Gene interactions and pathways from curated databases and text-mining

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TP53 — XRCC6

Pathways - manually collected, often from reviews:

  • NCI Pathway Database BARD1 signaling events: BARD1/DNA-PK/p53 complex (TP53-BARD1-PRKDC-XRCC6-XRCC5) → p53 (TP53) (modification, collaborate)
  • NCI Pathway Database BARD1 signaling events: BARD1/DNA-PK/p53 complex (TP53-BARD1-PRKDC-XRCC6-XRCC5) → BARD1/DNA-PK complex (BARD1-PRKDC-XRCC6-XRCC5) (modification, collaborate)
  • NCI Pathway Database BARD1 signaling events: p53 (TP53) → BARD1/DNA-PK complex (BARD1-PRKDC-XRCC6-XRCC5) (modification, collaborate)

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

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Abraham et al., Oncogene 1999 : Recent studies have indicated that DNA-PK is not required for the transactivation or apoptosis promoting activities of p53 protein
Kachnic et al., J Biol Chem 1999 : Taken together, these data suggest that loss of DNA-PK activity appears to attenuate the kinetics of p53 to activate downstream genes, implying that DNA-PK plays a role in post-translational modification of p53 , without affecting the increase in levels of p53 in response to DNA damage
Araki et al., Cancer Res 1999 (Mammary Neoplasms, Experimental) : Furthermore, we identified a missense point mutation in the p53 DNA binding motif region in SCGR11 cells, which were established from severe combined immunodeficient ( SCID ) mice and used for previous study on the role of DNA-PK in p53 transactivation
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
Jack et al., J Biol Chem 2004 : Using wortmannin, serine 15 mutants of p53, DNA-PK null cells and Chk2 null cells, we demonstrate that DNA-PK and Chk2 act independently and sequentially on p53
Soubeyrand et al., Eur J Biochem 2004 : Our results suggest a role for DNA-PK in the modulation of p53 activity resultant from the convergence of p53 and DNA-PK on structured DNA
Vidal et al., Thromb Haemost 2005 : Here, we show that ATM and ATR kinases, but not DNA-PK , which participate in DNA damage activated checkpoints, regulate the phosphorylation of p53 at serine 15 in response to MNNG cell treatment
Boehme et al., Proc Natl Acad Sci U S A 2008 : Correspondingly, down-regulation of DNA-PK prevented phosphorylation of Akt/PKB and GSK-3 after ionizing radiation and strongly reduced the accumulation of p53
Hill et al., DNA repair 2008 : Chromium induced apoptosis therefore involves DNA-PK mediated p53 activation followed by preferential transcription of pro-apoptotic PUMA over anti-apoptotic p21 genes
Sotiropoulou et al., Nat Cell Biol 2010 : The attenuated p53 activation is the consequence of a faster DNA repair activity, mediated by a higher non-homologous end joining ( NHEJ ) activity, induced by the key protein DNA-PK
Zhao et al., Mol Endocrinol 2011 (Carcinoma, Hepatocellular...) : Herein, we demonstrate that the orphan nuclear receptor TR3 suppresses DSB repair by blocking Ku80 DNA-end binding activity and promoting DNA-PK induced p53 activity in hepatoma cells ... Phosphorylated TR3, in turn, enhances DNA-PK induced phosphorylation and p53 transcription activity, thereby enhancing IR-induced apoptosis in hepatoma cells
Williamson et al., EMBO Mol Med 2012 (Disease Models, Animal...) : In ATM-deficient MCL cells, olaparib induced DNA-PK dependent phosphorylation and stabilization of p53 as well as expression of p53-responsive cell cycle checkpoint regulators, and inhibition of DNA-PK reduced the toxicity of olaparib in ATM-deficient MCL cells
Candéias et al., Biochimie 1997 : Thus, our results show that DNA-PK is not the main sensor for genotoxic stress and is not required for p53 activation ... In fact, they rather suggest that DNA-PK may play a role in p53 down-regulation
Woo et al., Nature 1998 : We find that p53 is incapable of binding to DNA in the absence of DNA-PK, that DNA-PK is necessary but not sufficient for activation of p53 sequence-specific DNA binding, and that this activation occurs in response to DNA damage