Mouse TIGIT / VSTM3 Protein

Sino Biological Inc. liefert Mouse TIGIT / VSTM3 Protein mit höherer Qualität und günstiger Kosten im Vergleich mit anderen globalen Lieferanten.

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Produkt-Information von TIGIT/ VSTM3 Protein

QC Testing von TIGIT/ VSTM3 Protein

Purity	> 90% as determined by SDS-PAGE	SDS-PAGE: TIGIT protein
Endotoxin	< 1.0 EU per μg of the protein as determined by the LAL method
Stability	Samples are stable for up to twelve months from date of receipt at -70℃
Predicted N terminal	Gly 26
Molecular Mass	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.
Formulation	Lyophilized from sterile PBS, pH7.4. Normally 5 % - 8 % trehalose and mannitol are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA.

Usage Guide von TIGIT/ VSTM3 Protein

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Beschreibung von TIGIT/ VSTM3 Protein

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.

References

1. Yu X. et al., 2009, Nat Immunol. 10 (1): 48-57.
2. Stanietsky N. et al., 2009, Proc Natl Acad Sci. 106 (42):17858-63.