Cyclic AMP stimulates MEG3 gene expression in cells through a cAMP-response element (CRE) in the MEG3 proximal promoter region

2006 ◽  
Vol 38 (10) ◽  
pp. 1808-1820 ◽  
Author(s):  
Jing Zhao ◽  
Xun Zhang ◽  
Yunli Zhou ◽  
Peter J. Ansell ◽  
Anne Klibanski
Keyword(s):  
Gene Expression ◽  
Cyclic Amp ◽  
Promoter Region ◽  
Proximal Promoter ◽  
Camp Response Element ◽  
Response Element ◽  
Proximal Promoter Region ◽  
In Cells

AVP-induced VIT32 gene expression in collecting duct cells occurs via trans-activation of a CRE in the 5′-flanking region of the VIT32 gene

2004 ◽  
Vol 287 (3) ◽  
pp. F460-F468 ◽  
Author(s):  
Christie P. Thomas ◽  
Randy W. Loftus ◽  
Kang Z. Liu
Keyword(s):  
Gene Expression ◽  
Promoter Region ◽  
Collecting Duct ◽  
Airway Epithelial Cells ◽  
Proximal Promoter ◽  
Xenopus Laevis Oocytes ◽  
Proximal Promoter Region ◽  
Duct Cells ◽  
Collecting Duct Cells ◽  
Flanking Region

VIT32, a vasopressin-induced transcript, inhibits Na+ transport when coexpressed with the epithelial sodium channel in Xenopus laevis oocytes ( EMBO J 21: 5109–5117, 2002). To understand the mechanism of VIT32 gene regulation, we examined the effect of DDAVP and cAMP stimulation on VIT32 expression in M-1 mouse collecting duct cells and in H441 human airway epithelial cells. Elevation of cAMP with forskolin and IBMX increased VIT32 gene expression with a peak effect at 2 h. The increase in gene expression was abolished by H89 and by actinomycin D, suggesting that cAMP stimulates VIT32 mRNA expression by a PKA-mediated increase in gene transcription. An ∼1.5-kb fragment of the 5′-flanking region of VIT32 was cloned and was able to confer cAMP-stimulated reporter gene activity when transfected into M-1 and H441 cells. By deletion analysis and site-directed mutagenesis, a cAMP response element (CRE) was identified within the proximal promoter region that was sufficient to account for the increase in VIT32 gene expression seen with DDAVP and elevation of cAMP. Furthermore, DDAVP-stimulated VIT32 promoter-reporter activity was inhibited by H89 and by a dominant negative CREB construct. Finally, we were able to identify CREB as a nuclear protein that bound to the VIT32 CRE in gel mobility shift assays. In summary, DDAVP stimulates transcription of VIT32 via a CRE within the proximal promoter region of the VIT32 gene.

Proximal promoter region of the wheat histone H3 gene confers S phase-specific gene expression in transformed rice cells

1993 ◽  
Vol 23 (3) ◽  
pp. 553-565 ◽  
Author(s):  
Norihiro Ohtsubo ◽  
Takuya Nakayama ◽  
Rie Terada ◽  
Ko Shimamoto ◽  
Masaki Iwabuchi
Keyword(s):  
Gene Expression ◽  
Promoter Region ◽  
Histone H3 ◽  
S Phase ◽  
Proximal Promoter ◽  
Specific Gene ◽  
Proximal Promoter Region ◽  
Specific Gene Expression ◽  
Histone H3 Gene

scholarly journals IL-1β induction ofMUC5ACgene expression is mediated by CREB and NF-κB and repressed by dexamethasone

2014 ◽  
Vol 306 (8) ◽  
pp. L797-L807 ◽  
Author(s):  
Yajun Chen ◽  
Lindsay M. Garvin ◽  
Tracey J. Nickola ◽  
Alan M. Watson ◽  
Anamaris M. Colberg-Poley ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Line ◽  
Interleukin 1 ◽  
A549 Cells ◽  
Cancer Cell Line ◽  
Nuclear Factor Κb ◽  
Camp Response Element Binding ◽  
Proximal Promoter ◽  
Camp Response Element ◽  
Response Element

Chronic airway diseases are characterized by inflammation and mucus overproduction. The MUC5AC mucin gene is upregulated by the proinflammatory cytokine interleukin-1 β (IL-1β) via activation of cAMP response element-binding protein (CREB) in the NCI-H292 cancer cell line and nuclear factor-κB (NF-κB) in the HBE1 transformed cell line, with each transcription factor binding to a cognate cis site in the proximal or distal region, respectively, of the MUC5AC promoter. We utilized primary differentiated human bronchial epithelial (HBE) and A549 lung adenocarcinoma cells to further investigate the contributions of CREB and NF-κB subunits to the IL-1β-induced upregulation of MUC5AC. Data show that ligand binding of IL-1β to the IL-1β receptor is required to increase MUC5AC mRNA abundance. Chromatin immunoprecipitation analyses show direct binding of CREB to the previously identified cAMP response element site and binding of p65 and p50 subunits to a novel NF-κB site in a mucin-regulatory domain in the proximal promoter and to a previously identified NF-κB site in the distal promoter. P50 binds to both NF-κB sites at 1 h following IL-1β exposure, but is replaced at 2 h by p65 in A549 cells and by a p50/p65 heterodimer in HBE cells. Thus IL-1β activates multiple domains in the MUC5AC promoter but exhibits some cell-specific responses, highlighting the complexity of MUC5AC transcriptional regulation. Data show that dexamethasone, a glucocorticoid that transcriptionally represses MUC5AC gene expression under constitutive conditions, also represses IL-1β-mediated upregulation of MUC5AC gene expression. A further understanding of mechanisms mediating MUC5AC regulation should lead to a honing of therapeutic approaches for the treatment of mucus overproduction in inflammatory lung diseases.

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