The DOI matches its Crossref record; 101 of the 101 references it cites were found in a registry or an index.
Flow-dependent regulation of endothelial nitric oxide synthase: role of protein kinases
Abstract
Vascular endothelial cells are directly and continuously exposed to fluid shear stress generated by blood flow. Shear stress regulates endothelial structure and function by controlling expression of mechanosensitive genes and production of vasoactive factors such as nitric oxide (NO). Though it is well known that shear stress stimulates NO production from endothelial nitric oxide synthase (eNOS), the underlying molecular mechanisms remain unclear and controversial. Shear-induced production of NO involves Ca 2+/calmodulin-independent mechanisms, including phosphorylation of eNOS at several sites and its interaction with other proteins, including caveolin and heat shock protein-90. There have been conflicting results as to which protein kinases—protein kinase A, protein kinase B (Akt), other Ser/Thr protein kinases, or tyrosine kinases—are responsible for shear-dependent eNOS regulation. The functional significance of each phosphorylation site is still unclear. We have attempted to summarize the current status of understanding in shear-dependent eNOS regulation.
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Cited by
Sessa, W. C. (2004) · Journal of Cell Science · doi:10.1242/jcs.01165 · Cited by 561
Nauli, S. M., Kawanabe, Y., Kaminski, J. J., Pearce, W. J., Ingber, D. E., & Zhou, J. (2008) · Circulation · doi:10.1161/circulationaha.107.710111 · Cited by 466
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Nitric Oxide and the Vascular Endothelium
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Metadata
- Authors
- Boo, Y. C., & Jo, H.
- Venue
- American Journal of Physiology-Cell Physiology
- Publisher
- American Physiological Society
- Published
- 2003-09
- Volume
- 285
- Issue
- 3
- Pages
- C499-C508
- ISSN
- 0363-6143 (ISSN-L)
- 1522-1563
- OpenAlex
- W2112837796
- Cited by
- 384
- References
- 101
- FWCI
- 15.92
- Type
- journal article
- Language
- en
- Open access
- closed
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