Human IL-12B / NKSF2 / p40 Protein, His Tag

Proteins and Peptides

貨號 Cat. No.
NK2-H52H7
規格 Size
1mg
品牌 Brand
ACROBiosystems
Species
Human
Conjugate
Unconjugated
Expression System
HEK293
Tag
His Tag

Description




Source : 


Human IL-12B, His Tag (NK2-H52H7) is expressed from human 293 cells (HEK293). It contains AA Ile 23 - Ser 328 (Accession # P29460-1).


 

Molecule : IL-12B


 

Synonyms : IL12B,CLMF,CLMF2,NKSF,NKSF2,p40


 

Format : Powder


 

Category : Cytokines&Growth Factors


 

Accession : AAH67499.1


 

Storage : -20℃


 

Shipping condition : Powder,RT


 

Molecular Weight : 36.6 kDa


 

Characteristics :


This protein carries a polyhistidine tag at the C-terminus. The protein has a calculated MW of 36.6 kDa. The protein migrates as 44 kDa and 46 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.


 

Endotoxin Level : Less than 1.0 EU per μg by the LAL method.


 

Buffer : PBS, pH7.4


 

Description :


Interleukin-12 (IL12) is also known as natural killer cell stimulatory factor (NKSF), cytotoxic lymphocyte maturation factor (CLMF) , is a heterodimeric cytokine encoded by two separate genes, IL-12A (p35) and IL-12B (p40). IL12 is naturally produced by dendritic cells, macrophages and human B-lymphoblastoid cells (NC-37) in response to antigenic stimulation. IL-12 is involved in the differentiation of naive T cells into Th0 cells and plays an important role in the activities of natural killer cells and T lymphocytes.IL-12 also has anti-angiogenic activity, which means it can block the formation of new blood vessels.
Interleukin-12 subunit beta (IL12B) also known as NKSF2, CLMF2 and P40. Interleukin-12 subunit beta has been shown to interact with IL23. A large excess of monomeric IL12B is also secreted by the cells producing IL12, and exhibits no demonstrable biological activity. Overexpression of IL12B gene has been shown to be associated with the pathogenesis of multiple sclerosis. In addition, studies have revealed that the promoter polymorphism of this gene is implicated in the severity of atopic and non-atopic asthma in children.


 

References :


(1) Kaliński P, et al., 1997, J. Immunol. 159 (1): 28–35.
(2) Chehimi J, et al., 1993, Eur J Immunol., 23(8):1826-30.
(3) Thierfelder WE, et al., Nature., 382(6587):171-4.
(4) Oppmann B., et al., 2000, Immunity (UNITED STATES) 13 (5): 715–25.





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