Gene interactions and pathways from curated databases and text-mining

◀ Back to TP53

DDB2 — TP53

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Tan et al., Mol Cell Biol 2002 (Xeroderma Pigmentosum) : Because DDB2 transcription increases after DNA damage in a p53 dependent manner, we searched for and found a region in the human DDB2 gene that binds and responds transcriptionally to p53 ... These results demonstrate direct activation of the human DDB2 gene by p53
Takimoto et al., Cancer Biol Ther 2002 : Thus the DNA repair function of BRCA1 may be attributed in part to p53 dependent transcriptional induction of DDB2
Tang et al., DNA repair 2002 (Xeroderma Pigmentosum) : When cells are exposed to UV, the resulting accumulation of p53 activates DDB2 transcription, which leads to increased levels of UV-DDB
Itoh et al., Mol Cell Biol 2003 (Xeroderma Pigmentosum) : We propose that both before and after UV irradiation, DDB2 directly regulates p53 levels, while DDB2 expression is itself regulated by p53
Ford et al., Mutat Res 2005 : The mechanisms involved in this process include both transcriptional and post-translational regulation by p53 of the DDB2 and XPC gene products, two critical DNA damage recognition proteins required for GGR
Prost et al., Oncogene 2007 : DDB2 , a gene mutated in XPE patients, is involved in global genomic repair especially the repair of cyclobutane pyrimidine dimers ( CPDs ), and is regulated by p53 in human cells
Stubbert et al., Cell cycle (Georgetown, Tex.) 2007 (Xeroderma Pigmentosum) : Surprisingly, DNA synthesis recovered normally in GG-NER-deficient XP complementation group E ( XP-E ) cells that carry mutations in the p53 regulated DNA repair gene DDB2 and are specifically defective in the repair of cyclobutane pyrimidine dimers (CPD) but not pyrimidine ( 6-4 ) pyrimidone photoproducts
Stubbert et al., Mutat Res 2009 (Xeroderma Pigmentosum) : The anti-apoptotic role for p53 following exposure to ultraviolet light does not involve DDB2 ... Collectively, these results indicate that p53 is primarily protective against UV-induced apoptosis in primary human fibroblasts and this activity of p53 does not require DDB2
Liu et al., Cancer Lett 1996 (Carcinoma, Hepatocellular...) : DDB ( 10 ( -4 ) M ) could significantly increase the content of cAMP in Bel-7402 cells, and also enhance the expression of anti-oncogene p53