CLEC12A/MICL/CLL-1 Protein, Human, Recombinant (His)

1.Loaded Monoclonal anti-human CLL-1 Antibody, human IgG1 on ProA Biosensor, can bind Recombinant Human CLL-1/CLEC12A Protein, His Tag (Cat#TMPY-02092) with an affinity constant of 9.15 nM as determined in BLI assay (Sartorius Octet RED384) (Routinely tested).
2.Immobilized anti-CLL-1, Human IgG1 at 2 μg/mL (100 μL/well) can bind Recombinant Human CLEC12A/CLL-1/DCAL2 Protein (His Tag) (Cat#TMPY-02092), the EC50 is 15-45 ng/mL(Routinely tested).
3.Immobilized Recombinant Human CLEC12A/CLL-1/DCAL2 Protein (His Tag) (Cat#TMPY-02092) at 1 μg/mL (100 μL/well) can bind KITE-222 derived anti-CLL-1 antibody, human IgG1, the EC50 is 1.25-3.75 ng/mL (QC tested).

CLEC12A/MICL/CLL-1 Protein, Human, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 41~45 kDa and the accession number is EAW96132.1.

Human

HEK293 Cells

≥ 95 % as determined by SDS-PAGE. ≥ 95 % as determined by SEC-HPLC.

CLEC12A is a member of the C-type lectin/C-type lectin-like domain (CTL/CTLD) superfamily. Members of this family share a common protein fold and have diverse functions, such as cell adhesion, cell-cell signaling, glycoprotein turnover, and roles in inflammation and immune response. CLEC12A is a negative regulator of granulocyte and monocyte function. Several alternatively spliced transcript variants of this gene have been described, but the full-length nature of some of these variants has not been determined. C-type lectins are the most diverse and prevalent lectin family in immunity. Using a novel CLEC12A -specific monoclonal antibody, experiments had shown that human CLEC12A was expressed primarily on myeloid cells, including granulocytes, monocytes, macrophages, and dendritic cells. Although CLEC12A was highly N-glycosylated in primary cells, the level of glycosylation was found to vary between cell types. CLEC12A surface expression was down-regulated during inflammatory/activation conditions in vitro, as well as during an in vivo model of acute inflammation. This suggests that CLEC12A may be involved in the control of myeloid cell activation during inflammation.