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Regulation of CLC-Ka/barttin by the ubiquitin ligase Nedd4-2 and the serum- and glucocorticoid-dependent kinases.
ClC-Ka/barttin channels are regulated by SGK1 and SGK3, which may participate in the regulation of transport in kidney and inner ear and be down-regulated by Nedd4-2.
Targeted disruption of the protein kinase SGK3/CISK impairs postnatal hair follicle development.
A role for SGK3 in normal postnatal hair follicle development is established, possibly involving effects on beta-catenin/Lef-1-mediated gene transcription.
SGK1-dependent cardiac CTGF formation and fibrosis following DOCA treatment
The results suggest that SGK1 plays a decisive role in mineralocorticoid-induced CTGF expression and cardiac fibrosis.
Modulation of the L-arginine/nitric oxide signalling pathway in vascular endothelial cells.
In addition to acute stimulatory actions of D-glucose and insulin on L-arginine transport and NO synthesis, gestational diabetes, intrauterine growth retardation and pre-eclampsia induce phenotypic changes in the fetal vasculature, resulting in alterations in the L- arginine/NO signalling pathway and regulation of [Ca2+]i.
Experience-Dependent Formation and Recruitment of Large Vesicles from Reserve Pool
The Isoflavone Equol Mediates Rapid Vascular Relaxation
These findings provide the first evidence that nutritionally relevant plasma concentrations of equol (and other soy protein isoflavones) rapidly stimulate phosphorylation of ERK1/2 and phosphatidylinositol 3-kinase/Akt, leading to the activation of NOS and increased NO production at resting cytosolic Ca2+ levels.
Early activation of the p42/p44MAPK pathway mediates adenosine‐induced nitric oxide production in human endothelial cells: a novel calcium‐insensitive mechanism
The results provide the first evidence that adenosine stimulates the endothelial cell L‐arginine‐NO pathway in aCa2+‐insensitive manner involving p42/p44MAPK, with release of NO leading to a membrane hyperpolarization and activation of L‐ arginine transport.
Nitric oxide-induced cardioprotection in cultured rat ventricular myocytes.
No is implicated as a trigger in this model of early PC via activation of a constitutive NOS isoform and the mechanism of cardioprotection is cGMP dependent but independent of protein kinase C or ATP-sensitive K(+) channels, which differs from the proposed mechanism of NO-induced cardioprotsection in late PC.
SGK1 as a determinant of kidney function and salt intake in response to mineralocorticoid excess.
- V. Vallon, D. Huang, F. Lang
- Biology, MedicineAmerican journal of physiology. Regulatory…
- 1 August 2005
DOCA/1% NaCl treatment enhanced renal Na(+) excretion significantly more in sgk1(+/+) mice (from 3 +/- 1 to 134 +/- 32 micromol.g body wt(-1)), pointing to SGK1-dependent stimulation of salt intake, kidney growth, proteinuria, and renal K(+)excretion during mineralocorticoid excess.
DOCA-induced Phosphorylation of Glycogen Synthase Kinase 3ß
In conclusion, mineralocorticoid excess leads to phosphorylation and thus inactivation of GSK3ß, an effect not only due to upregulation of SGK1 but as well due to activation of additional kinases.