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CD1-H82E3-25ug
$350.00
CD1-H82E3-200ug
$1,380.00
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  • Performance Data
  • Reviews & Citations
  • Important Statement
  • Resources

分子别名(Synonym)

CD161, C-type lectin domain family 5 member B, HNKR-P1a, NKR-P1A, Natural killer cell surface protein P1A

表达区间及表达系统(Source)

Biotinylated Human CD161, His,Avitag (CD1-H82E3) is expressed from human 293 cells (HEK293). It contains AA Gln 67 - Ser 225 (Accession # Q12918-1).

Predicted N-terminus: His

蛋白结构(Molecular Characterization)

This protein carries a polyhistidine tag at the N-terminus, followed by an Avi tag (Avitag™)

The protein has a calculated MW of 41.0 kDa.

标记(Labeling)

Biotinylation of this product is performed using Avitag™ technology. Briefly, the single lysine residue in the Avitag is enzymatically labeled with biotin.

蛋白标记度(Protein Ratio)

Passed as determined by the HABA assay / binding ELISA.

制剂(Formulation)

Please contact us for detailed information.

Contact us for customized product form or formulation.

重构方法(Reconstitution)

Please see Certificate of Analysis for specific instructions.

For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.

存储(Storage)

For long term storage, the product should be stored at lyophilized state at -20°C or lower.

Please avoid repeated freeze-thaw cycles.

This product is stable after storage at:

  1. -20°C to -70°C for 12 months in lyophilized state;
  2. -70°C for 3 months under sterile conditions after reconstitution.

Background

CD161 is also known as NKR-P1A, CLEC5B and KLRB1which plays an inhibitory role on natural killer (NK) cells cytotoxicity. Activation results in specific acid sphingomyelinase/SMPD1 stimulation with subsequent marked elevation of intracellular ceramide. Activation also leads to AKT1/PKB and RPS6KA1/RSK1 kinases stimulation as well as markedly enhanced T-cell proliferation induced by anti-CD3. Acts as a lectin that binds to the terminal carbohydrate Gal-alpha Gal epitope as well as to the N-acetyllactosamine epitope. Binds also to CLEC2D/LLT1 as a ligand and inhibits NK cell-mediated cytotoxicity as well as interferon-gamma secretion in target cells. New research shows that genetic inactivation of KLRB1 or antibody-mediated CD161 blockade enhances T cell-mediated killing of glioma cells in vitro and their anti-tumor function in vivo. KLRB1 and its associated transcriptional program are also expressed by substantial T cell populations in other human cancers. The reference provides an atlas of T cells in gliomas and highlights CD161 and other NK cell receptors as immunotherapy targets.