Anti-TIGIT/VSTM3 antibody

Anti-TIGIT/VSTM3 antibody

• DataSheet
• Material Safety Data Sheets (MSDS)

Rabbit polyclonal to TIGIT/VSTM3

ELISA, IHC-P

Mouse TIGIT / VSTM3

WUCAM antibody; DKFZp667A205 antibody; ENSMUSG00000071552 antibody; FLJ39873 antibody; VSIG9 antibody; VSTM3 antibody; WUCAM antibody; Vstm3 antibody; ENSMUSG00000071552 antibody; TIGIT antibody; Tigit antibody; VSIG9 antibody; VSTM3 antibody; Vstm3 antibody

Rabbit IgG

Produced in rabbits immunized with purified, recombinant Mouse TIGIT / VSTM3 (rM TIGIT / VSTM3; NP_001139797.1; Met1-Gly141). TIGIT / VSTM3 specific IgG was purified by Mouse TIGIT / VSTM3 affinity chromatography.

Polyclonal

0.2 μm filtered solution in PBS with 5% trehalose

This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -80℃. Preservative-Free.
Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles.

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.