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ULBP2 Antibody (Center) Blocking Peptide

Synthetic peptide

     
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Product Information
Primary Accession Q9BZM5
Clone Names 100712070
Peptide ID 100712070
Additional Information
Gene ID 80328
Other Names NKG2D ligand 2, N2DL-2, NKG2DL2, ALCAN-alpha, Retinoic acid early transcript 1H, UL16-binding protein 2, ULBP2, N2DL2, RAET1H
Format Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.
StorageMaintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.
PrecautionsThis product is for research use only. Not for use in diagnostic or therapeutic procedures.
Protein Information
Name ULBP2
Synonyms N2DL2, RAET1H
Function 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.
Cellular Location Cell membrane; Lipid-anchor, GPI-anchor. Secreted
Tissue Location Expressed in various types of cancer cell lines and in the fetus, but not in normal tissues
Research Areas
Citations (0)

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Background

Ligand for the 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 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 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.

References

McGilvray, R.W., et al. Int. J. Cancer 127(6):1412-1420(2010)Nuckel, H., et al. Leukemia 24(6):1152-1159(2010)Antoun, A., et al. Hum. Immunol. 71(6):610-620(2010)Davila, S., et al. Genes Immun. 11(3):232-238(2010)Ward, J., et al. PLoS Pathog. 5 (10), E1000613 (2009) :

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$ 80.00
Cat# BP17088c
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