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SRP4187

Sigma-Aldrich

IL-27 from mouse

recombinant, expressed in E. coli, ≥97% (SDS-PAGE), ≥97% (HPLC)

Synonyme(s) :

IL 27, Interleukin27

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About This Item

Code UNSPSC :
12352202
Nomenclature NACRES :
NA.32

Source biologique

mouse

Produit recombinant

expressed in E. coli

Pureté

≥97% (HPLC)
≥97% (SDS-PAGE)

Forme

lyophilized

Poids mol.

~23.7 kDa

Conditionnement

pkg of 10 μg

Impuretés

endotoxin, tested

Numéro d'accès NCBI

Numéro d'accès UniProt

Conditions d'expédition

wet ice

Température de stockage

−20°C

Informations sur le gène

mouse ... Il27(246779)

Description générale

Recombinant mouse IL-27/p28 Subunit, also known as Interleukin-30, is a member of the IL-12 family of Cytokines. When combined with EBI3 (Epstein-Barr virus induced gene 3), the heterodimer formed is IL-27. Mouse p28 is a proinflammatory cytokine inducing immunomodulatory effects. Current research is underway to delineate specific biological functions. Recombinant mouse p28 is a single-chain 207 amino acid peptide with a mass of approximately 23.7 kDa.

Forme physique

Lyophilized from 10 mM NaP, pH 7.5.

Reconstitution

Centrifuge the vial prior to opening. Avoid freeze-thaw cycles.
Reconstitute in water to a concentration of 0.1-1.0 μg/μL. The solution can then be diluted into other aqueous buffers.

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Denada Dibra et al.
PloS one, 6(4), e19072-e19072 (2011-05-12)
Crosstalk between tumor cells and the cognate microenvironment plays a crucial role in tumor initiation and progression. However, only a few genes are known to affect such a crosstalk. This study reveals that WSX1 plays such a role when highly
Jui-Hung Yen et al.
Journal of leukocyte biology, 98(5), 689-702 (2015-06-11)
MS is an autoimmune disease characterized by immune cell infiltration in the CNS, leading to cumulative disability. IFN-β, used clinically in RR-MS reduces lesion formation and rates of relapse. Although the molecular mechanisms are not entirely elucidated, myeloid cells appear
Juan Liao et al.
PloS one, 9(9), e108777-e108777 (2014-10-01)
The pathogenesis of complex diseases, such as type 1 diabetes (T1D), derives from interactions between host genetics and environmental factors. Previous studies have suggested that viral infection plays a significant role in initiation of T1D in genetically predisposed individuals. T1D

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