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ESR1 — FOS

Pathways - manually collected, often from reviews:

• FastForward regulation: ESR1 → FOS (transcriptional regulation, unknown) Kapranov et al., Science 2002, Elias et al., Semin Dermatol 1992
  Evidence: DNABINDING
• NCI Pathway Database AP-1 transcription factor network: ER alpha (ESR1) → JUN/FOS complex (FOS-JUN) (modification, collaborate) Lambertini et al., J Cell Physiol 2008*
  Evidence: physical interaction
• NCI Pathway Database AP-1 transcription factor network: ER alpha (ESR1) → JUN/FOS/ER alpha complex (FOS-JUN-ESR1) (modification, collaborate)
  Lambertini et al., J Cell Physiol 2008*
  Evidence: physical interaction
• NCI Pathway Database AP-1 transcription factor network: JUN/FOS complex (FOS-JUN) → JUN/FOS/ER alpha complex (FOS-JUN-ESR1) (modification, collaborate)
  Lambertini et al., J Cell Physiol 2008*
  Evidence: physical interaction
• NCI Pathway Database FOXA1 transcription factor network: E2/ERA complex (ESR1) → AP1 complex (FOS-JUN) (transcription, activates) Eeckhoute et al., Genes Dev 2006
  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: FOS — ESR1 (physical association, affinity chromatography technology) Baron et al., J Biol Chem 2007*

Text-mined interactions from Literome

Planas-Silva et al., Cancer Res 1999 (Breast Neoplasms) : Other transcriptional cofactors that allow estrogen receptor to induce expression of AP-1 may be required for estrogen to act as a mitogen
Walters et al., J Biol Chem 2002 : Overexpression of the AP-1 protein c-Jun, but not c-Fos , strongly enhanced SKF induced ERalpha target gene expression but only when the TRE was present
Petz et al., Endocrinology 2002 (Breast Neoplasms) : Purified estrogen receptor ( ER ) enhanced binding of Fos and Jun to the +90 AP-1 site and bound to an adjacent imperfect ERE half-site
Gréco et al., Horm Behav 2003 : To determine whether cells in which Fos is induced by a particular mating stimulus coexpress ERalpha , ERbeta, or both, we used a triple-label immunofluorescent technique to visualize ERalpha-, ERbeta-, and mating induced Fos-immunoreactivity (Fos-ir) in neurons in which mating stimulation reliably increases Fos expression
Wang et al., Cell Biol Toxicol 2010 (Adenoma...) : In this study, we made the following observations : ( a ) 0.01 % ( v/v ) ethanol ( corresponding to 1.7 mM ) significantly elevated estrogen receptor alpha (ERalpha) protein content, stimulated activator protein-1 (AP-1) dependent ERalpha transcriptional activities, and ultimately enhanced GH4C1 cells growth in vitro and ( b ) the same concentration of ethanol suppressed the stimulatory effects of 17beta-estradiol ( E2 ; 10 nM ) on both cell growth and cellular PRL accumulate through attenuation of ERalpha actions at both the estrogen response element and the AP-1 site
Pedraza-Alva et al., Biochem Biophys Res Commun 2009 : Estrogen receptor regulates MyoD gene expression by preventing AP-1 mediated repression
Schmitt et al., J Neurosci Res 1995 : Using transient transfections in neuroblastoma NE-1-115 and COS-1 cells, we show that ligand activated estrogen receptor ( HEGo ) represses the transcriptional activation by c-Fos/c-Jun