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ESR1 — RELA

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: ESR1 — RELA (physical association, affinity chromatography technology) Rubio et al., Oncogene 2006*
• IRef Biogrid Interaction: ESR1 — RELA (physical association, affinity chromatography technology) Olivier et al., Mol Pharmacol 2006*
• IRef Biogrid Interaction: ESR1 — RELA (physical association, affinity chromatography technology) Nettles et al., Mol Endocrinol 2008*
• IRef Biogrid Interaction: ESR1 — RELA (direct interaction, pull down) Nettles et al., Mol Endocrinol 2008*
• MIPS CORUM ESR1-RELA-BCL3-NCOA3 complex: ESR1-RELA-BCL3-NCOA3 complex complex (BCL3-ESR1-NCOA3-RELA) Rubio et al., Oncogene 2006*
• IRef Corum Interaction: Complex of BCL3-ESR1-RELA-NCOA3 (association, coimmunoprecipitation) Rubio et al., Oncogene 2006*
• IRef Hprd Interaction: ESR1 — RELA (in vitro) Stein et al., Mol Cell Biol 1995*
• IRef Intact Interaction: ESR1 — RELA (direct interaction, pull down) Stein et al., Mol Cell Biol 1995*
• IRef Intact Interaction: ESR1 — RELA (physical association, anti bait coimmunoprecipitation) Nettles et al., Mol Endocrinol 2008*
• IRef Intact Interaction: ESR1 — RELA (direct interaction, pull down) Nettles et al., Mol Endocrinol 2008*
• IRef Intact Interaction: ESR1 — RELA (direct interaction, pull down) Gionet et al., J Cell Biochem 2009*
• IRef Intact Interaction: ESR1 — RELA (physical association, anti bait coimmunoprecipitation) Gionet et al., J Cell Biochem 2009*

Text-mined interactions from Literome

Valentine et al., J Biol Chem 2000 : Both ERalpha and ERbeta inhibit RelA in response to 17beta-estradiol but not in the presence of antihormones
Harnish et al., Endocrinology 2000 : Ligand bound ERalpha did not inhibit NF-kappaB binding to DNA, but it did decrease the histone acetyltransferase activity required for NF-kappaB transcriptional activity ... Coexpression of the transcription coactivator CREB binding protein (CBP), but not steroid receptor coactivator 1a, reversed the ERalpha mediated inhibition of NF-kappaB activity
Sharma et al., J Appl Physiol 2001 : We investigated the effects of E2 treatment and adenovirus mediated estrogen receptor (ER)-alpha gene transfer on cell proliferation and NF-kappaB activation using VSM cells cultured from 3-mo-old and 24-mo-old Fischer 344 female rats ... In conclusion, our data demonstrate that constitutive and IL-1beta stimulated NF-kappaB activation is increased in VSM cells from aged female rats due to loss of E2 and this can be restored back to normal levels by ER-alpha gene transfer and E2 treatment
Osipo et al., J Natl Cancer Inst 2003 (Breast Neoplasms) : Paradoxically, fulvestrant reversed this effect and stimulated MCF-7TAMLT tumor growth apparently through ERalpha mediated regulation of Fas, HER2/neu, and NF-kappaB
Wang et al., Nat Cell Biol 2007 (Breast Neoplasms...) : ERalpha signalling reduced levels of functional NF-kappaB and Fra-2 AP-1 and inhibited de novo RelB synthesis, leading to an inverse correlation between RELB and ERalpha gene expression in human breast cancer tissues and cell lines
Caggiano et al., J Med Chem 2007 (Arthritis, Experimental...) : Estrogen receptor dependent inhibitors of NF-kappaB transcriptional activation-1 synthesis and biological evaluation of substituted 2-cyanopropanoic acid derivatives : pathway selective inhibitors of NF-kappaB, a potential treatment for rheumatoid arthritis
Gionet et al., J Cell Biochem 2009 (Breast Neoplasms) : Ectopic expression of the ERalpha reduced cell numbers in ER+ and ER- breast cancer cell lines while NF-kappaB binding activity and the expression of several NF-kappaB regulated proteins were reduced in ER- cells
Wang et al., Mol Cell Biol 2009 (Breast Neoplasms...) : RelB NF-kappaB represses estrogen receptor alpha expression via induction of the zinc finger protein Blimp1
Cerillo et al., J Steroid Biochem Mol Biol 1998 : Furthermore, the expression of SRC-1alpha or RIP-140 does not enable the ERalpha to repress NFkappaB or to potentiate an AP-1 response in HEK-293 cells