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Review
. 2004 Jun;24(11):4605-12.
doi: 10.1128/MCB.24.11.4605-4612.2004.

Molecular and cellular determinants of estrogen receptor alpha expression

Joseph J Pinzone  1 , Holly Stevenson, Jeannine S Strobl, Patricia E Berg
Affiliations
Review

Molecular and cellular determinants of estrogen receptor alpha expression

Joseph J Pinzone et al. Mol Cell Biol. 2004 Jun.
No abstract available

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Figures

FIG. 1.
FIG. 1.
Transcriptional regulation of the ER gene by epigenetic mechanisms. The ER gene is transcriptionally regulated by epigenetic mechanisms including methylation and acetylation. The methyltransferase DNMT1 transfers methyl groups (circles) to cytosine bases located within CpG islands in exon 1 and upstream regulatory regions of ER, thereby inhibiting transcription. Transcriptionally active ER is characterized by the presence of acetyl groups (wavy lines) on histones H3 and H4, which promotes an open, accessible chromatin conformation. Upon removal of the acetyl groups by HDAC, the chromatin becomes condensed where ER is now in a transcriptionally inactive state. The DNMT inhibitor 5-aza-dC and the HDAC inhibitor TSA work synergistically to allow the reexpression of ER in cells with methylated DNA and acetylated histones.
FIG. 2.
FIG. 2.
Hormonal pathways involved in regulation of ER transcription. (A) Nuclear hormone effects on ER transcription. ERAG, estrogen receptor agonist; ERANT, estrogen receptor antagonist; PRAG, progesterone receptor agonist; T, testosterone; AR, androgen receptor; VDRAG, vitamin D receptor agonist; RXR, retinoid X receptor. (B) Protein hormone effects on ER transcription. HCG, human chorionic gonadotropin; INS, insulin; ↓ and ⊥, stimulation and inhibition within the nucleus, respectively.
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