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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 25 Jan 2016.

Serum/glucocorticoid regulated kinase 1

This gene encodes a serine/threonine protein kinase that plays an important role in cellular stress response. This kinase activates certain potassium, sodium, and chloride channels, suggesting an involvement in the regulation of processes such as cell survival, neuronal excitability, and renal sodium excretion. High levels of expression of this gene may contribute to conditions such as hypertension and diabetic nephropathy. Several alternatively spliced transcript variants encoding different isoforms have been noted for this gene. [provided by RefSeq, Jan 2009] (from NCBI)
Top mentioned proteins: Akt, V1a, ENaC, Insulin, CAN
Papers using SGK1 antibodies
Biphasic effects of ANP infusion in conscious, euvolumic rats: roles of AQP2 and ENaC trafficking
Sands Jeff M., In PLoS ONE, 2005
... Antibodies used included anti-actin (Sigma), anti-SGK (serum and glucocorticoid-induced kinase) (Cell Signaling Technology, Beverly, MA) and ...
Papers on SGK1
(Pro)renin receptor contributes to regulation of renal epithelial sodium channel.
Siragy et al., Charlottesville, United States. In J Hypertens, 14 Feb 2016
We hypothesized that PRR plays a role in regulation of renal epithelial sodium channel (ENaC) through serum and glucocorticoid-inducible kinase isoform 1 (SGK-1)-neural precursor cell expressed, developmentally downregulated 4-2 (Nedd4-2) signaling pathway.
Up-Regulation of FGF23 Release by Aldosterone.
Lang et al., Tübingen, Germany. In Biochem Biophys Res Commun, 07 Feb 2016
The present study explored a putative aldosterone sensitivity of Fgf23 transcription and secretion and the putative involvement of the aldosterone sensitive serum & glucocorticoid inducibe kinase SGK1 and SGK1 sensitive transcription factor NFκB and store operated Ca(2+) entry (SOCE).
A novel rat model of gestational diabetes induced by intrauterine programming is associated with alterations in placental signaling and fetal overgrowth.
Jawerbaum et al., Buenos Aires, Argentina. In Mol Cell Endocrinol, 30 Jan 2016
In this intrauterine programmed GDM model, the placentas showed alterations in mTOR pathway: unchanged phosphorylation of 4EBP-1 and PKCα despite reduced total expression of 4EBP-1 and PKCα, and increased phosphorylation of SGK1.
Hormone stimulation of androgen receptor mediates dynamic changes in DNA methylation patterns at regulatory elements.
Smiraglia et al., Buffalo, United States. In Oncotarget, 15 Jan 2016
Here we demonstrate in normal prostate cells that hormone stimulated AR activity results in dynamic changes in the transcription rate and DNA methylation patterns at the AR target genes, TIPARP and SGK1.
Highly recurrent mutations of SGK1, DUSP2 and JUNB in nodular lymphocyte predominant Hodgkin lymphoma.
Hansmann et al., Frankfurt am Main, Germany. In Leukemia, 10 Jan 2016
The analysis of 62 selected genes in NLPHL by targeted ultra-deep sequencing revealed three novel highly recurrently mutated genes (each mutated in ~50% of cases), that is, DUSP2, SGK1 and JUNB.
Aldosterone Induces Renal Fibrosis and Inflammatory M1-Macrophage Subtype via Mineralocorticoid Receptor in Rats.
Moreno et al., Madrid, Spain. In Plos One, 31 Dec 2015
Relative kidney weight, collagen content, fibronectin, macrophage infiltrate, CTGF, Col I, MMP2, TNF-α, CD68, Arg2, and SGK-1 were increased (p<0.05) in aldosterone + salt-treated rats, being reduced by spironolactone (p<0.05).
The histone demethylase JMJD2A/KDM4A links ribosomal RNA transcription to nutrients and growth factors availability.
Vandromme et al., Toulouse, France. In Nat Commun, 31 Dec 2015
We show that PI3K, a major signalling transducer central for cell proliferation and survival, controls cellular localization of KDM4A and consequently its association with ribosomal DNA through the SGK1 downstream kinase.
Mir-27a promotes apoptosis of cochlear sensory epithelium in Cx26 knockout mice.
Li et al., Shanghai, China. In Front Biosci, 31 Dec 2015
The abnormal expression of mir-27a and sgk1 in Cx26 knockout mice was verified with real-time PCR.
miRNA and target gene expression in menstrual endometria and early pregnancy decidua.
Wang et al., Hohhot, China. In Eur J Obstet Gynecol Reprod Biol, 27 Dec 2015
METHODS: Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to measure the expression of the miR-146b-5p, miR-181b-5p, miR-424, miR-532, miR-199a-3p, miR-423, miR-22-3p, let-7i-5p, and miR-1 and the predicted target genes IGF2R, LEPR, SGK1, MMP2, MMP10, LIF, IL6, and STAT3 in menstrual endometria and early pregnancy decidua.
High-Salt Enhances the Inflammatory Response by Retina Pigment Epithelium Cells following Lipopolysaccharide Stimulation.
Yang et al., Chongqing, China. In Mediators Inflamm, 2014
Coculture of ARPE-19 cells with NaCl resulted in significant increases in the phosphorylation of p38 MAPK, Akt, and NF-κB and an upregulation of the transcription factors NFAT5 and SGK1.
The AGC kinase SGK1 regulates TH1 and TH2 differentiation downstream of the mTORC2 complex.
Powell et al., Baltimore, United States. In Nat Immunol, 2014
SGK1 is an AGC kinase that regulates the expression of membrane sodium channels in renal tubular cells in a manner dependent on the metabolic checkpoint kinase complex mTORC2.
Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells.
Hafler et al., New Haven, United States. In Nature, 2013
High-salt conditions activate the p38/MAPK pathway involving nuclear factor of activated T cells 5 (NFAT5; also called TONEBP) and serum/glucocorticoid-regulated kinase 1 (SGK1) during cytokine-induced TH17 polarization.
Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1.
Kuchroo et al., Boston, United States. In Nature, 2013
We identified serum glucocorticoid kinase 1 (SGK1), a serine/threonine kinase, as an essential node downstream of IL-23 signalling.
Serum-glucocorticoid regulated kinase 1 regulates alternatively activated macrophage polarization contributing to angiotensin II-induced inflammation and cardiac fibrosis.
Du et al., Beijing, China. In Arterioscler Thromb Vasc Biol, 2012
SGK1 may play an important role in macrophage recruitment and M2 macrophage activation by activating the STAT3 pathway, which leads to angiotensin II-induced cardiac fibrosis.
Hepatic mTORC2 activates glycolysis and lipogenesis through Akt, glucokinase, and SREBP1c.
Hall et al., Basel, Switzerland. In Cell Metab, 2012
Mammalian target of rapamycin complex 2 (mTORC2) phosphorylates and activates AGC kinase family members, including Akt, SGK1, and PKC, in response to insulin/IGF1.
Inducible kidney-specific Sgk1 knockout mice show a salt-losing phenotype.
Staub et al., Lausanne, Switzerland. In Am J Physiol Renal Physiol, 2012
The impaired ability of Sgk1 knockout mice to retain Na+ increased significantly with a low-salt diet despite higher plasma aldosterone levels. On a low-Na+ diet, the Sgk1 knockout mice were also hyperkaliuric and lost body weight.
Serum- and glucocorticoid-dependent kinase-1-induced cell migration is dependent on vinculin and regulated by the membrane androgen receptor.
Stournaras et al., Tübingen, Germany. In Febs J, 2012
Data show that SGK1 regulates cell migration via vinculin dephosphorylation, a mechanism that is controlled by membrane androgen receptor function.
Phosphorylation of nicastrin by SGK1 leads to its degradation through lysosomal and proteasomal pathways.
Park et al., Kwangju, South Korea. In Plos One, 2011
SGK1 is a gamma-secretase regulator presumably effective through phosphorylation and degradation of NCT.
SGK1 sensitivity of platelet migration.
Lang et al., Tübingen, Germany. In Cell Physiol Biochem, 2011
SGK1 participates in the signaling of platelet migration
Deregulation of the serum- and glucocorticoid-inducible kinase SGK1 in the endometrium causes reproductive failure.
Brosens et al., London, United Kingdom. In Nat Med, 2010
Data show that deregulated SGK1 activity in cycling endometrium interferes with embryo implantation, leading to infertility, or predisposes to pregnancy complications by rendering the feto-maternal interface vulnerable to oxidative damage.
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