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ESR1 — NCOA3

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: Complex of ESR1-NCOA3 → estradiol/ESR1 complex (ESR1) (increases)
  
  Evidence: in a substantial proportion of patients with primary breast cancer, and in all patients with ER positive metastatic disease, resistance eventually develops to all strategies that are designed to limit ER activation by oestrogen. ER binds as a dimer to small palindromic DNA motifs - known as oestrogen response elements (EREs) - in the promoters of these genes, through the action of two ZINC FINGERS 29. AF1 and AF2 activate transcription independently and/or synergistically. There is evidence that...
• OpenBEL Selventa BEL large corpus: ESR1 → Complex of CARM1-NCOA3 (directlyIncreases, CARM1/NCOA3 Activity)
  Evidence: The C-terminal region of the p160 proteins mediates interaction with other factors with a role in ER signaling including CBP (CREB-binding protein), p300 and arginine methyltransferase 1 (CARM-1) [32].
• OpenBEL Selventa BEL large corpus: ESR1 → Complex of EP300-NCOA3 (directlyIncreases, EP300/NCOA3 Activity)
  Evidence: The C-terminal region of the p160 proteins mediates interaction with other factors with a role in ER signaling including CBP (CREB-binding protein), p300 and arginine methyltransferase 1 (CARM-1) [32].
• OpenBEL Selventa BEL large corpus: ESR1 → Complex of EP300-NCOA3 (directlyIncreases, EP300/NCOA3 Activity)
  Evidence: ER coregulators are also targets of many of the same signaling pathways that affect ER directly. MAPK can phosphorylate p160 coactivators NCoA-1 and NCoA-3, and can enhance their transcriptional activities partly by facilitating their interaction with CBP/p300 [87,88].
• OpenBEL Selventa BEL large corpus: ESR1 → Complex of ESR1-NCOA3 (directlyIncreases, ESR1/NCOA3 Activity)
  Evidence: There are three members of the p160 family of coactivators, NCoA-1 (SRC-1) [22], NCoA-2 (TIF2, GRIP1) [23,24], and NCoA-3 (AIB1, ACTR, RAC3, p/CIP, TRAM-1) [25-30],
• OpenBEL Selventa BEL large corpus: ESR1 → Complex of ESR1-NCOA3 (directlyIncreases, ESR1/NCOA3 Activity)
  Evidence: in a substantial proportion of patients with primary breast cancer, and in all patients with ER positive metastatic disease, resistance eventually develops to all strategies that are designed to limit ER activation by oestrogen. ER binds as a dimer to small palindromic DNA motifs - known as oestrogen response elements (EREs) - in the promoters of these genes, through the action of two ZINC FINGERS 29. AF1 and AF2 activate transcription independently and/or synergistically. There is evidence that...
• OpenBEL Selventa BEL large corpus: ESR1 → NCOA3 (directlyIncreases, NCOA3 Activity)
  Evidence: ER coregulators are also targets of many of the same signaling pathways that affect ER directly. MAPK can phosphorylate p160 coactivators NCoA-1 and NCoA-3, and can enhance their transcriptional activities partly by facilitating their interaction with CBP/p300 [87,88].
• NCI Pathway Database FOXA1 transcription factor network: E2/ERA complex (ESR1) → AIB1 (NCOA3) (transcription, activates) Carroll et al., Cell 2005
  Evidence: mutant phenotype, physical interaction
• NCI Pathway Database FOXA1 transcription factor network: E2/ERA complex (ESR1) → AIB1 (NCOA3) (transcription, activates) Carroll et al., Cell 2005
  Evidence: mutant phenotype, physical interaction
• NCI Pathway Database FOXA1 transcription factor network: E2/ERA complex (ESR1) → AIB1 (NCOA3) (transcription, activates) Carroll et al., Cell 2005
  Evidence: mutant phenotype, physical interaction
• NCI Pathway Database Validated nuclear estrogen receptor alpha network: E2/ERA (dimer) complex (ESR1) → E2/ERA (dimer)/AIB1 complex (ESR1-NCOA3) (modification, collaborate)
  Katzenellenbogen et al., Ann N Y Acad Sci 2001
  Evidence: physical interaction
• NCI Pathway Database Validated nuclear estrogen receptor alpha network: E2/ERA (dimer) complex (ESR1) → AIB1 (NCOA3) (modification, collaborate) Katzenellenbogen et al., Ann N Y Acad Sci 2001
  Evidence: physical interaction
• NCI Pathway Database Validated nuclear estrogen receptor alpha network: E2/ERA (dimer)/AIB1 complex (ESR1-NCOA3) → AIB1 (NCOA3) (modification, collaborate) Katzenellenbogen et al., Ann N Y Acad Sci 2001
  Evidence: 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, 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) → DSCAM (DSCAM) (transcription, activates) Carroll et al., Cell 2005
  Evidence: physical interaction
• NCI Pathway Database FOXA1 transcription factor network: E2/ERA complex (ESR1) → AIB1 (NCOA3) (transcription, activates) Carroll et al., Cell 2005
  Evidence: mutant phenotype, physical interaction
• NCI Pathway Database Validated nuclear estrogen receptor alpha network: E2/ERA (dimer)/AIB1 complex (ESR1-NCOA3) → NRIP1 (NRIP1) (transcription, activates) Lin et al., Genome Biol 2004*, Carroll et al., Cell 2005
  Evidence: physical interaction
• NCI Pathway Database FOXA1 transcription factor network: E2/ERA complex (ESR1) → AIB1 (NCOA3) (transcription, activates) Beck et al., DNA Cell Biol 1999*, Carroll et al., Cell 2005, Laganière et al., Proc Natl Acad Sci U S A 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

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

Studies that report less than 10 interactions are marked with *

• IRef Bind_translation Interaction: NCOA3 — ESR1 (affinity chromatography technology) Takeshita et al., J Biol Chem 1997*
• IRef Bind_translation Interaction: ESR1 — NCOA3 (affinity chromatography technology) Wu et al., Mol Cell 2004
• IRef Bind_translation Interaction: ESR1 — NCOA3 (coimmunoprecipitation) Wu et al., Mol Cell 2004
• IRef Biogrid Interaction: ESR1 — NCOA3 (direct interaction, two hybrid) Monroe et al., J Endocrinol 2003*
• IRef Biogrid Interaction: ESR1 — NCOA3 (direct interaction, fluorescent resonance energy transfer) Bai et al., Mol Endocrinol 2003*
• IRef Biogrid Interaction: ESR1 — NCOA3 (direct interaction, unspecified method) Bramlett et al., Mol Endocrinol 2001*
• IRef Biogrid Interaction: ESR1 — NCOA3 (direct interaction, two hybrid) Suen et al., J Biol Chem 1998*
• IRef Biogrid Interaction: ESR1 — NCOA3 (direct interaction, pull down) Wong et al., Biochemistry 2001*
• IRef Biogrid Interaction: ESR1 — NCOA3 (physical association, affinity chromatography technology) Tikkanen et al., Proc Natl Acad Sci U S A 2000*
• IRef Biogrid Interaction: ESR1 — NCOA3 (direct interaction, pull down) Tikkanen et al., Proc Natl Acad Sci U S A 2000*
• IRef Biogrid Interaction: ESR1 — NCOA3 (physical association, affinity chromatography technology) Feng et al., Mol Cell Biol 2006*
• IRef Biogrid Interaction: ESR1 — NCOA3 (direct interaction, two hybrid) Long et al., Mol Cancer Ther 2008*
• IRef Biogrid Interaction: ESR1 — NCOA3 (physical association, affinity chromatography technology) Long et al., Mol Cancer Ther 2008*
• IRef Biogrid Interaction: ESR1 — NCOA3 (direct interaction, two hybrid) Dutertre et al., Mol Endocrinol 2003*
• IRef Biogrid Interaction: ESR1 — NCOA3 (direct interaction, two hybrid) Jaber et al., J Mol Endocrinol 2004*
• IRef Biogrid Interaction: ESR1 — NCOA3 (physical association, affinity chromatography technology) Torchia et al., Nature 1997
• IRef Biogrid Interaction: ESR1 — NCOA3 (direct interaction, pull down) Torchia et al., Nature 1997
• IRef Biogrid Interaction: ESR1 — NCOA3 (physical association, affinity chromatography technology) Karmakar et al., Mol Endocrinol 2010*
• IRef Biogrid Interaction: ESR1 — NCOA3 (direct interaction, pull down) Takeshita et al., J Biol Chem 1997*
• IRef Biogrid Interaction: ESR1 — NCOA3 (direct interaction, pull down) Zhao et al., J Biol Chem 2001*
• IRef Biogrid Interaction: ESR1 — NCOA3 (physical association, affinity chromatography technology) Wu et al., Mol Cell 2004
• IRef Biogrid Interaction: ESR1 — NCOA3 (physical association, affinity chromatography technology) Lanz et al., Mol Endocrinol 2010*
• IRef Biogrid Interaction: ESR1 — NCOA3 (physical association, affinity chromatography technology) Heck et al., Cancer Res 2009*
• IRef Biogrid Interaction: ESR1 — NCOA3 (direct interaction, two hybrid) Heck et al., Cancer Res 2009*
• IRef Biogrid Interaction: ESR1 — NCOA3 (direct interaction, fluorescent resonance energy transfer) Heck et al., Cancer Res 2009*
• IRef Biogrid Interaction: ESR1 — NCOA3 (direct interaction, fluorescent resonance energy transfer) Gunther et al., ACS Chem Biol 2008*
• IRef Biogrid Interaction: ESR1 — NCOA3 (physical association, affinity chromatography technology) Amazit et al., Mol Cell Biol 2007*
• IRef Biogrid Interaction: ESR1 — NCOA3 (physical association, affinity chromatography technology) Mc Ilroy et al., Endocr Relat Cancer 2006*
• IRef Biogrid Interaction: ESR1 — NCOA3 (direct interaction, two hybrid) Shao et al., J Steroid Biochem Mol Biol 2004*
• MIPS CORUM ESR1-RELA-BCL3-NCOA3 complex: ESR1-RELA-BCL3-NCOA3 complex complex (BCL3-ESR1-NCOA3-RELA) Rubio et al., Oncogene 2006*
• MIPS CORUM IKK-alpha--ER-alpha-AIB1 complex: IKK-alpha--ER-alpha-AIB1 complex complex (CHUK-ESR1-NCOA3) Park et al., Mol Cell 2005
• 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 BCL3-ESR1-RELA-NCOA3 (association, coimmunoprecipitation) Rubio et al., Oncogene 2006*
• IRef Hprd Interaction: ESR1 — NCOA3 (in vitro) Tikkanen et al., Proc Natl Acad Sci U S A 2000*, Zhao et al., J Biol Chem 2001*, Shao et al., J Steroid Biochem Mol Biol 2004*
• IRef Innatedb Interaction: Complex of ESR1-CCND1-CHUK-NCOA3 (unknown, -) Park et al., Mol Cell 2005
• IRef Intact Interaction: NCOA3 — ESR1 (physical association, pull down) Zhao et al., J Biol Chem 2001*
• IRef Intact Interaction: Complex of 143 proteins (association, cosedimentation through density gradient) Nassa et al., Proteomics 2011
• IRef Intact Interaction: Complex of 43 proteins (association, pull down) Nassa et al., Proteomics 2011
• IRef Ophid Interaction: NCOA3 — ESR1 (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

Planas-Silva et al., Cancer Res 2001 (Breast Neoplasms) : We show here that AIB1 and other steroid receptor coactivators can enhance the functional interaction of the estrogen receptor with the cyclin D1 promoter
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
Hossain et al., Mol Cell Biol 2006 (Breast Neoplasms) : We also found that downregulation of AIB1 by Mir-17-5p resulted in decreased estrogen receptor mediated, as well as estrogen receptor independent, gene expression and decreased proliferation of breast cancer cells
Li et al., Mol Cell 2008 (Breast Neoplasms) : PDXP and PP2A dephosphorylate SRC-3 and inhibit its ligand dependent association with estrogen receptor
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