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 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.

The estrogen receptor gene: Promoter organization and expression

1997 ◽  
Vol 29 (12) ◽  
pp. 1343-1369 ◽  
Author(s):  
Kaj Grandien ◽  
Anders Berkenstam ◽  
Jan-Åke Gustafsson
Keyword(s):  
Estrogen Receptor ◽  
Receptor Gene ◽  
Gene Promoter ◽  
Estrogen Receptor Gene

scholarly journals A Novel Cyclic Adenosine 3′,5′-Monophosphate-Responsive Element Involved In the Transcriptional Regulation of the Lutropin Receptor Gene in Granulosa Cells

2000 ◽  
Vol 14 (9) ◽  
pp. 1498-1508
Author(s):  
Shiyou Chen ◽  
Xuebo Liu ◽  
Deborah L. Segaloff
Keyword(s):  
Granulosa Cells ◽  
Promoter Region ◽  
Receptor Gene ◽  
Consensus Sequence ◽  
Protein S ◽  
Luciferase Reporter ◽  
The Core ◽  
Lutropin Receptor ◽  
Flanking Region ◽  
Responsive Element

Abstract The induction of the lutropin receptor (LHR) in granulosa cells by FSH is mediated, at least in part, by cAMP. However, the classic cAMP-responsive element (CRE) is not present in the 5′-flanking region of the rat LHR gene. Previous studies from our laboratory had shown that three Sp1 sites within the promoter region of the rat LHR (rLHR) bind Sp1 and Sp3 and are involved in the basal and cAMP-mediated transcription of the rLHR gene. In the present studies we show that the rLHR promoter region forms a complex (designated complex A) with nuclear extracts from rat granulosa cells, and the abundance of complex A is markedly increased when using cells that had been pretreated with 8-bromo (Br)-cAMP. We have localized the binding of the protein(s) in complex A to a DNA sequence immediately upstream and partially overlapping with the Sp1c binding site. The core site (designated SAS for Sp1c adjacent sequence) is localized to nucleotide (nt) −146 to −142 and contains the sequence GGGGG. The consensus sequence for the core portion of this element appears to be (G/T)GGGG. Mutations of the SAS site, but not SP1c site, abolish complex A formation. Experiments utilizing rat granulosa cells transfected with luciferase reporter genes driven by the 5′-flanking region of the rLHR gene demonstrate a functional role for the SAS site in the cAMP responsiveness of the rLHR gene.

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