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Citations in the corpus

How shelterin protects mammalian telomeres. (2008, background): “Mammalian cells are alerted to lesions in their genome by two phosphatidylinositol 3kinase-related protein kinases, ATM and ATR (Figure 6) [reviewed in (170)].”
Tumour suppression by p53: a role for the DNA damage response? (2009, background): “ATM and ATR are members of the phosphatidylinositol-3 kinase-like kinase family and coordinate a complex signalling network in response to various forms of DNA damag”
Immunogenicity of induced pluripotent stem cells (2011, neutral): “This ‘‘off-target’’ effect of the designed ZFN would be even more problematic when the targeted genes are involved in maintaining genomic stability in hESCs, because multiple double-strand breaks introduced by ZFN in the genome will promote chromosomal translations, especially when the DNA damage re”
Regulation of oxidative stress by ATM is required for self-renewal of haematopoietic stem cells (2004, background): “gif" NDATA ITEM> ]> The ‘ataxia telangiectasia mutated’ ( Atm ) gene maintains genomic stability by activating a key cell-cycle checkpoint in response to DNA damage, telomeric instability or oxidative stres”
p53-deficient cells rely on ATM- and ATR-mediated checkpoint signaling through the p38MAPK/MK2 pathway for survival after DNA damage. (2007, background): “Disruption of normal checkpoint function from inherited and acquired genetic mutations is increasingly recognized as a pathophysiological mechanism responsible for tumor-prone human disease syndromes (Bartek and Lukas, 2003; Kastan and Bartek, 2004; O'Driscoll et al., 2004; Shiloh, 2003).”
Metabolic regulation of hematopoietic stem cells in the hypoxic niche. (2011, background): “These proteins belong to the phosphoinositide-3-like kinase kinase family and share similar domain architecture and regulation (Shiloh, 2003).”
DNA damage sensing by the ATM and ATR kinases. (2013, background): “The activation of ATM by DSBs leads to the phosphorylation of a number of substrates, such as Brca1, Chk2, and p53, mediating the effects of ATM on DNA repair, cell-cycle arrest, apoptosis, and other downstream processes (Shiloh 2003; Lavin 2008).”
ATM- and cell cycle-dependent regulation of ATR in response to DNA double-strand breaks (2006, background): “The survival of cells with impaired ATM or ATR function after DNA damage is compromised and they are defective in initiating DNA-damage-induced cell-cycle arres”
CCRK is a novel signalling hub exploitable in cancer immunotherapy (2018, neutral): “P300, once phosphorylated by CDK1/2 at S1038 and S2039, is susceptible for degradation (Wang et al., 2014).”
Donor-Derived Brain Tumor Following Neural Stem Cell Transplantation in an Ataxia Telangiectasia Patient (2009, methodology): “Since the patient is affected by AT, known to be characterized by genetic instability [19], we used several complementary methodologies to prove that the nonidentity of the tumor and the patient is not due to chromosomal and genetic instability.”
A DNA damage checkpoint response in telomere-initiated senescence (2003, background): “Enforcement of the DNA damage checkpoint relies on the concerted activities of the upstream protein kinases ATM and ATR, the downstream transducer kinases CHK1 and CHK2, and mediators such as 53BP1 and MDC1 (ref”
Identification and Characterization of a Novel and Specific Inhibitor of the Ataxia-Telangiectasia Mutated Kinase ATM (2004, background): “ATM is a protein kinase member of the phosphatidylinositol 3 -kinase (PI3K)–related kinase (PIKK) family (2) that plays a critical role in the maintenance of genome integrity (3, 4).”