Human TIGIT / VSTM3 Protein (His Tag)
VSIG9,VSTM3,WUCAM
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| Catalog Number | P10917-H08H |
|---|---|
| Organism Species | Human |
| Host | Human Cells |
| Synonyms | VSIG9,VSTM3,WUCAM |
| Molecular Weight | The secreted recombinant human TIGIT comprises 128 amino acids with a predicted molecular mass of 14.2 kDa. |
| predicted N | Met 22 |
| SDS-PAGE |  |
| Purity | > 85 % as determined by SDS-PAGE |
| Protein Construction | A DNA sequence encoding the extracellular domain of human TIGIT (NP_776160.2) (Met 1-Phe 138) with a C-terminal polyhistidine tag was expressed. |
| Bio-activity | 1. Measured by its ability to bind with human CD155-Fc (P10109-H02H) in a functional ELISA. 2. Measured by its ability to bind with mouse PVR-Fch (P50259-M03H) in a functional ELISA. |
| Research Area | Immunology |Adaptive Immunity |T Cell |Non-CD of T cell |
| Formulation | Lyophilized from sterile PBS, pH 7.4 1. Normally 5 % - 8 % trehalose, mannitol and 0.01% Tween80 are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA. |
| Background | TIGIT, also known as V-set and transmembrane domain-containing protein 3 (VSTM3) or V-set and immunoglobulin domain-containing protein 9 (VSIG9) is a new surface protein containing an immunoglobulin variable domain, a transmembrane domain and an immunoreceptor tyrosine-based inhibitory motif (ITIM). TIGIT is expressed on regulatory, memory, activated T cells and NK cells. It binds PVR with high affinity, and PVRL2 with lower affinity, but not PVRL3. Knockdown of TIGIT with siRNA in human memory T cells did not affect T cell responses, however, TIGIT inhibits NK cytotoxicity directly through its ITIM. TIGIT suppresses T cell activation by promoting the generation of mature immunoregulatory dendritic cells. The binding of PVR to TIGIT on human dendritic cells enhanced the production of IL-10 and diminished the production of IL-12p40. In addition, TIGIT counter inhibits the NK-mediated killing of tumor cells and protects normal cells from NK-mediated cytotoxicity thus providing an "alternative self" mechanism for MHC class I inhibition. |
| Reference |