◀ Back to TP53
HDAC2 — TP53
Pathways - manually collected, often from reviews:
-
NCI Pathway Database Direct p53 effectors:
HDAC2 (HDAC2)
→
p53 (tetramer) complex (TP53)
(transcription, inhibits)
Le Cam et al., Cell 2006, Harms et al., Cancer Res 2007, Shi et al., Mol Cell 2007, Das et al., Cell 2007, Xu et al., J Biol Chem 2007, Gamper et al., Mol Cell Biol 2008, el-Deiry et al., Cancer Res 1995
Evidence: mutant phenotype, reporter gene, physical interaction
-
NCI Pathway Database Direct p53 effectors:
HDAC2 (HDAC2)
→
p53 (tetramer) complex (TP53)
(transcription, inhibits)
Wang et al., Oncogene 2000*, Shou et al., Oncogene 2002*, Harms et al., Cancer Res 2007
Evidence: mutant phenotype, reporter gene, physical interaction
-
NCI Pathway Database Direct p53 effectors:
HDAC2 (HDAC2)
→
p53 (tetramer) complex (TP53)
(transcription, inhibits)
Harms et al., Cancer Res 2007, Shi et al., Mol Cell 2007, Das et al., Cell 2007, Xu et al., J Biol Chem 2007, Gamper et al., Mol Cell Biol 2008, Tang et al., Cell 2008, el-Deiry et al., Cancer Res 1995
Evidence: mutant phenotype, reporter gene, physical interaction
-
NCI Pathway Database Direct p53 effectors:
HDAC2 (HDAC2)
→
p53 (tetramer) complex (TP53)
(transcription, inhibits)
Harms et al., Cancer Res 2007, Shi et al., Mol Cell 2007, Das et al., Cell 2007, Xu et al., J Biol Chem 2007, Gamper et al., Mol Cell Biol 2008, Jansson et al., Nat Cell Biol 2008, el-Deiry et al., Cancer Res 1995
Evidence: mutant phenotype, reporter gene, physical interaction
-
NCI Pathway Database Direct p53 effectors:
HDAC2 (HDAC2)
→
p53 (tetramer) complex (TP53)
(transcription, inhibits)
Ard et al., Mol Cell Biol 2002*, Harms et al., Cancer Res 2007, Zauberman et al., Nucleic Acids Res 1995*, Wu et al., Genes Dev 1993
Evidence: mutant phenotype, reporter gene, physical interaction
-
NCI Pathway Database Direct p53 effectors:
HDAC2 (HDAC2)
→
p53 (tetramer) complex (TP53)
(transcription, inhibits)
Liu et al., Oncogene 2002*, Harms et al., Cancer Res 2007
Evidence: mutant phenotype, reporter gene, physical interaction
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
IRef Biogrid Interaction:
HDAC2
—
TP53
(physical association, affinity chromatography technology)
Insinga et al., EMBO J 2004*
-
IRef Biogrid Interaction:
HDAC2
—
TP53
(physical association, affinity chromatography technology)
Sun et al., J Biol Chem 2007
-
IRef Biogrid Interaction:
HDAC2
—
TP53
(physical association, affinity chromatography technology)
Tian et al., J Cell Physiol 2011*
-
IRef Biogrid Interaction:
HDAC2
—
TP53
(physical association, affinity chromatography technology)
Adenuga et al., Arch Biochem Biophys 2010*
-
IRef Biogrid Interaction:
HDAC2
—
TP53
(physical association, affinity chromatography technology)
Brandl et al., Journal of molecular cell biology 2012*
-
IRef Biogrid Interaction:
HDAC2
—
TP53
(direct interaction, pull down)
Li et al., Oncogene 2010*
-
IRef Hprd Interaction:
TP53
—
HDAC2
(in vitro)
Juan et al., J Biol Chem 2000*
-
IRef Hprd Interaction:
TP53
—
HDAC2
(in vivo)
Juan et al., J Biol Chem 2000*
Text-mined interactions from Literome
Juan et al., J Biol Chem 2000
:
Down-regulation of
p53 activity by HDACs is
HDAC dosage
dependent , requires the deacetylase activity of HDACs, and depends on the region of p53 that is acetylated by p300/CREB binding protein (CBP)
Koumenis et al., Mol Cell Biol 2001
(Cell Transformation, Neoplastic) :
At the molecular level, DNA damage
induces the interaction of
p53 with the transcriptional activator p300 as well as with the transcriptional corepressor
mSin3A ... In contrast, hypoxia primarily
induces an interaction of
p53 with
mSin3A , but not with p300
Wilkinson et al., Mol Cell Biol 2005
:
p53 promotes SnoN and
histone deacetylase interaction at an overlapping Smad binding, p53 regulatory element ( SBE/p53RE ) in AFP
Peltonen et al., Pigment Cell Res 2005
(Melanoma) :
Inhibiting p53 function by a dominant negative p53 ( p53 ( 175His ) ) confirmed that the
HDAC inhibitor induced apoptosis was
independent of wild-type
p53 , even though TSA slightly activated p53 in a reporter assay
Shetty et al., Mol Cell Biol 2005
(Breast Neoplasms) :
Indeed,
HDAC inhibitors
activate NF-kappaB and
p53 and upregulate DR5 expression
Blagosklonny et al., Cancer Res 2005
:
We suggest that, by either restoring or mimicking p53 trans-functions,
histone deacetylase inhibitors
initiate degradation of mutant
p53
Tsuyama et al., Biochem Biophys Res Commun 2005
(Multiple Myeloma) :
Expression of
p53 , a direct target gene of Bcl6, was downregulated in the IL-6 stimulated cells, and this process was
impaired by an
HDAC inhibitor
Zhang et al., Cancer Lett 2008
(Carcinoma, Hepatocellular...) :
Researches have shown that
ING2 can
activate p53 and p53 mediated apoptotic pathway involved in the hepatocarcinogenesis
Chang et al., J Virol 2008
:
Critical
role of
p53 in
histone deacetylase inhibitor induced Epstein-Barr virus Zta expression
Chen et al., EMBO J 2010
:
MDM2 also
inhibits p53 transcriptional activity by recruiting
histone deacetylase and corepressors to p53
LeBoeuf et al., Dev Cell 2010
:
Mutant embryos display increased levels of acetylated
p53 , which opposes p63 functions, and p53 is
required for
HDAC inhibitor mediated p21 expression in keratinocytes ... Our data identify critical requirements for HDAC1/2 in epidermal development and indicate that
HDAC1/2 directly mediate repressive functions of p63 and
suppress p53 activity
Zeng et al., Cancer Res 2011
:
We show that
p53 is
required for both
HDAC and PcG to repress Arf expression
Zhang et al., Genes Dev 2011
:
Accumulation of
HDAC2 in Mule-deficient cells
leads to compromised p53 acetylation as well as crippled
p53 transcriptional activation, accumulation, and apoptotic response upon DNA damage and Nutlin-3 treatments
McCormack et al., Leukemia 2012
(Leukemia, Myeloid, Acute) :
Our results suggest the concomitant targeting of
MDM2-p53 and
HDAC inhibition , may be an effective therapeutic strategy for the treatment of AML
Li et al., Cancer Lett 2012
(Bone Neoplasms...) :
Pharmacologic inhibitor of
HDAC , trichostatin A (TSA)
promoted p53-p300 interaction and recruitment of p53 Lys-382 to promoter regions of its target genes p21 and Puma, consequently inducing apoptosis and stabilizing the acetylation of p53 at Lys-382 together with the upregulation of p21 and Puma, which were impaired in EFTs cells after the knockdown of p53 expression
Yan et al., Oncogene 2013
:
Here we found that
histone deacetylase (HDAC) inhibitors
suppress both wild-type and mutant
p53 transcription in time- and dose dependent manners
Madapura et al., Cell cycle (Georgetown, Tex.) 2012
:
Modifying
p53 levels using Nutlin-3, which specifically dissociates the MDM2-p53 interaction, was
sufficient to upregulate
SAP expression, indicating that SAP is a target of p53 in T cells