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S5188

Sigma-Aldrich

Anti-SGK antibody produced in rabbit

buffered aqueous solution, IgG fraction of antiserum

Synonym(s):

Anti-SGK

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About This Item

MDL number:
UNSPSC Code:
12352203
NACRES:
NA.44

biological source

rabbit

Quality Level

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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wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificates of Analysis (COA)

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Natalie S McGuier et al.
Addiction biology, 21(6), 1097-1112 (2016-10-26)
Alcohol use disorders (AUDs) are a major public health issue and produce enormous societal and economic burdens. Current Food and Drug Administration (FDA)-approved pharmacotherapies for treating AUDs suffer from deleterious side effects and are only effective in a subset of
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
Characterization of sgk, a novel member of the serine/threonine protein kinase gene family which is transcriptionally induced by glucocorticoids and serum.
Webster MK, et al.
Molecular and Cellular Biology, 13(4), 2031-2040 (1993)
Cloning and characterization of a putative human serine/threonine protein kinase transcriptionally modified during anisotonic and isotonic alterations of cell volume
Waldegger S, et al.
Proceedings of the National Academy of Sciences of the USA, 94(9), 4440-4445 (1997)
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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