The GIGD7 monoclonal antibody reacts with mouse T cell immunoreceptor with Ig and ITIM domains (TIGIT, VSTM3, WUCAM), a 26 kDa protein that is a member of the poliovirus receptor (PVR) family. In mice, the expression of TIGIT has been reported in follicular T helper cells, while in humans, the expression of TIGIT has been reported on NK cells, regulatory T cells, follicular T helper cells, memory CD4+ T cells, and CD8+ T cells. TIGIT is not expressed on B cells or naive CD4+ T cells. TIGIT is upregulated on CD4+ T cells following activation. TIGIT can interact with certain members of the PVR and PVR-like families, including CD155, and also mediates the interaction of NK cells and T cells with antigen presenting cells, fibroblasts and endothelial cells that express PVR and PVR-like proteins. This GIGD7 antibody has been tested by flow cytometric analysis of mouse splenocytes. This can be used at less than or equal to 1 µg per test. A test is defined as the amount (µg) of antibody that will stain a cell sample in a final volume of 100 µL. Cell number should be determined empirically but can range from 10^5 to 10^8 cells/test. It is recommended that the antibody be carefully titrated for optimal performance in the assay of interest. Filtration: 0.2 µm post-manufacturing filtered.Binds with high affinity to the poliovirus receptor (PVR) which causes increased secretion of IL10 and decreased secretion of IL12B and suppresses T cell activation by promoting the generation of mature immunoregulatory dendritic cells.
|4° C, store in dark, DO NOT FREEZE!|
|PBS with 0.1% gelatin and 0.09% sodium azide|
For Research Use Only
The Fisher Scientific Encompass Program offers items which are not part of our distribution portfolio. These products typically do not have pictures or detailed descriptions. However, we are committed to improving your shopping experience. Please use the form below to provide feedback related to the content on this product.
Your feedback has been submitted. Fisher Scientific is always working to improve our content for you. We appreciate your feedback.Ok