◀ Back to CDKN1A
CDKN1A — HDAC4
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Xiao et al., J Cell Biochem 1999
:
Both Sp1 and Sp3 are responsible for
p21waf1 promoter activity
induced by
histone deacetylase inhibitor in NIH3T3 cells
Sowa et al., Cancer Res 1999
:
Sp3, but not Sp1, mediates the transcriptional
activation of the
p21/WAF1/Cip1 gene promoter by
histone deacetylase inhibitor
Xiao et al., J Biol Chem 2000
:
p300 collaborates with Sp1 and Sp3 in
p21 ( waf1/cip1 ) promoter activation
induced by
histone deacetylase inhibitor
Shin et al., Cancer Res 2000
(Stomach Neoplasms) :
The
p21 gene was
activated only by
histone deacetylase inhibitor
Claassen et al., Proc Natl Acad Sci U S A 2000
:
Repression of
p21 ( CIP1 ) transcription by c-Myc occurred at the promoter level in a region near the start site of transcriptional initiation and was
independent of
histone deacetylase activity
Huang et al., Oncogene 2000
(Breast Neoplasms) :
Activation of the
p21WAF1/CIP1 promoter independent of p53 by the
histone deacetylase inhibitor suberoylanilide hydroxamic acid ( SAHA ) through the Sp1 sites
Sowa et al., Biofactors 2000
(Colorectal Neoplasms...) :
As a model of this, we found that
histone deacetylase inhibitors such as butyrate or trichostatin A dramatically
stimulate the
p21/WAF1 gene promoter through the Spl sites, resulting in cell cycle arrest
Han et al., J Biol Chem 2001
:
Activation of
p21 ( WAF1/Cip1 ) transcription through Sp1 sites by
histone deacetylase inhibitor apicidin : involvement of protein kinase C
Burgess et al., Mol Pharmacol 2001
:
Up-regulation of
p21 ( WAF1/CIP1 ) by
histone deacetylase inhibitors reduces their cytotoxicity
Blagosklonny et al., Mol Cancer Ther 2002
:
By preventing deacetylation of histones,
histone deacetylase inhibitors ( HDIs ) transcriptionally
induce p21
Sowa et al., Nihon Eiseigaku Zasshi 2003
(Neoplasms) :
As a model of our hypothesis, we found that
histone deacetylase inhibitors such as butyrate and trichostatin A dramatically
stimulate the
p21/WAF1 gene promoter through the Sp1 sites, resulting in cell cycle arrest
Piekarz et al., Blood 2004
(Lymphoma, T-Cell) :
Treatment with depsipeptide, as well as other
histone deacetylase inhibitors,
caused induction of histone acetylation, induction of
p21 expression, and substantial apoptosis without significant cell cycle arrest
Wilson et al., Mol Biol Cell 2008
:
Down regulating
HDAC4 expression by small interfering RNA ( siRNA ) in HCT116 cells induced growth inhibition and apoptosis in vitro, reduced xenograft tumor growth, and
increased p21 transcription ... Conversely, overexpression of
HDAC4 repressed
p21 promoter activity
Mottet et al., Oncogene 2009
(Bone Neoplasms...) :
HDAC4 represses
p21 ( WAF1/Cip1 ) expression in human cancer cells through a Sp1 dependent, p53 independent mechanism ... HDAC4 interacts with Sp1, binds and reduces histone H3 acetylation at the Sp1/Sp3 binding site-rich p21 ( WAF1/Cip1 ) proximal promoter, suggesting a key role for Sp1 in
HDAC4 mediated repression of
p21 ( WAF1/Cip1 ) ... Induction of
p21 ( WAF1/Cip1 )
mediated by silencing of
HDAC4 arrested cancer cell growth in vitro and inhibited tumor growth in an in vivo human glioblastoma model
Liu et al., Cancer Res 2009
(Breast Neoplasms) :
Short hairpin RNA silencing of either HDAC2 or
HDAC4 is
sufficient to induce
p21 expression