The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Cellular regulation of endothelial nitric oxide synthase
Abstract
Renal function is highly dependent on endothelium-derived nitric oxide (NO). Several renal disorders have been linked to impaired NO bioavailability. The enzyme that is responsible for the synthesis of NO within the renal endothelium is endothelial NO synthase (eNOS). eNOS-mediated NO generation is a highly regulated cellular event, which is induced by calcium-mobilizing agonists and fluid shear stress. eNOS activity is regulated at the transcriptional level but also by a variety of modifications, such as acylation and phosphorylation, by its cellular localization, and by protein-protein interactions. The present review focuses on the complex regulation of eNOS within the endothelial cell.
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“This has been confirmed by Sessa and co-workers (103), whose studies implicated that Akt-mediated eNOS phosphorylation reduces the dissociation of calmodulin from activated eNOS.”
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Deanfield, J. E., Halcox, J. P., & Rabelink, T. J. (2007) · Circulation · doi:10.1161/circulationaha.106.652859 · Cited by 2,710
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Positive and Negative Regulation of Insulin Signaling by Reactive Oxygen and Nitrogen Species
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Cahill, P. A., & Redmond, E. M. (2016) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2016.03.007 · Cited by 518
Nitrite as Regulator of Hypoxic Signaling in Mammalian Physiology
van Faassen, E. E., Bahrami, S., Feelisch, M., Hogg, N., Kelm, M., Kim‐Shapiro, D. B., Kozlov, A. V., Li, H., Lundberg, J. O., Mason, R., et al. (2009) · Medicinal Research Reviews · doi:10.1002/med.20151 · Cited by 435
Metadata
- Authors
- Govers, R., & Rabelink, T. J.
- Venue
- American Journal of Physiology-Renal Physiology
- Publisher
- American Physiological Society
- Published
- 2001-02-01
- Volume
- 280
- Issue
- 2
- Pages
- F193-F206
- ISSN
- 1522-1466 (ISSN-L)
- 1931-857X
- OpenAlex
- W2103790130
- Cited by
- 472
- References
- 9
- FWCI
- 21.37
- Type
- journal article
- Language
- en
- Open access
- closed
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