S5188
Anti-SGK antibody produced in rabbit
buffered aqueous solution, IgG fraction of antiserum
Synonym(s):
Anti-SGK
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About This Item
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biological source
rabbit
conjugate
unconjugated
antibody form
IgG fraction of antiserum
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
mol wt
antigen 50 kDa
species reactivity
human
technique(s)
indirect immunofluorescence: 1:2,000 using 3% paraformaldehyde-fixed, 0.5% Triton X-100 treated human epidermal carcinoma A431cell line
microarray: suitable
western blot: 1:2,000 using whole cell extract of the human epidermal carcinoma A431 cell line
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... SGK1(6446)
General description
Anti-SGK is developed in rabbit using a synthetic peptide corresponding to the C-terminus of human SGK conjugated to KLH (keyhole limpet hemocyanin). SGK is localized to the perinuclear or cytoplasmic compartment as a hypophosphorylated protein.
SGK (serum and glucocorticoid-regulated protein kinase) is a 50 kDa member of Ser/Thr kinase family. Sequence of sgk is well conserved across species, the human and rat SGK amino acid sequences are 96-98% identical.
Application
Anti-SGK antibody produced in rabbit has been used in :
- immunoprecipitation
- western blotting
- immunofluorescence
Biochem/physiol Actions
SGK (serum and glucocorticoid-regulated protein kinase) plays an important role in signal transduction activated by mineral corticoids. It is also regulated at the transcription level by stimuli including glucocorticoid, serum, follicle stimulating hormone as well as changes in cell volume. SGK levels are strongly affected by osmotic changes. SGK is strongly and rapidly stimulated in kidney cells in response to aldosterone and stimulates epithelial Na+ channels, suggesting a central role of SGK in the regulation of sodium transport and homeostasis. SGK transcription is markedly increased in diabetic nephropathy, in response to excessive extracellular glucose concentrations. The localization of SGK in the cell is regulated by hormones or serum. For cell cycle progression, the shuttling of SGK between nucleus and cytoplasm is required.
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Storage Class Code
10 - Combustible liquids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
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cell cycle and hormonal control of nuclear-cytoplasmic localization of the serum-and glucocorticoid-inducible protein kinase, sgk, in mammary tumor cells a novel convergence point of anti-proliferative and proliferative cell signaling pathways
Buse P, et al.
The Journal of biological chemistry, 274(11), 7253-7263 (1999)
Joseph R Shaw et al.
Aquatic toxicology (Amsterdam, Netherlands), 98(2), 157-164 (2010-03-09)
Seawater acclimation in killifish, Fundulus heteroclitus, is mediated in part by a rapid (1h) translocation of CFTR Cl(-) channels from an intracellular pool to the plasma membrane in gill and increased CFTR-mediated Cl(-) secretion. This effect is mediated by serum
Differential ubiquitylation of the mineralocorticoid receptor is regulated by phosphorylation
Faresse N, et al.
Faseb Journal, 26(10), 4373-4382 (2012)
D Pearce et al.
Kidney international, 57(4), 1283-1289 (2000-04-12)
Mineralocorticoids stimulate electrogenic Na+ transport in tight epithelia by altering the transcription of specific genes. Although the earliest mineralocorticoid effect is to increase the activity of the epithelial sodium channel (ENaC), ENaC mRNA and protein levels do not change. Instead
A Náray-Fejes-Tóth et al.
Kidney international, 57(4), 1290-1294 (2000-04-12)
The sgk, an aldosterone-induced gene in mineralocorticoid target cells, regulates the epithelial sodium channel. Aldosterone increases sodium reabsorption in tight epithelia. The early phase of this stimulatory effect is thought to involve activation of apical sodium channels. To identify immediate-early
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