scholarly journals Endothelin-1 and angiotensin II contribute to BNP but not c-fos gene expression response to elevated load in isolated mice hearts

2007 ◽  
Vol 1772 (3) ◽  
pp. 338-344 ◽  
Author(s):  
Jarkko Piuhola ◽  
István Szokodi ◽  
Heikki Ruskoaho
Keyword(s):  
Gene Expression ◽  
Angiotensin Ii ◽  
Gene Expression Response ◽  
Endothelin 1 ◽  
Expression Response

scholarly journals RNA Decay Controls the Kinetics of the Angiotensin II Gene Expression Response

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A508-A509
Author(s):  
Kimberly Wellman ◽  
Rui Fu ◽  
Amber Baldwin ◽  
Kent Riemondy ◽  
Neelanjan Mukherjee
Keyword(s):  
Gene Expression ◽  
Blood Pressure ◽  
Angiotensin Ii ◽  
Decay Rates ◽  
Rna Decay ◽  
Type I ◽  
Specific Expression ◽  
Gene Expression Response ◽  
Aldosterone Production ◽  
Expression Response

Abstract Complex cellular resonses require the temporal coordination of stimulus-induced gene expression programs. Angiotensin II (AngII) is the active 8 amino acid peptide in the renin-angiotensin-aldosterone system that controls blood pressure and fluid balance. AngII binds to type I angiotensin receptor in the adrenal cortex to initiate a cascade of temporally coordinated events leading to the production of aldosterone, a master regulator of blood pressure and volume. We stimulated a steroidogenic human cell line (H295R) with AngII and performed RNA-seq at twelve points. We identified twelve distict temporally distinct groups of gene expression responses each encoding functionally related proteins important for various steps of aldosterone productionl. Interstingly, the shape of the impulse response suggested a key role for RNA decay. Indeed, RNA decay rates in unstimulated H295R cells strongly correlated with the amplitude and peakiness of the gene expression response for each group of genes. We also found evidence for increases in RNA decay during the AngII response. Next, we selected candidate RBPs based on motif finding, adrenal specific expression, and AngII responsiveness. We performed an siRNA knockdown screen on these 22 candidates to identify RBPs that regulate aldosterone levels. Eight of these RBPs exhibited statistically significant changes in aldosterone for at least two independent siRNAs. Interestingly, multiple RBPs that promote RNA decay were found to suppress aldosterone production and induced in response to AngII-stimulation. These RBPs could be responsible for our observed increases in RNA decay. Altogether, these data support a model in which RNA decay is a critical regulator of the timing and strength of AngII-induced gene expression and ultimately aldosterone production.

Gene expression response of mouse lung, liver and white adipose tissue to β-carotene supplementation, knockout of Bcmo1 and sex

2011 ◽  
Vol 55 (10) ◽  
pp. 1466-1474 ◽  
Author(s):  
Yvonne G. J. van Helden ◽  
Roger W. L. Godschalk ◽  
Johannes von Lintig ◽  
Georg Lietz ◽  
Jean-Francois Landrier ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Mouse Lung ◽  
Gene Expression Response ◽  
Expression Response ◽  
Β Carotene

Gene expression response of the alga Fucus virsoides (Fucales, Ochrophyta) to glyphosate solution exposure

2020 ◽  
Vol 267 ◽  
pp. 115483
Author(s):  
Marco Gerdol ◽  
Andrea Visintin ◽  
Sara Kaleb ◽  
Francesca Spazzali ◽  
Alberto Pallavicini ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Expression Response ◽  
Expression Response

scholarly journals VExD: A curated resource for human gene expression following viral infection

2021 ◽  
Author(s):  
Phillip J Dexheimer ◽  
Mario Pujato ◽  
Krishna Roskin ◽  
Matthew T Weirauch
Keyword(s):  
Gene Expression ◽  
Viral Infection ◽  
Human Gene ◽  
Application Programming Interface ◽  
Gene Expression Response ◽  
Human Gene Expression ◽  
Link Type ◽  
Uniform Manner ◽  
Expression Response ◽  
Virus Expression

AbstractMotivationHuman viruses cause significant mortality, morbidity, and economic disruption worldwide. The human gene expression response to viral infection can yield important insights into the detrimental effects to the host. To date, hundreds of studies have performed genome-scale profiling of the effect of viral infection on human gene expression. However, no resource exists that aggregates human expression results across multiple studies, viruses, and tissue types.ResultsWe developed the Virus Expression Database (VExD), a comprehensive curated resource of transcriptomic studies of viral infection in human cells. We have processed all studies within VExD in a uniform manner, allowing users to easily compare human gene expression changes across conditions.Availability and ImplementationVExD is freely accessible at https://vexd.cchmc.org for all modern web browsers. An Application Programming Interface (API) for VExD is also available. The source code is available at https://github.com/pdexheimer/[email protected], [email protected]

scholarly journals Disruption of TFIIH activities generates a stress gene expression response and reveals possible new targets against cancer

2019 ◽  
Author(s):  
Maritere Urioistegui-Arcos ◽  
Rodrigo Aguayo-Ortiz ◽  
María del Pilar Valencia-Morales ◽  
Erika Melchy-Pérez ◽  
Yvonne Rosenstein ◽  
...  
Keyword(s):  
Gene Expression ◽  
Tumour Growth ◽  
Transformed Cells ◽  
Rna Seq ◽  
Gene Expression Response ◽  
New Targets ◽  
Increased Sensitivity ◽  
Promoter Occupancy ◽  
Expression Response ◽  
Stress Gene

AbstractDisruption of the enzymatic activities of the transcription factor TFIIH by Triptolide (TPL) or THZ1 could be used against cancer. Here, we used an oncogenesis model to compare the effect of TFIIH inhibitors between transformed cells and their progenitors. We report that tumour cells exhibited highly increased sensitivity to TPL or THZ1 and that the combination of both had an additive effect. TPL affects the interaction between XPB and P52, causing a reduction in the levels of XPB, P52, and P8, but not other TFIIH subunits. RNA-Seq and RNAPII-ChIP-Seq experiments showed that although the levels of many transcripts were reduced, the levels of a significant number were increased after TPL treatment, with maintained or increased RNAPII promoter occupancy. A significant number of these genes encode for factors that have been related to tumour growth and metastasis. Some of these genes were also overexpressed in response to THZ1, which depletion enhances the toxicity of TPL and are possible new targets against cancer.

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