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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