Gene interactions and pathways from curated databases and text-mining

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ATM — TP53

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Taylor et al., Oncogene 2001 : Chk1, Chk2, Atm and Atr also contribute to the activation of p53 in response to genotoxic stress and therefore play multiple roles
Silins et al., Carcinogenesis 2001 (Liver Neoplasms...) : An inhibitor of DNA dependent protein kinase (DNA-PK) and ataxia telangiectasia mutated (ATM) , wortmannin, blocked the DEN induced p53 response in non-EAF hepatocytes
Das et al., Am J Physiol Lung Cell Mol Physiol 2004 (Adenocarcinoma...) : Although H2O2 and other peroxides have been shown to induce ataxia telangiectasia mutated (ATM) dependent p53 phosphorylation in response to DNA damage, the signal transduction mechanisms in response to hyperoxia are currently unknown
Rogoff et al., Mol Cell Biol 2004 : Both Atm and Nbs1 contribute to Chk2 activation and p53 phosphorylation following deregulation of normal Rb growth control
Yoon et al., Mol Cell Biol 2004 : UVB induced C/EBPalpha was accompanied by an increase in p53 protein and caffeine, an inhibitor of ataxia-telangiectasia mutated kinase, and ataxia-telangiectasia mutated and Rad3 related kinase inhibited UVB induced increases in both C/EBPalpha and p53
Lozano et al., J Pathol 2005 (Disease Models, Animal...) : Additionally, upstream regulators of p53 activity, such as p19(Arf) and Atm , are themselves critical tumour modifiers/suppressors
Al Rashid et al., Cancer Res 2005 : Despite a clear link between ataxia-telangiectasia mutated (ATM) dependent phosphorylation of p53 and cell cycle checkpoint control, the intracellular biology and subcellular localization of p53 phosphoforms during the initial sensing of DNA damage is poorly understood
Song et al., Nat Cell Biol 2007 (Cell Transformation, Neoplastic...) : These acquired oncogenic properties of mutant p53 could be explained by the findings that these p53 mutants interact with the nuclease Mre11 and suppress the binding of the Mre11-Rad50-NBS1 (MRN) complex to DNA double stranded breaks ( DSBs ), leading to impaired Ataxia-telangiectasia mutated (ATM) activation
Gurley et al., Mol Cancer Res 2007 : Ataxia-telangiectasia mutated is not required for p53 induction and apoptosis in irradiated epithelial tissues ... Although Atm can regulate p53 , it is not known if this Atm function varies between tissues
Nalapareddy et al., EMBO Rep 2010 : Telomere shortening limits the proliferation of primary human fibroblasts by the induction of senescence, which is mediated by ataxia telangiectasia mutated dependent activation of p53
Yuan et al., J Biol Chem 2010 : HDAC9 deacetylates ATDC, alters the ability of ATDC to associate with p53 , and consequently inhibits the cell proliferation promoting activity of ATDC
Santoro et al., Oncogene 2012 : Melatonin induced p53 phosphorylation at Ser-15 residue does not require ataxia telangiectasia mutated activity, whereas it is severely impaired upon chemical inhibition of p38 mitogen activated protein kinase activity
Zhang et al., PloS one 2013 : We found that 5-Iodotubercidin could cause DNA damage, verified by induction of DNA breaks and nuclear foci positive for ?H2AX and TopBP1, activation of Atm and Chk2, and S15 phosphorylation and up-regulation of p53
Wang et al., International journal of biomedical science : IJBS 2007 : DNA damage response is triggered by double stranded DNA breaks, single stranded DNA breaks as well as other types of lesions, which recruit and activate Ser/Thr kinases such as Atm to the damaged sites, where Atm activates p53 to promote apoptosis, cell cycle arrest, and DNA repair
Barlow et al., Nat Genet 1997 (Ataxia Telangiectasia...) : Thus, Atm deficiency results in lack of p53 induction by IR, but only selective disruption of p53 dependent functions