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ABL1 — CDKN1A

Text-mined interactions from Literome

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
Pierce et al., Hematol J 2001 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive) : This enhanced BCR/ABL mediated growth inhibition occurred over a range of growth factor concentrations and was independent of changes in p21 ( Cip1 ) and p27 ( Kip ) levels
Keeshan et al., Br J Haematol 2003 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive) : Bcr-Abl upregulates cytosolic p21WAF-1/CIP-1 by a phosphoinositide-3-kinase (PI3K) independent pathway
Li et al., Mol Cell Biol 2004 (Ovarian Neoplasms) : Conversely, reduction of endogenous levels of p150 ( Sal2 ) in HOSE resulted in reduced p21 expression and increased DNA synthesis
Rangatia et al., Leukemia 2006 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive) : Lack of BCR-ABL leads to cell cycle arrest in G1 phase as observed by decrease in cyclin D1 and increase in p21 and p27 cdk inhibitors mRNA
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 ... Furthermore, not only the activation of p21 promoter but also the recruitment to p21 promoter by c-Abl is dependent on the interaction between c-Abl and p53 protein
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