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CDKN1A — CDKN2A
Pathways - manually collected, often from reviews:
-
NCI Pathway Database Validated transcriptional targets of TAp63 isoforms:
TAp63g (tetramer)/p14ARF complex (TP63-CDKN2A)
→
p21CIP1 (CDKN1A)
(transcription, inhibits)
MacPartlin et al., J Biol Chem 2005, Kommagani et al., Oncogene 2006*, Guo et al., Nat Cell Biol 2009*, Deutsch et al., Cell 2011*
Evidence: mutant phenotype, reporter gene, physical interaction
Text-mined interactions from Literome
Mitra et al., Mol Cell Biol 1999
:
Induction of
p21 ( WAF1/CIP1 ) and inhibition of Cdk2
mediated by the tumor suppressor
p16(INK4a)
Kurokawa et al., Oncogene 1999
:
Induction of
p19ARF activated p53 by increasing its stability, and
allowed the expression of
p21Cip1 , which bound to all of the cyclin D1-cdk complexes ( cyclin D1-cdk2, -cdk4, and -cdk6 ) thereby inhibiting their kinase activities
Kapelko-Słowik et al., Pol Arch Med Wewn 2002
(Leukemia, Myeloid, Acute...) :
[ Expression of
p16INK4a , p15INK4b,
p21WAF1/Clip1 cell cycle
inhibitors on blastic cells in patients with acute myeloblastic leukemia ( AML ) and acute lymphoblastic leukemia ( ALL ) ]
Gao et al., Am J Physiol Cell Physiol 2004
(Ovarian Neoplasms) :
Expression of the cyclin kinase inhibitor
p16(INK4a) was
induced by the PI3K inhibitor, whereas steady-state levels of
p21 ( CIP1/WAF1 ) were decreased in the same experiment
Xue et al., FEBS Lett 2004
:
Sp1 is involved in the transcriptional
activation of
p16(INK4) by
p21 ( Waf1 ) in HeLa cells ... In this study we examined the
effects of
p21 ( Waf1 ) on the transcription of
p16(INK4) ... We determined that
p21 ( Waf1 ) can
activate the transcription of
p16(INK4) , and that this effect is GC-box dependent ... Upregulation of Sp1 contributes to the transcriptional activation and protein level of
p16(INK4) mediated by
p21 ( Waf1 ), and is a potential point of cooperation between the p16/pRb and p14 (ARF)/p53 tumor suppressor pathways
Skinner et al., Oncogene 2004
(Neoplasms) :
A concentration dependent induction of the cyclin dependent kinase (CDK) inhibitor
p21WAF1 was observed in both cell types, but
p16Ink4a was
induced by ras only in fibroblasts
Balsitis et al., J Virol 2005
(Hyperplasia...) :
While E7-mediated p21 induction was partially p53 dependent, neither p53 nor
p21 induction by E7
required p19(ARF)
Saegusa et al., Int J Cancer 2006
(Disease Progression...) :
In cell lines, transcriptional
activation of
p16(INK) (4A) promoter by active form beta-catenin, as well as
p21 ( WAF1 ), occurred through the region from -385 to -280 bp relative to the translation start site, in a TCF4 independent manner ... These findings indicate that induction of
p16(INK4A) mediated by nuclear beta-catenin and
p21 ( WAF1 ), along with loss of pRb expression, may be important for initial steps during trans-differentiation of Em Ca cells
Han et al., Chin Med J (Engl) 2007
:
Previous reports showed that
p16(INK4) could be
activated by
p21 ( Waf1 ) through transcriptional factor Sp1 in HeLa cells ... This study was undertaken to determine the
effects of
p16(INK4) on the expression and functions of
p21 ( Waf1 )
Sekaric et al., Oncogene 2007
:
Moreover, depletion of hAda3 by siRNA inhibited endogenous p53 acetylation and accumulation of
p21cip1 in
response to ectopic
p14ARF
Al-Khalaf et al., PloS one 2013
:
Furthermore, ectopic expression of
p16(INK4A) in p16(INK4A)-deficient breast epithelial MCF-10A cells significantly
increased the level of
p21 ( WAF1 ), with no effect on cell proliferation
Robles et al., Oncogene 1998
:
This scenario, where a transient increase in
p21 is
followed by a delayed induction of
p16INK4a , also happens with the permanent arrest that occurs with cellular senescence