Although there is not a classical estrogen response element ...

created [InstanceEdit:9009656] Rothfels, Karen, 2017-06-21
dbId 9009655
displayName Although there is not a classical estrogen response element ...
modified [InstanceEdit:9024214] Rothfels, Karen, 2017-10-02
schemaClass Summation
text Although there is not a classical estrogen response element (ERE) in the proximal CCND1 promoter, estrogen-responsive transcription is mediated through recruitment of hormone-bound ESR1 by other DNA-binding proteins (reviewed in Guo et al, 2011; Klein and Assoian, 2008). A heterodimer of JUN:FOS binds to an estrogen-responsive G1 element (ERGE) between nucleotides -948 and -925 and is responsible for recruitment of ESR1 and estrogen to this site. OCT1 may facilitate this binding by displacing a YY1:HDAC1 repressive complex that occupies an adjacent site in unstimulated cells (Albanese et al, 1995; Cicatiello et al, 2004; Shen et al, 2007). Binding of ATF2:JUN heterodimers to a cyclic AMP response element (CRE) located 52 nucleotides upstream of the transcriptional start site may also contribute to estrogen-responsive signaling (Sabbah et al, 1999; Castro-Rivera at al, 2001). An ERE has been identified in an enhancer element downstream of the CCND1 gene (enh2). This enhancer binds to FOXA1, and also mediates recruitment of the histone acetyltransferase p300 to the CCND1 promoter (Eeckhoute et al, 2006).
Although FOXA1 and GATA3 were initially characterized as 'pioneer' transcription factors that bind to closed chromatin conformations and prime recruitment of sequence-specific DNA binding factors, more recent studies have questioned the order of recruitment of the estrogen receptors, FOXA1 and GATA3 to estrogen-responsive targets (Swinstead et al, 2016).
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