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For reconstitution, add sterile, distilled water to achieve a final antibody concentration of 1 mg/mL. Gently shake to solubilize the protein completely. Do not vortex. Reconstituted products should be stored at -80 °.
Cell-mediated immune responses are initiated by T lymphocytes that are themselves stimulated by cognate peptides bound to MHC molecules on antig en-presenting cells (APC). T-cell activation is generally self-limited as activated T cells express receptors such as PD-1 (also known as PDCD-1) that mediate inhibitory signals from the APC. PD-1 can bind two different but related ligands, PDL-1 and PDL-2. Upon binding to either of these ligands, signals generated by PD-1 inhibit the activation of the immune response in the absence of "danger signals" such as LPS or other molecules associated with bacteria or other pathogens. Evidence for this is seen in PD1-null mice who exhibit hyperactivated immune systems and autoimmune diseases. Despite its predicted molecular weight, PD-1 often migrates at higher molecular weight in SDS-PAGE.
TIGIT is a 26 kDa protein that belongs to the poliovirus receptor (PVR) family. It is expressed on NK cells, regulatory T cells, follicular T helper cells, memory CD4+ T cells, and CD8+ T cells, but not on B cells or naive CD4+ T cells. However, TIGIT can be upregulated on naive CD4+ T cells upon activation. TIGIT interacts with members of the PVR and PVR-like families, including CD155. This interaction mediates the engagement of NK and T cells with antigen-presenting cells, fibroblasts, and endothelial cells expressing PVR and PVR-like proteins. Binding of TIGIT to PVR leads to increased secretion of IL-10 and decreased secretion of IL-12B, promoting the generation of mature immunoregulatory dendritic cells and suppressing T cell activation. Through these interactions, TIGIT plays a significant role in modulating immune responses and maintaining immune homeostasis.
仅用于科研。不用于诊断过程。未经明确授权不得转售。