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ABL1 — TP53

Pathways - manually collected, often from reviews:

• BioCarta tumor suppressor arf inhibits ribosomal biogenesis: p53 (TP53) → c-ABL (ABL1) (transcription, inhibits)

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: ABL1 — TP53 (direct interaction, pull down) Nie et al., Mol Cell Biol 2000*
• IRef Hprd Interaction: TP53 — ABL1 (in vivo) Nie et al., Mol Cell Biol 2000*, Shaul et al., Cell Death Differ 2000*
• IRef Hprd Interaction: TP53 — ABL1 (in vitro) Nie et al., Mol Cell Biol 2000*, Shaul et al., Cell Death Differ 2000*
• IRef Ophid Interaction: TP53 — ABL1 (aggregation, interologs mapping) Brown et al., Bioinformatics 2005
• IRef Ophid Interaction: TP53 — ABL1 (aggregation, confirmational text mining) Nie et al., Mol Cell Biol 2000*
• IRef Ophid Interaction: TP53 — ABL1 (aggregation, confirmational text mining) Yuan et al., J Biol Chem 1996*

Text-mined interactions from Literome

Sionov et al., J Biol Chem 1999 : We demonstrate that c-Abl increases the expression level of the p53 protein
Sionov et al., Mol Cell Biol 2001 : c-Abl regulates p53 levels under normal and stress conditions by preventing its nuclear export and ubiquitination ... Here we demonstrate a key role for c-Abl in the nuclear accumulation of endogenous p53 in cells exposed to DNA damage
Keeshan et al., Leukemia 2001 : Despite the drug-resistant phenotype, high Bcr-Abl levels concomitantly increased the expression of p53 , p21, Bax and down-regulated Bcl-2
Goldberg et al., EMBO J 2002 : Our results suggest that phosphorylation of Mdm2 by c-Abl impairs the inhibition of p53 by Mdm2, hence defining a novel mechanism by which c-Abl activates p53
Wei et al., J Biol Chem 2005 : Here we show that interaction with c-Abl stabilized p53 tetrameric conformation, and as a consequence c-Abl stimulated p53 DNA binding only when all quarter binding sites ( a perfect binding sequence ) on p53-responsive promoters were present ... This result suggests that in response to DNA damage, c-Abl binding may specifically stimulate p53 DNA binding on the promoters with perfect binding sequences ... These results suggest that the promoter specificity plays an important role in selective activation of p53 DNA binding by c-Abl
Levav-Cohen et al., Biochem Biophys Res Commun 2005 : Surprisingly, the oncogenic form of c-Abl , the Bcr-Abl fusion protein in CML cells, also promotes the accumulation of wt p53 ... However, in contrast to the activation of p53 by c-Abl , its oncogenic form, Bcr-Abl, counteracts the growth inhibitory activities of p53 by modulating the p53-Mdm2 loop
Wendel et al., Proc Natl Acad Sci U S A 2006 (Disease Progression...) : We show that the tumor suppressor p53 is selectively activated by imatinib in BCR-ABL expressing cells as a result of BCR-ABL kinase inhibition
Kamath et al., Mol Pharmacol 2007 : Although p53 induction in response to curcumin treatment is dependent on Abl , we found that Abl -- > p53 signaling is not necessary for curcumin induced cell death
Jing et al., J Biochem 2007 : We found that p53 is involved in the activation of p21 promoter by c-Abl , and integrative structure of p53 is required for regulating p21 transcription ... In addition, the chromatin immunoprecipitation study demonstrated that c-Abl and p53 can be recruited to the region containing p53 binding site of p21 promoter, and c-Abl increases the DNA binding activity of p53 to the p21 promoter
Lee et al., J Biol Chem 2008 : Cooperative roles of c-Abl and Cdk5 in regulation of p53 in response to oxidative stress ... c-Abl mediates down-regulation of HDM2, leading to an increase of p53 level ... Our results show that c-Abl and Cdk5 cooperatively regulate maximal activation of p53 , resulting in neuronal death in response to oxidative stress by hydrogen peroxide
Zuckerman et al., J Biol Chem 2009 : c-Abl phosphorylates Hdmx and regulates its interaction with p53
Furlan et al., J Hepatol 2012 : We investigated the mechanism leading to p53 regulation by Met and found that Abl and p38MAPK are required for p53 phosphorylation on S ( 389 ), Mdm2 upregulation, and hepatocyte survival
Sridevi et al., Cell Death Differ 2013 (Acute Kidney Injury...) : When injected with cisplatin, we found similar levels of platinum in the Abl ( +/+ ) and the Abl ( µ/µ ) kidneys, as well as similar initial inductions of p53 and PUMAa expression
Goga et al., Oncogene 1995 : We find that c-Abl requires p53 but not Rb to suppress growth ... An Abl mutant which no longer binds p53 does not enhance p53 transcriptional activity and fails to suppress growth
Wen et al., EMBO J 1996 (Cell Transformation, Neoplastic) : The cytostatic function of c-Abl is controlled by multiple nuclear localization signals and requires the p53 and Rb tumor suppressor gene products ... Further, we demonstrate that the Abl cytostatic effect requires both the Rb and p53 tumor suppressor gene products
Kharbanda et al., Oncogene 1998 : The demonstration that c-Abl binds to p53, induces the transactivation function of p53 and activates p21 expression has supported involvement of c-Abl in regulation of the p53 dependent G1 arrest response