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Shear Stress Stimulates Phosphorylation of Endothelial Nitric-oxide Synthase at Ser1179 by Akt-independent Mechanisms
It is demonstrated that shear stimulates phosphorylation of eNOS-S1179 in a PKA-dependent, but Aktindependent manner, whereas the NO⋅ production is regulated by the mechanisms dependent on both PKA and Akt.
Shear stress stimulates phosphorylation of eNOS at Ser(635) by a protein kinase A-dependent mechanism.
The results suggest that shear stress stimulates eNOS by two different mechanisms: 1) PKA- and PI3K-dependent and 2) Pka-dependent but PI3k-independent pathways.
Flow-dependent regulation of endothelial nitric oxide synthase: role of protein kinases.
The current status of understanding in shear-dependent eNOS regulation is summarized and there have been conflicting results as to which protein kinases-protein kinase A, protein kinase B (Akt), other Ser/Thrprotein kinases, or tyrosine kinase-are responsible for shear to shear stress regulation.
Bone Morphogenic Protein 4 Produced in Endothelial Cells by Oscillatory Shear Stress Stimulates an Inflammatory Response*
It is suggested that BMP4 is a mechanosensitive, inflammatory factor playing a critical role in early steps of atherogenesis in the lesion-prone areas.
Oscillatory shear stress stimulates endothelial production of O2- from p47phox-dependent NAD(P)H oxidases, leading to monocyte adhesion.
It is suggested that chronic exposure of endothelial cells to OS stimulates O2- and/or its derivatives produced from p47phox-dependent NAD(P)H oxidase, which, in turn, leads to monocyte adhesion, an early and critical atherogenic event.
Compensatory Phosphorylation and Protein-Protein Interactions Revealed by Loss of Function and Gain of Function Mutants of Multiple Serine Phosphorylation Sites in Endothelial Nitric-oxide Synthase*
Multiple serine phosphorylation events regulate basal and stimulate NO release with Ser-635 and Ser-1179 being important positive regulatory sites andSer-116 as a negative regulatory, and serines 635 and 1179 are important positive regulators of basal and stimulated NO release.
Chronic shear induces caveolae formation and alters ERK and Akt responses in endothelial cells.
It is suggested that chronic shear stimulates caveolae formation by translocating caveolin-1 from the Golgi to the luminal plasma membrane and alters cell signaling responses.
Flavonoids, taxifolin and luteolin attenuate cellular melanogenesis despite increasing tyrosinase protein levels
When tested in murine melanoma B16F10 cells activated by α‐melanocyte stimulating hormone (α‐MSH), taxifolin and luteolin inhibited the cellular melanogenesis as effectively as arbutin, one of the most widely used hypopigmenting agents in cosmetics.
Endothelial NO synthase phosphorylated at SER635 produces NO without requiring intracellular calcium increase.
Protein kinase B/Akt activates c-Jun NH(2)-terminal kinase by increasing NO production in response to shear stress.
It is suggested that shear stress triggers activation of PI3K, Akt, and endothelial NO synthase, leading to production of NO, which (along with O(2-), which is also produced by shear) activates Ras-JNK pathway.