ULBP2 antibody
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Description
Ligand for the KLRK1/NKG2D receptor, together with at least ULBP1 and ULBP3. ULBPs activate multiple signaling pathways in primary NK cells, resulting in the production of cytokines and chemokines. Binding of ULBPs ligands to KLRK1/NKG2D induces calcium mobilization and activation of the JAK2, STAT5, ERK and PI3K kinase/Akt signal transduction pathway. In CMV infected cells, interacts with soluble CMV glycoprotein UL16. The interaction with UL16 blocked the interaction with the KLRK1/NKG2D receptor, providing a mechanism by which CMV infected cells might escape the immune system. UL16 also causes ULBP2 to be retained in the ER and cis-Golgi apparatus so that it does not reach the cell surface.
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Product specifications
| Category | Primary Antibodies |
| Immunogen Target | UL16 binding protein 2 (ULBP2) |
| Host | Rabbit |
| Reactivity | Human |
| Recommended Dilution | WB: 1:500-1:5000 |
| Clonality | polyclonal |
| Conjugation | Unconjugated |
| Isotype | IgG |
| Observed MW | 30-35 kDa |
| Purity | ≥95% as determined by SDS-PAGE |
| Purification | Immunogen affinity purified |
| Size 1 | 100µg |
| Form | liquid |
| Tested Applications | ELISA, WB |
| Storage | PBS with 0.02% sodium azide and 50% glycerol pH 7.3, -20℃ for 12 months(Avoid repeated freeze / thaw cycles.) |
| UniProt ID | Q9BZM5 |
| Gene ID | 80328 |
| Alias | UL16-binding protein 2,ALCAN-alpha,NKG2D ligand 2 (N2DL-2, NKG2DL2),Retinoic acid early transcript 1H,ULBP2,N2DL2,RAET1H |
| Background | Antibody anti-ULBP2 |
| Status | RUO |
| Note | Mol. Weight 30-35 kDa |
Descripción
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ULBP2 antibody
Ligand for the KLRK1/NKG2D receptor, together with at least ULBP1 and ULBP3. ULBPs activate multiple signaling pathways in primary NK cells, resulting in the production of cytokines and chemokines. Binding of ULBPs ligands to KLRK1/NKG2D induces calcium mobilization and activation of the JAK2, STAT5, ERK and PI3K kinase/Akt signal transduction pathway. In CMV infected cells, interacts with soluble CMV glycoprotein UL16. The interaction with UL16 blocked the interaction with the KLRK1/NKG2D receptor, providing a mechanism by which CMV infected cells might escape the immune system. UL16 also causes ULBP2 to be retained in the ER and cis-Golgi apparatus so that it does not reach the cell surface.
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