Human NKG2A / CD159a Protein, His Tag

Proteins and Peptides

貨號 Cat. No.
NKA-H5244
規格 Size
1mg
品牌 Brand
ACROBiosystems
Species
Human
Conjugate
Unconjugated
Expression System
HEK293
Tag
His Tag

Description




Source : 


Human NKG2A, His Tag (NKA-H5244) is expressed from human 293 cells (HEK293). It contains AA Pro 94 - Leu 233 (Accession # P26715-1).


 

Molecule : NKG2A


 

Synonyms : NKG2A,CD159a,KLRC1,NK cell receptor A


 

Format : Powder


 

Category : Other Recombinant Proteins


 

Accession : NP_002250.1


 

Storage : -20℃


 

Shipping condition : Powder,RT


 

Molecular Weight : 17.9 kDa


 

Characteristics :


This protein carries a polyhistidine tag at the N-terminus. The protein has a calculated MW of 17.9 kDa. The protein migrates as 30-40 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 :


NKG2A/CD159a is a transmembrane protein belonging to the CD94/NKG2 family of C-type lectin-like receptors that inhibits innate immune system activation, also known as KLRC1, CD159a, NK cell receptor A and NKG2-A/NKG2-B type II integral membrane protein. NKG2A marks a unique immune effector subset preferentially co-expressing the tissue-resident CD103 molecule, but not immune checkpoint inhibitors. NKG2A blockade therapy operated through CD8 T cells, but not NK cells. The increase in NKG2A expression might be induced by IL-10, which was present at a high level in the plasma of HCC patients. Blocking IL-10 could specifically inhibit NKG2A expression in NK cells. These findings indicate that NKG2A expression is influenced by factors from cancer nests and contributes to NK cell exhaustion, suggesting that NKG2A blockade has the potential to restore immunity against liver tumors by reversing NK cell exhaustion.


 

References :


(1) Sun C, et al. Oncoimmunology. 2016. 6(1):e1264562.
(2) McWilliams EM, et al. Oncoimmunology. 2016. 5(10).
(3) van Montfoort N, et al. Cell. 2018. 175(7):1744-1755.





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