Thermo Fisher Scientific ULBP1 Polyclonal Antibody

Applications

Tested Dilution

Publications

Western Blot (WB)

0.2-1 µg/mL

-

Product Specifications

Species Reactivity

Human

Host/Isotype

Rabbit / IgG

Class

Polyclonal

Type

Antibody

Immunogen

Synthetic peptide directed towards the N-terminal of human ULBP1 (aa 1-50). if (typeof window.$mangular === undefined || !window.$mangular) { window.$mangular = {}; } $mangular.antigenJson = \[{targetFamily:ULBP1,uniProtId:Q9BZM6-1,ncbiNodeId:9606,antigenRange:1-50,antigenLength:244,antigenImageFileName:PA5-43459_ULBP1_Q9BZM6-1_Rabbit.svg,antigenImageFileNamePDP:PA5-43459_ULBP1_Q9BZM6-1_Rabbit_PDP.jpeg,sortOrder:1}\]; $mangular.isB2BCMGT = false; $mangular.isEpitopesModalImageMultiSizeEnabled = true;

View immunogen .st0{fill:#FFFFFF;} .st1{fill:#1E8AE7;}

Conjugate

Unconjugated Unconjugated Unconjugated

Form

Liquid

Concentration

0.5 mg/mL

Purification

Affinity Chromatography

Storage buffer

PBS with 2% sucrose

Contains

0.09% sodium azide

Storage conditions

-20° C, Avoid Freeze/Thaw Cycles

Shipping conditions

Wet ice

RRID

AB_2605618

Product Specific Information

Peptide sequence: MAAAASPAFL LCLPLLHLLS GWSRAGWVDT HCLCYDFIIT PKSRPEPQWC

Sequence homology: Human: 100%

Target Information

ULBP1 is the ligand for the NKG2D receptor, together with at least ULBP2 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 ULBP1 to be retained in the ER and cis-Golgi apparatus so that it does not reach the cell surface.

For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.