scholarly journals A 13 bp palindrome is a functional estrogen responsive element and interacts specifically with estrogen receptor

1988 ◽  
Vol 16 (2) ◽  
pp. 647-663 ◽  
Author(s):  
Ludger Klein-Hitpass ◽  
Gerhart U. Ryffel ◽  
Ellen Heitlinger ◽  
Andrew C.B. Cato
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Responsive Element ◽  
Responsive Element

scholarly journals In VitroBinding of the Purified Hormone-Binding Subunit of the Estrogen Receptor to Oligonucleotides Containing Natural or Modified Sequences of an Estrogen-Responsive Element

1991 ◽  
Vol 5 (4) ◽  
pp. 555-563 ◽  
Author(s):  
Nicola Medici ◽  
Vincenzo Nigro ◽  
Ciro Abbondanza ◽  
Bruno Moncharmont ◽  
Anna Maria Molinari ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Hormone Binding ◽  
Estrogen Responsive Element ◽  
Responsive Element ◽  
Binding Subunit

Characterization of an estrogen-responsive element implicated in regulation of the rainbow trout estrogen receptor gene

1995 ◽  
Vol 15 (1) ◽  
pp. 37-47 ◽  
Author(s):  
Y Le Dréan ◽  
G Lazennec ◽  
L Kern ◽  
D Saligaut ◽  
F Pakdel ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Rainbow Trout ◽  
Receptor Gene ◽  
Expression System ◽  
Consensus Sequence ◽  
Gene Promoter ◽  
Dnase I Footprinting ◽  
Estrogen Responsive Element ◽  
Responsive Element ◽  
Simplex Virus

ABSTRACT We previously reported that the expression of the rainbow trout estrogen receptor (rtER) gene is markedly increased by estradiol (E2). In this paper, we have used transient transfection assays with reporter plasmids expressing chloramphenicol acetyl transferase (CAT), linked to 5′ flanking regions of the rtER gene promoter, to identify cis-elements responsible for E2 inducibility. Deletion analysis localized an estrogen-responsive element (ERE), at position +242, with one mutation on the first base compared with the consensus sequence. This element confers estrogen responsiveness to CAT reporter linked to both the herpes simplex virus thymidine kinase promoter and the homologous rtER promoter. Moreover, using a 0·2 kb fragment of the rtER promoter encompassing the ERE and the rtER DNA binding domain obtained from a bacterial expression system, DNase I footprinting experiments demonstrated a specific protection covering 20 bp (+240/+260) containing the ERE sequence. Based on these studies, we believe that this ERE sequence, identified in the rtER gene promoter, may be a major cis-acting element involved in the regulation of the gene by estrogen.

scholarly journals Krüppel-Like Factor 9 Is a Negative Regulator of Ligand-Dependent Estrogen Receptor α Signaling in Ishikawa Endometrial Adenocarcinoma Cells

2007 ◽  
Vol 21 (12) ◽  
pp. 2988-3001 ◽  
Author(s):  
Michael C. Velarde ◽  
Zhaoyang Zeng ◽  
Jennelle R. McQuown ◽  
Frank A. Simmen ◽  
Rosalia C. M. Simmen
Keyword(s):  
Estrogen Receptor ◽  
Epithelial Cells ◽  
Promoter Region ◽  
Small Interfering Rna ◽  
Negative Regulator ◽  
Luciferase Reporter ◽  
Target Cells ◽  
Estrogen Responsive Element ◽  
Responsive Element ◽  
Interfering Rna

Abstract Estrogen and progesterone, acting through their respective receptors and other nuclear proteins, exhibit opposing activities in target cells. We previously reported that Krüppel-like factor 9 (KLF9) cooperates with progesterone receptor (PR) to facilitate P-dependent gene transcription in uterine epithelial cells. Here we evaluated whether KLF9 may further support PR function by directly opposing estrogen receptor (ER) signaling. Using human Ishikawa endometrial epithelial cells, we showed that 17β-estradiol (E2)-dependent down-regulation of ERα expression was reversed by a small interfering RNA to KLF9. Transcription assays with the E2-sensitive 4× estrogen-responsive element-thymidine kinase-promoter-luciferase reporter gene demonstrated inhibition of ligand-dependent ERα transactivation with ectopic KLF9 expression. E2 induced PR-A/B and PR-B isoform expression in the absence of effects on KLF9 levels. Addition of KLF9 small interfering RNA augmented E2 induction of PR-A/B while abrogating that of PR-B, indicating selective E2-mediated inhibition of PR-A by KLF9. Chromatin immunoprecipitation of the ERα minimal promoter demonstrated KLF9 promotion of E2-dependent ERα association to a region containing functional GC-rich motifs. KLF9 inhibited the recruitment of the ERα coactivator specificity protein 1 (Sp1) to the PR proximal promoter region containing a half-estrogen responsive element and GC-rich sites, but had no effect on Sp1 association to the PR distal promoter region containing GC-rich sequences. In vivo association of KLF9 and Sp1, but not of ERα with KLF9 or Sp1, was observed in control and E2-treated cells. Our data identify KLF9 as a transcriptional repressor of ERα signaling and suggest that it may function at the node of PR and ER genomic pathways to influence cell proliferation.

scholarly journals Estrogen Receptor β Activation Inhibits Colitis by Promoting NLRP6-Mediated Autophagy

2021 ◽  
Author(s):  
Wentao Fan ◽  
Chenchen Ding ◽  
Shuihui Liu ◽  
Xiaona Gao ◽  
Xiaofei Shen ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Inflammatory Response ◽  
Gene Promoter ◽  
Estrogen Receptor Β ◽  
Autophagic Flux ◽  
Intestinal Epithelial ◽  
Estrogen Responsive Element ◽  
Underlying Mechanisms ◽  
Responsive Element ◽  
And Control

Abstract Estrogen receptor β (ERβ) and NLRP6 are highly expressed in intestinal tissues. Loss of ERβ and NLRP6 exacerbate colitis in mouse models. However, the underlying mechanisms are incompletely understood. Here, we report that ERβ attenuates inflammation by inducing NLRP6-mediated autophagy. Specifically, ERβ directly activates the NLRP6 gene expression via binding to estrogen responsive element (ERE) of Nlrp6 gene promoter. ERβ also physically interacts with the NLRP6 nucleotide-binding domain and promotes NLRP6 inflammasome assembly. The ERβ-NLRP6 axis then interacts with multiple autophagy-related proteins including ULK1, BECN1, ATG16L1, LC3B, p62 to affect the autophagosome biogenesis and control autophagic flux. Finally, NLRP6-mediated autophagy suppresses the inflammatory response by promoting the K48-linked polyubiquitination of ASC, Casp-1 p20, IL-1β, TNF-α, and prohibitin-2. Thus, ERβ-NLRP6 direct an anti-inflammatory response by promoting autophagy. Our work uncovers an ERβ-NLRP6-autophagy pathway as an unrecognized regulatory mechanism that maintains intestinal epithelial cell homeostasis and facilitates tissue repair in colitis.

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