The Soluble Guanylyl Cyclase Activator YC-1 Increases Intracellular cGMP and cAMP via Independent Mechanisms in INS-1E Cells
The Journal of Pharmacology and Experimental Therapeutics, ISSN: 0022-3565, Vol: 338, Issue: 3, Page: 925-931
2011
- 7Citations
- 16Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations7
- Citation Indexes7
- CrossRef6
- Captures16
- Readers16
- 16
Article Description
In addition to increasing cGMP, the soluble guanylyl cyclase (sGC) activator 3-(5′-hydroxymethyl-2′-furyl)-1-benzylindazole (YC-1) can elevate intracellular cAMP levels. This response was assumed to be as a result of cGMP-dependent inhibition of cAMP phosphodiesterases; however, in this study, we show that YC-1-induced cAMP production in the rat pancreatic beta cell line INS-1E occurs independent of its function as a sGC activator and independent of its ability to inhibit phosphodiesterases. This YC-1-induced cAMP increase is dependent upon soluble adenylyl cyclase and not on transmembrane adenylyl cyclase activity. We previously showed that soluble adenylyl cyclase-generated cAMP can lead to extracellular signal-regulated kinase activation and that YC-1-stimulated cAMP production also stimulates extracellular signal-regulated kinase. Although YC-1 has been used as a tool for investigating sGC and cGMP-mediated pathways, this study reveals cGMP-independent pharmacological actions of this compound.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0022356524465373; http://dx.doi.org/10.1124/jpet.111.184135; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=80052173193&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/21665942; https://linkinghub.elsevier.com/retrieve/pii/S0022356524465373; https://dx.doi.org/10.1124/jpet.111.184135; https://jpet.aspetjournals.org/content/338/3/925
Elsevier BV
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