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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

◀ Back to HDAC3

HDAC3 — TBL1XR1

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Herdick et al., J Mol Biol 2000 : This study demonstrates that the interaction of the VDR with NCoR results in a preferential stabilization of the VDR in a non-agonistic conformation ( silent state ), whereas within a complex with SRC-1 VDR is in its agonistic conformation ( activated state )
Guenther et al., Mol Cell Biol 2001 : In contrast, SMRT does not activate the class II HDAC4 , with which it also interacts
Guenther et al., Genes Dev 2002 : Histone deacetylase 3 (HDAC3) requires the nuclear receptor corepressor SMRT for HDAC enzyme activity
Sohn et al., Mol Endocrinol 2003 : First, corepressor SMRT [ for silencing mediator of thyroid hormone receptor ( TR ) and retinoic acid receptor ( RAR ) ] inhibits the interaction of coactivator steroid receptor coactivator-1 with liganded TR/RAR
Dong et al., Oncogene 2003 : Studies comparing NuMA-RARalpha with NuMA-RARalpha ( deltaCC ) demonstrated that the dimerization or alpha-helical coiled-coil domain of NuMA was required for homodimer formation, transcriptional repression of wild-type RARalpha, transcriptional activation of STAT3 , and stability of the NuMA-RARalpha/SMRT complex
Wu et al., J Biol Chem 2003 : NCoR enhanced DACH1 repression, and the repression of TGF-beta induced AP-1 or Smad signaling by DACH1 required the DACH1 DS domain ... NCoR enhanced DACH1 repression, and the repression of TGF-beta induced AP-1 or Smad signaling by DACH1 required the DACH1 DS domain ... NCoR enhanced DACH1 repression, and the repression of TGF-beta induced AP-1 or Smad signaling by DACH1 required the DACH1 DS domain
Takahashi et al., Blood 2004 (Leukemia) : In the presence of Flt3-ITD , PLZF-SMRT interaction was reduced, transcriptional repression by PLZF was inhibited, and PLZF mediated growth suppression of leukemia cells was partially blocked
Ishii et al., Mol Endocrinol 2004 (Thyroid Hormone Resistance Syndrome) : TR and NCoR were located on the promoter, and T3 caused NCoR dissociation and steroid receptor coactivator-1 recruitment
Akaike et al., Mol Cell Biol 2004 : Furthermore, association of ERK5a and PPARgamma1 disrupted the interaction of SMRT and PPARgamma1, thereby inducing PPARgamma activation
Zhang et al., Genes Dev 2005 : Here we demonstrate that, in addition to protein-protein interactions with NCoR/SMRT , the activity of HDAC3 is regulated by both phosphorylation and dephosphorylation
Ki et al., Mol Cell Biol 2005 : The small interference RNA ( siRNA ) against SMRT abolished SMRT repression of the gene induction by C/EBPbeta or Nrf2
Zhang et al., Mol Cell Biol 2005 : We demonstrated that JMJD2A selectively represses the expression of the ASCL2 gene but not other imprinted genes in the same imprinted locus in HeLa cells and that this repression required a functional N-CoR complex and the tandem Tudor domain of JMJD2A ... We demonstrated that JMJD2A selectively represses the expression of the ASCL2 gene but not other imprinted genes in the same imprinted locus in HeLa cells and that this repression required a functional N-CoR complex and the tandem Tudor domain of JMJD2A
Hoberg et al., Mol Cell Biol 2006 : Introduction of nonphosphorylatable mutants of RelA/p65 and SMRT proteins or the inhibition of IKK activity results in active repression of NF-kappaB promoters by tethering the SMRT-HDAC3 complex
Lefebvre et al., Mol Endocrinol 2006 : Through direct phosphorylation of the corepressor silencing mediator for retinoic and thyroid hormone receptors ( SMRT ), Akt stabilized RAR/SMRT interaction, leading to an increased tethering of SMRT to the RARbeta2 promoter, decreased histone acetylation, down-regulation of the RARbeta2 expression, and impaired cellular differentiation in response to retinoid
Hatchell et al., Mol Cell 2006 (Breast Neoplasms) : SLIRP is recruited to endogenous promoters ( pS2 and metallothionein ), the latter in a SRA dependent manner, while NCoR promoter recruitment is dependent on SLIRP
Grégoire et al., Mol Cell Biol 2007 : Furthermore, the nuclear receptor corepressor SMRT ( silencing mediator of retinoid acid and thyroid hormone receptor ) stimulated the deacetylase activity of HDAC3 towards MEF2 and PCAF
Hoshino et al., J Biochem 2007 : Co-repressor SMRT and class II histone deacetylases promote Bach2 nuclear retention and formation of nuclear foci that are responsible for local transcriptional repression
Matsuoka et al., Biochem Pharmacol 2007 : Disruption of HDAC4/N-CoR complex by histone deacetylase inhibitors leads to inhibition of IL-2 gene expression ... We therefore focused on the role of HDAC4/N-CoR complex in the transcriptional regulation of IL-2
Peterson et al., Mol Cell Biol 2007 (Breast Neoplasms) : SMRT is required for full expression of the ERalpha target genes cyclin D1, BCL-2 , and progesterone receptor but not pS2, and its depletion significantly attenuated estrogen dependent proliferation of MCF-7 cells ... SMRT is required for full expression of the ERalpha target genes cyclin D1 , BCL-2, and progesterone receptor but not pS2, and its depletion significantly attenuated estrogen dependent proliferation of MCF-7 cells ... SMRT is required for full expression of the ERalpha target genes cyclin D1, BCL-2, and progesterone receptor but not pS2, and its depletion significantly attenuated estrogen dependent proliferation of MCF-7 cells ... SMRT is required for full expression of the ERalpha target genes cyclin D1, BCL-2, and progesterone receptor but not pS2, and its depletion significantly attenuated estrogen dependent proliferation of MCF-7 cells ... SMRT is required for full expression of the ERalpha target genes cyclin D1, BCL-2, and progesterone receptor but not pS2 , and its depletion significantly attenuated estrogen dependent proliferation of MCF-7 cells ... SMRT is required for full expression of the ERalpha target genes cyclin D1, BCL-2 , and progesterone receptor but not pS2, and its depletion significantly attenuated estrogen dependent proliferation of MCF-7 cells
Furuya et al., Mol Cell Biol 2007 (Thyroid Neoplasms) : Since NCoR is known to modulate the actions of TRbeta mutants in vivo and in vitro, we asked whether NCoR regulates PV-activated PI3K signaling ... Overexpression of NCoR in thyroid tumor cells of TRbetaPV/PV mouse reduced PI3K signaling, as indicated by the decrease in the phosphorylation of its immediate downstream effector, p-AKT ... Conversely, lowering cellular NCoR by siRNA knockdown in tumor cells led to overactivated p-AKT and increased cell proliferation and motility
Brayman et al., Mol Endocrinol 2007 (Breast Neoplasms) : Overexpression of PIASy did not affect P receptor B binding to the MUC1 promoter but surprisingly led to a loss of nuclear receptor corepressor (NCoR) , which was recruited to the promoter in response to P. Collectively, these data indicate that PIASy may be a useful target for down-regulation of MUC1 expression in various contexts
Sundaram et al., J Cell Biochem 2008 : Co-expression of NCoR with DACH1 significantly decreased ( 5.3-fold ) and siRNA suppression of NCoR in DACH1 co-transfected cells increased ( 3.6-fold ) RANKL promoter activity ... Co-expression of NCoR with DACH1 significantly decreased ( 5.3-fold ) and siRNA suppression of NCoR in DACH1 co-transfected cells increased ( 3.6-fold ) RANKL promoter activity
Higgins et al., Mol Endocrinol 2008 : This study illustrates that both SMRT and NCoR are involved in E2-dependent repression of VEGFR2 in MCF-7 cells ... This study illustrates that both SMRT and NCoR are involved in E2-dependent repression of VEGFR2 in MCF-7 cells
Song et al., J Biol Chem 2008 : Overexpression of SMRT and NCoR attenuated the transcription of beta-catenin-TCF4-specific reporter gene and of CCND1, an endogenous beta-catenin target gene ... Overexpression of SMRT and NCoR attenuated the transcription of beta-catenin-TCF4-specific reporter gene and of CCND1 , an endogenous beta-catenin target gene ... Overexpression of SMRT and NCoR attenuated the transcription of beta-catenin-TCF4-specific reporter gene and of CCND1, an endogenous beta-catenin target gene
Jennewein et al., J Immunol 2008 : Chromatin immunoprecipitation analysis demonstrated that AC prevented the LPS induced removal of nuclear receptor corepressor (NCoR) from the kappaB site within the TNF-alpha promoter
Stanya et al., J Cell Biol 2008 : Cdk2 and Pin1 negatively regulate the transcriptional corepressor SMRT ... Cdk2 and Pin1 negatively regulate the transcriptional corepressor SMRT ... Pin1 regulates SMRT protein stability, thereby affecting SMRT dependent transcriptional repression ... SMRT phosphorylation at multiple sites is required for Pin1 interaction, and these sites can be phosphorylated by Cdk2, which interacts with SMRT
Furuya et al., Steroids 2009 (Thyroid Neoplasms) : Over-expression of NCoR in thyroid tumor cells of TRbeta ( PV/PV ) mice reduces AKT-mTOR-p70 ( S6K ) signaling ... Over-expression of NCoR in thyroid tumor cells of TRbeta ( PV/PV ) mice reduces AKT-mTOR-p70 ( S6K ) signaling ... Over-expression of NCoR in thyroid tumor cells of TRbeta ( PV/PV ) mice reduces AKT-mTOR-p70 ( S6K ) signaling ... Conversely, lowering cellular NCoR by siRNA knockdown in tumor cells leads to over activated PI3K-AKT signaling to increase cell proliferation and motility ... Conversely, lowering cellular NCoR by siRNA knockdown in tumor cells leads to over activated PI3K-AKT signaling to increase cell proliferation and motility
Zhang et al., J Biol Chem 2009 : DBC1 stabilized the interaction between COUP-TFI and NCoR by interacting directly with both proteins
Wang et al., Mol Endocrinol 2009 : These findings demonstrate the critical role of NCoR/HDAC3 complex in negative regulation of TSHalpha gene expression and show that similar complexes and overlapping epigenetic modifications can participate in both negative and positive transcriptional regulation
Karmakar et al., Mol Endocrinol 2010 (Breast Neoplasms) : Our data link the SMRT corepressor directly with SRC family coactivators in positive regulation of ERalpha dependent gene expression and, taken with the positive correlation found for SMRT and SRC-3 in human breast tumors, suggest that SMRT can promote ERalpha- and SRC-3 dependent gene expression in breast cancer
Hodgson et al., Cancer Res 2011 (Neoplasm Recurrence, Local...) : Optimal induction of INPP4B by an androgen receptor required the expression of the transcriptional coactivator NCoR ... Optimal induction of INPP4B by an androgen receptor required the expression of the transcriptional coactivator NCoR
Portal et al., Proc Natl Acad Sci U S A 2011 (Cell Transformation, Viral) : These data strongly support a model in which EBNA2 association with NCoR-deficient RBPJ enhances transcription and EBNALP dismisses NCoR and RBPJ repressive complexes from enhancers to coactivate hes1 and arglu1 but not cd21 or cd23
Zhou et al., PloS one 2012 (MAP Kinase Signaling System) : Importantly, miR-16 targeted the 3'-untranslated region of SMRT and caused translational suppression of SMRT
Finlin et al., Metab Syndr Relat Disord 2012 : Small interfering RNA ( siRNA ) -mediated knockdown of SUMO-1 decreased PPAR?, HDAC3, and NCoR in THP-1 cells and increased tumor necrosis factor-a (TNF-a) induction in response to lipopolysaccharide (LPS)
Liu et al., J Biol Chem 2012 : SUMO1 was required for the T3-induced recruitment of the co-activator CREB binding protein (CBP) and release of nuclear receptor co-repressor (NCoR) on a TRE but had no significant effect on TR DNA binding
Choi et al., J Cell Physiol 2013 (Prostatic Neoplasms) : We demonstrated that the Serine-70 of NCoR is identified the critical amino acid for PKA dependent NCoR phosphorylation ... More importantly, the activation of PKA enhanced the repressive activity of NCoR in a reporter assay and potentiated the antagonist activity in the Androgen Receptor (AR) mediated transcription
Lit et al., Anticancer Res 2013 (Breast Neoplasms...) : At the protein level, inhibition of LATS2 reduces the expression of cyclin-D1 and Nuclear Receptor Co-Repressor (NCoR) while increasing the expression of p27