Identification of functional glucocorticoid response elements in the mouse FoxO1 promoter

2014 ◽  
Vol 450 (2) ◽  
pp. 979-983 ◽  
Author(s):  
Weiping Qin ◽  
Jiangping Pan ◽  
Yiwen Qin ◽  
David N. Lee ◽  
William A. Bauman ◽  
...  
Keyword(s):  
Response Elements ◽  
Glucocorticoid Response ◽  
Glucocorticoid Response Elements

scholarly journals The Glucose-6-Phosphatase Catalytic Subunit Gene Promoter Contains Both Positive and Negative Glucocorticoid Response Elements

2005 ◽  
Vol 19 (12) ◽  
pp. 3001-3022 ◽  
Author(s):  
Beth T. Vander Kooi ◽  
Hiroshi Onuma ◽  
James K. Oeser ◽  
Christina A. Svitek ◽  
Shelley R. Allen ◽  
...  
Keyword(s):  
Gene Promoter ◽  
Catalytic Subunit ◽  
Subunit Gene ◽  
Response Elements ◽  
Glucocorticoid Response ◽  
Glucocorticoid Response Elements

Identification of two glucocorticoid response elements in the promoter region of the ubiquitous isoform of glutamine synthetase in gulf toadfish, Opsanus beta

2009 ◽  
Vol 297 (4) ◽  
pp. R1075-R1081 ◽  
Author(s):  
Andrew J. Esbaugh ◽  
Patrick J. Walsh
Keyword(s):  
Gene Expression ◽  
Glutamine Synthetase ◽  
Luciferase Activity ◽  
Nitrogen Excretion ◽  
Luciferase Reporter ◽  
Response Elements ◽  
Glucocorticoid Response ◽  
Glucocorticoid Response Elements ◽  
Gulf Toadfish

Unlike most teleosts, gulf toadfish have the capacity to switch from ammoniotely to ureotely as the predominate means of nitrogen excretion during periods of stress. The switch to ureotely is a result of increased glutamine synthetase (GS) mRNA expression/enzyme activity in the liver and muscle, which is initiated by cortisol. Cortisol typically affects gene expression through the action of cortisol-activated transcription factors, such as glucocorticoid receptors, which bind to glucocorticoid response elements (GRE) in the upstream regulatory region of genes. The purpose of the present study was to identify the GRE responsible for increased GS gene expression during crowding/confinement in gulf toadfish using an in vivo luciferase reporter assay. Upstream promoter regions for both the ubiquitous and gill GS isoforms were amplified by PCR. Additionally, an intron was amplified from the ubiquitous GS isoform that suggested the possibility of two discreet transcripts for the mitochondrial and cytoplasmic proteins. When tested via in vivo reporter assays, both the cytoplasmic and mitochondrial ubiquitous GS promoters showed increased luciferase activity during crowding vs. noncrowded controls; the gill GS promoter showed no effects in response to crowding. In silico analysis of the mitochondrial and cytoplasmic ubiquitous GS promoter constructs showed an overlapping section of 565 bp containing two potential GREs. Mutation of either site alone had no effect on luciferase activity vs. wild-type controls. However, when both sites were mutated a significant decrease in luciferase activity was observed. We conclude that two functional GREs combine to confer cortisol-inducible GS expression in the liver of gulf toadfish.

scholarly journals The permissive role of glucocorticoids on interleukin-1 stimulation of angiotensinogen gene transcription is mediated by an interaction between inducible enhancers.

1990 ◽  
Vol 10 (8) ◽  
pp. 4389-4395 ◽  
Author(s):  
D Ron ◽  
A R Brasier ◽  
K A Wright ◽  
J F Habener
Keyword(s):  
Acute Phase ◽  
Acute Phase Response ◽  
Interleukin 1 ◽  
Luciferase Reporter ◽  
Nf Kappa B ◽  
Response Elements ◽  
Glucocorticoid Response ◽  
Glucocorticoid Response Elements ◽  
Permissive Role

The acute-phase activation of the rat angiotensinogen (rAT) gene in liver cells is a transcriptional event mediated through an interleukin-1-inducible, NF kappa B-binding, cis-acting element (the acute-phase response element [APRE]). Using a cell culture model for the acute-phase response, we showed that the increase in angiotensionogen mRNA in H35 rat hepatoma cells requires costimulation with glucocorticoids and cytokines. Stably transfected rAT promoter-luciferase reporter genes were also activated by cytokines only in the presence of glucocorticoids. This permissive role of glucocorticoids is dependent on the expression of functional glucocorticoid receptors, because in HepG2 cells naturally deficient in such receptors, rAT gene-luciferase reporter constructs responded to interleukin-1 only when cotransfected with an expression vector for the glucocorticoid receptor. Point mutations in the two rAT gene glucocorticoid response elements located adjacent to the APRE led to loss of interleukin-1 inducibility. Induction of luciferase activity in transfected cells occurred even in the presence of cycloheximide, demonstrating that this synergistic response did not depend on new protein synthesis. Thus, a direct interaction between the interleukin-1-inducible NF kappa B-binding APRE and glucocorticoid response elements, located in cis, underlies the acute-phase activation of the rAT gene.

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