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

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ESR1 — JUN

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

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
Holloway et al., Mol Endocrinol 2004 (Breast Neoplasms...) : Despite up-regulated activator protein-1 activity in response to ERK1/2 activation, and in ERalpha ( - ) and hormone independent breast cancers, we find that increased activator protein-1 activity is not responsible for ERalpha down-regulation
del Río et al., J Biol Chem 2004 : Here we present the characterization of its mechanism of action showing that melatonin is a specific inhibitor of E ( 2 ) -induced ERalpha mediated transcription in both estrogen response element- and AP1 containing promoters, whereas ERbeta mediated transactivation is not inhibited or even activated at certain promoters
Dong et al., Mol Endocrinol 2007 (Breast Neoplasms) : Moreover, it was indicated that estrogen stimulated PADI4 expression through binding of estrogen receptor (ER)-alpha to the upstream of the PADI4 gene and ERalpha mediated enhancement of activator protein-1 , Sp1, and nuclear factor-Y levels
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