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CHUK — NCOA3
Pathways - manually collected, often from reviews:
-
NCI Pathway Database Validated nuclear estrogen receptor alpha network:
E2/ERA (dimer)/AIB1 complex (ESR1-NCOA3)
→
IKK alpha (CHUK)
(transcription, activates)
Park et al., Mol Cell 2005
Evidence: mutant phenotype, reporter gene, physical interaction
-
NCI Pathway Database Validated nuclear estrogen receptor alpha network:
E2/ERA (dimer)/AIB1 complex (ESR1-NCOA3)
→
IKK alpha (CHUK)
(transcription, activates)
Park et al., Mol Cell 2005
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Validated nuclear estrogen receptor alpha network:
E2/ERA (dimer)/AIB1 complex (ESR1-NCOA3)
→
IKK alpha (CHUK)
(transcription, activates)
Park et al., Mol Cell 2005
Evidence: mutant phenotype, physical interaction
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
IRef Biogrid Interaction:
CHUK
—
NCOA3
(colocalization, imaging technique)
Park et al., Mol Cell 2005
-
IRef Biogrid Interaction:
CHUK
—
NCOA3
(physical association, affinity chromatography technology)
Wu et al., Mol Cell Biol 2002
-
IRef Biogrid Interaction:
CHUK
—
NCOA3
(direct interaction, pull down)
Wu et al., Mol Cell Biol 2002
-
IRef Biogrid Interaction:
CHUK
—
NCOA3
(direct interaction, enzymatic study)
Wu et al., Mol Cell Biol 2002
-
IRef Biogrid Interaction:
CHUK
—
NCOA3
(physical association, affinity chromatography technology)
Jung et al., Mol Endocrinol 2005
-
IRef Biogrid Interaction:
CHUK
—
NCOA3
(direct interaction, enzymatic study)
Wu et al., Mol Cell 2004
-
MIPS CORUM IKK-alpha--ER-alpha-AIB1 complex:
IKK-alpha--ER-alpha-AIB1 complex complex (CHUK-ESR1-NCOA3)
Park et al., Mol Cell 2005
-
MIPS CORUM SRC-3 complex:
SRC-3 complex complex (CHUK-CREBBP-IKBKB-IKBKG-NCOA2-NCOA3-TROVE2)
Wu et al., Mol Cell Biol 2002
-
IRef Corum Interaction:
Complex of NCOA3-NCOA3-ESR1-CHUK-CHUK-ESR1
(association, chromatin immunoprecipitation assay)
Park et al., Mol Cell 2005
-
IRef Corum Interaction:
Complex of 22 proteins
(association, molecular sieving)
Wu et al., Mol Cell Biol 2002
-
IRef Hprd Interaction:
CHUK
—
NCOA3
(in vitro)
Wu et al., Mol Cell Biol 2002
-
IRef Hprd Interaction:
CHUK
—
NCOA3
(in vivo)
Wu et al., Mol Cell Biol 2002
-
IRef Innatedb Interaction:
Complex of ESR1-CCND1-CHUK-NCOA3
(unknown, -)
Park et al., Mol Cell 2005
-
IRef Innatedb Interaction:
CHUK
—
NCOA3
(unknown, -)
Park et al., Mol Cell 2005
-
IRef Innatedb Interaction:
CHUK
—
NCOA3
(unknown, -)
Wu et al., Mol Cell Biol 2002
-
IRef Intact Interaction:
Complex of NCOA3-NCOA2-CHUK-TRIM21-IKBKG-IKBKB-CREBBP
(association, affinity chromatography technology)
Wu et al., Mol Cell Biol 2002
-
IRef Intact Interaction:
CHUK
—
NCOA3
(physical association, coimmunoprecipitation)
Wu et al., Mol Cell Biol 2002
Text-mined interactions from Literome
Wu et al., Mol Cell Biol 2002
:
Taken together, our results not only reveal the
IKK mediated phosphorylation of
SRC-3 to be a regulated event that plays an important role but also substantiate the role of SRC-3 in multiple signaling pathways
Zheng et al., Mol Cell Biol 2005
:
Together these data demonstrate that E2-induced
SRC-3 phosphorylation is
dependent on a direct interaction between SRC-3 and
ERalpha and can occur outside of the nucleus ... Together these data demonstrate that E2-induced
SRC-3 phosphorylation is
dependent on a direct interaction between
SRC-3 and ERalpha and can occur outside of the nucleus
Zhou et al., Cell 2006
:
In this issue of Cell, challenge this notion by revealing that the proteasomal activator
REGgamma directs degradation of the steroid receptor coactivator
SRC-3 by the 20S proteasome in an ATP- and ubiquitin independent manner
Lin et al., J Biochem Mol Biol 2006
:
In summary, our present study showed for the first time that the 160
RAC3/SRC3 is involved in the functional transactivation of TAD of Nrf2 and that the other nuclear co-regulators such as CBP/p300, CARM1,
PRMT1 and p/CAF can also transcriptionally
activate this TAD of Nrf2 and that they could further enhance the transactivation activity mediated by RAC3/SRC3 ... In summary, our present study showed for the first time that the 160
RAC3/SRC3 is involved in the functional transactivation of TAD of Nrf2 and that the other nuclear co-regulators such as CBP/p300,
CARM1 , PRMT1 and p/CAF can also transcriptionally
activate this TAD of Nrf2 and that they could further enhance the transactivation activity mediated by RAC3/SRC3 ... In summary, our present study showed for the first time that the 160
RAC3/SRC3 is involved in the functional transactivation of TAD of Nrf2 and that the other nuclear co-regulators such as CBP/p300, CARM1, PRMT1 and
p/CAF can also transcriptionally
activate this TAD of Nrf2 and that they could further enhance the transactivation activity mediated by RAC3/SRC3
Mussi et al., Mol Endocrinol 2006
:
Furthermore, overexpression of
E2F1 significantly
increases the promoter activity of the endogenous
SRC-3 gene and boosts SRC-3 expression in vivo
Mc Ilroy et al., Endocr Relat Cancer 2006
(Breast Neoplasms...) :
In HER2 ( human epidermal growth factor receptor 2 ) positive primary tumour cell cultures 17beta-estradiol
induced a decrease in
SRC-3 , whereas upregulated
SRC-3 expression
Li et al., Mol Cell 2007
(Thyroid Neoplasms) :
We previously demonstrated that the proteasome activator
REGgamma directs degradation of the steroid receptor coactivator
SRC-3 by the 20S proteasome in an ATP- and ubiquitin independent manner
Yan et al., Cancer Res 2008
(Carcinoma...) :
In addition,
SRC-3/AIB1 directly
regulates transcription of matrix metalloproteinase (MMP)-2 and
MMP-13 through its coactivation of AP-1 and PEA3 ... In addition,
SRC-3/AIB1 directly
regulates transcription of
matrix metalloproteinase (MMP)-2 and MMP-13 through its coactivation of AP-1 and PEA3
Agoulnik et al., Steroids 2009
(Prostatic Neoplasms) :
SRC-3 is
required for optimal androgen dependent induction of PSA,
TMPRSS2 , and PMEPA1 whereas SRA is required only for optimal induction of the TMPRSS2 gene ...
SRC-3 is
required for optimal androgen dependent induction of PSA, TMPRSS2, and
PMEPA1 whereas SRA is required only for optimal induction of the TMPRSS2 gene ...
SRC-3 is
required for optimal androgen dependent induction of
PSA , TMPRSS2, and PMEPA1 whereas SRA is required only for optimal induction of the TMPRSS2 gene
Wang et al., PloS one 2010
(Anoxia) :
Knocking down
SRC-3 , but not SRC-1 or SRC-2, using short interfering RNAs ( siRNAs ),
reduced EPO transcriptional activity
Karmakar et al., Mol Endocrinol 2010
(Breast Neoplasms) :
SMRT and SRC-3 bind directly in an ERalpha independent manner, and this interaction
promotes E2-dependent
SRC-3 binding to ERalpha measured by co-IP and SRC-3 recruitment to the cyclin D1 gene as measured by chromatin IP assays
Suen et al., J Biol Chem 1998
:
SRC-3 enhanced
ERalpha and progesterone receptor stimulated gene transcription in a ligand dependent manner, but stimulation of ERbeta mediated transcription was not observed