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SRP5143

Sigma-Aldrich

STAT6, GST tagged human

recombinant, expressed in baculovirus infected Sf9 cells, ≥70% (SDS-PAGE), buffered aqueous glycerol solution

Sinónimos:

D12S1644, IL-4-STAT, STAT6B, STAT6C

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About This Item

Número de CAS:
168115-60-4
UNSPSC Code:
12352200
NACRES:
NA.32

biological source

human

recombinant

expressed in baculovirus infected Sf9 cells

assay

≥70% (SDS-PAGE)

form

buffered aqueous glycerol solution

mol wt

~138 kDa

NCBI accession no.

BC075852

application(s)

cell analysis

shipped in

dry ice

storage temp.

−70°C

Gene Information

human ... STAT6(6778)

General description

The STAT6 protein is a member of the STAT family of transcription factors that are activated by cytokines and phosphorylated by the receptor associated kinases. STATs form homo- or hetero-dimers that translocate to the cell nucleus where they act as transcription activators. STAT6 plays a central role in exerting IL4 mediated biological responses. STAT6 induces the expression of BCL2L1/BCL-XL, which is responsible for the anti-apoptotic activity of IL4. STAT6 mRNA has been detected in various tissues including peripheral blood lymphocytes, colon, intestine, ovary, prostate, thymus, spleen, kidney, liver, lung and placenta. STAT6 is critically involved in Th2 immune response.

Physical form

Supplied in 50mM Tris-HCl, pH 7.5, 150mM NaCl, 10mM glutathione, 0.1mM EDTA, 0.25mM DTT, 0.1mM PMSF, 25% glycerol.

Preparation Note

after opening, aliquot into smaller quantities and store at -70 °C. Avoid repeating handling and multiple freeze/thaw cycles

Storage Class

10 - Combustible liquids

wgk_germany

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable

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S Weidinger et al.
Journal of medical genetics, 41(9), 658-663 (2004-09-03)
Several studies have shown linkage of chromosome 12q 13-24 with atopy related phenotypes. Among candidate genes in this region is STAT6 (signal transducer and activator of transcription), which is essential for Th2 cell differentiation, recruitment, and effector function. We evaluated
Wei Wang et al.
Journal of immunology (Baltimore, Md. : 1950), 172(1), 97-103 (2003-12-23)
Autoantibodies to the muscle acetylcholine receptor (AChR) cause the symptoms of human and experimental myasthenia gravis (EMG). AChR-specific CD4+ T cells permit development of these diseases, but the role(s) of the Th1 and Th2 subsets is unclear. The STAT4 and

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