Immunohistochemistry-Paraffin: TIGIT Antibody (TIGIT/3017) [NBP2-79793] - Formalin-fixed, paraffin-embedded human Prostate Carcinoma stained with TIGIT Antibody (TIGIT/3017).
Flow Cytometry: TIGIT Antibody (TIGIT/3017) [NBP2-79793] - Flow Cytometric Analysis of PFA-fixed MOLT4 cells. TIGIT Antibody (TIGIT/3017) followed by goat anti-Mouse IgG-CF488 (Blue); Isotype Control (Red).
Protein Array: TIGIT Antibody (TIGIT/3017) [NBP2-79793] - Analysis of Protein Array containing more than 19,000 full-length human proteins using TIGIT Antibody (TIGIT/3017). Z- and S- Score: The Z-score represents the ...read more
ELISA: For coating, order antibody without BSA). Immunohistochemistry (Formalin-fixed): 1-2ug/ml for 30 minutes at RT. Staining of formalin-fixed tissues requires heating tissue sections in 10mM Tris with 1mM EDTA, pH 9.0, for 45 min at 95C followed by cooling at RT for 20 minutes. Optimal dilution for a specific application should be determined.
26 kDa. Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.
Read Publication using NBP2-79793 in the following applications:
200ug/ml of antibody purified from Bioreactor Concentrate by Protein A or G. Prepared in 10 mM PBS with 0.05% BSA & 0.05% azide. Also available WITHOUT BSA & azide at 1.0 mg/ml. (NBP2-79927)
Antibody with azide - store at 2 to 8C. Antibody without azide - store at -20 to -80C. Antibody is stable for 24 months. Non-hazardous.
Alternate Names for TIGIT Antibody (TIGIT/3017)
T cell immunoreceptor with Ig and ITIM domains
TIGIT (T cell Immunoreceptor with Ig and ITIM domains), also called Vstm3 (V-set and transmembrane domain-containing 3), Vsig9 (V-set and Ig domain-containing 9) and WUCAM (Washington University cell adhesion molecule), is a 30-34 kDa type I transmembrane protein that is a member of the CD28 family within the Ig superfamily of proteins (1-3). Human TIGIT cDNA encodes 244 amino acids (aa) including a 21 aa signal sequence, a 120 aa extracellular region with a V-type Ig-like domain and two potential N-glycosylation sites, a 21 aa transmembrane sequence, an 82 aa cytoplasmic domain with an immunoreceptor tyrosine-based inhibitory motif (ITIM) and has a theoretical molecular weight of ~27 kDa (3). TIGIT is expressed as a homodimer receptor on NK cells and subsets of activated, memory and regulatory T (Treg) cells, and on follicular helper T cells within secondary lymphoid organs (4). TIGIT has three known homodimer ligands that belong to the nectin family that are expressed on antigen presenting cells (APCs) or tumor cells (5). CD155 is the primary ligand for TIGIT, but it is also capable of binding CD112 and CD113 (5). The CD155/TIGIT signaling axis is an emerging immune checkpoint that inhibits function of T cells and NK cells. Upon TIGIT ligation, CD155 signaling leads to increased secretion of interleukin 10 (IL-10) and decreased secretion of proinflammatory cytokine IL-12 (5). TIGIT is a promising target for cancer immunotherapy and is the center of many pre-clinical studies investigating checkpoint blockade utilizing monoclonal antibodies either as a monotherapy or combination therapy (5).
TIGIT is commonly used as a marker for T cell exhaustion and its expression correlates with disease progression. Furthermore, in viral infections including HIV and SIV, TIGIT serves as a target for immune restoration (6). In cancer detection, TIGIT is upregulated and coexpressed with programmed cell death protein 1 (PD-1) on the majority of circulating tumor antigen (TA)-specific CD8+ T cells (7). In addition to this, TIGIT can inhibit immune cells at multiple steps within the cancer immunity cycle. These include inhibiting NK cell effector function, suppressing dendritic cell costimulatory abilities, suppressing CD8+ T cell effector function by Tregs or polio virus receptor (PVR)-stimulated myeloid cells, and by directly inhibiting CD8+ T cells and preventing elimination of cancer cells (7).
1. Joller, N., & Kuchroo, V. K. (2017). Tim-3, Lag-3, and TIGIT. Current topics in microbiology and immunology, 410, 127-156. https://doi.org/10.1007/82_2017_62
2. Xu, Z., Jin, B. A novel interface consisting of homologous immunoglobulin superfamily members with multiple functions. Cell Mol Immunol 7, 11-19 (2010). https://doi.org/10.1038/cmi.2009.108
4. Khan, M., Arooj, S., & Wang, H. (2020). NK Cell-Based Immune Checkpoint Inhibition. Frontiers in immunology, 11, 167. https://doi.org/10.3389/fimmu.2020.00167
5. Harjunpaa, H., & Guillerey, C. (2020). TIGIT as an emerging immune checkpoint. Clinical and experimental immunology, 200(2), 108-119. https://doi.org/10.1111/cei.13407
6. Blake, S. J., Dougall, W. C., Miles, J. J., Teng, M. W., & Smyth, M. J. (2016). Molecular Pathways: Targeting CD96 and TIGIT for Cancer Immunotherapy. Clinical cancer research: an official journal of the American Association for Cancer Research, 22(21), 5183-5188. https://doi.org/10.1158/1078-0432.CCR-16-0933
7. Manieri, N. A., Chiang, E. Y., & Grogan, J. L. (2017). TIGIT: A Key Inhibitor of the Cancer Immunity Cycle. Trends in immunology, 38(1), 20-28. https://doi.org/10.1016/j.it.2016.10.002
This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.
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