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Mouse TIGIT / VSTM3 Protein (Fc Tag)

ENSMUSG00000071552,Vstm3

Catalog Number P50939-M02H
Organism Species Mouse
Host Human Cells
Synonyms ENSMUSG00000071552,Vstm3
Molecular Weight The recombinant mouse TIGIT /Fc is a disulfide-linked homodimer. The reduced monomer comprises 357 amino acids and has a predicted molecular mass of 39.8 kDa. The apparent molecular mass of the protein is approximately 52 kDa in SDS-PAGE under reducing conditions due to glycosylation.
predicted N Gly 26
SDS-PAGE
Purity > 90 % as determined by SDS-PAGE
Protein Construction A DNA sequence encoding the mouse TIGIT (PP86176) (Met1-Gly141) was expressed, fused with the Fc region of human IgG1 at the C-terminus.
Bio-activity Immobilized mouse PVR-His (P50259-M08H) at 10 μg/ml (100 μl/well) can bind mouse TIGIT-Fc, The EC50 of mouse TIGIT-Fc is 0.25-0.55 μg/ml.
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.
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