R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
TIM-3 (D5D5R™) XP® Rabbit mAb #45208
Filter:
- WB
- IP
- IHC
- F
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 45-70 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- IHC-Immunohistochemistry
- F-Flow Cytometry
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:50 |
| IHC Leica Bond | 1:50 - 1:200 |
| Immunohistochemistry (Paraffin) | 1:200 - 1:800 |
| Flow Cytometry (Live) | 1:50 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.
For a carrier free (BSA and azide free) version of this product see product #81229.
For a carrier free (BSA and azide free) version of this product see product #81229.
Protocol
Specificity / Sensitivity
TIM-3 (D5D5R™) XP® Rabbit mAb recognizes endogenous levels of total TIM-3 protein.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with recombinant protein specific to the extracellular domain of human TIM-3 protein.
Background
T cell Ig- and mucin-domain-containing molecules (TIMs) are a family of transmembrane proteins expressed by various immune cells. TIM-3 is an inhibitory molecule that is induced following T cell activation (1-3 ). TIM-3 is expressed by exhausted T cells in the settings of chronic infection and cancer (4,5), and tumor-infiltrating T cells that coexpress PD-1 and TIM-3 exhibit the most severe exhausted phenotype (5). Tumor-infiltrating dendritic cells (DCs) also express TIM-3. TIM-3 expression on DCs was found to suppress innate immunity by reducing the immunogenicity of nucleic acids released by dying tumor cells (6). Research studies show that heterodimerization of TIM-3 with CEACAM-1 is critical for the inhibitory function of TIM-3, and co-blockade of TIM-3 and CEACAM-1 enhanced anti-tumor responses in a mouse model of colorectal cancer (7). In addition, blockade of TIM-3 in mouse models of autoimmunity enhanced the severity of disease (1). Finally, binding of Galectin-9 to TIM-3 expressed by Th1 cells induces T cell death (8).
- Monney, L. et al. (2002) Nature 415, 536-41.
- Sánchez-Fueyo, A. et al. (2003) Nat Immunol 4, 1093-101.
- Sabatos, C.A. et al. (2003) Nat Immunol 4, 1102-10.
- Jones, R.B. et al. (2008) J Exp Med 205, 2763-79.
- Sakuishi, K. et al. (2010) J Exp Med 207, 2187-94.
- Chiba, S. et al. (2012) Nat Immunol 13, 832-42.
- Huang, Y.H. et al. (2015) Nature 517, 386-90.
- Zhu, C. et al. (2005) Nat Immunol 6, 1245-52.
限制使用
除非 CST 的合法授书代表以书面形式书行明确同意，否书以下条款适用于 CST、其关书方或分书商提供的书品。 任何书充本条款或与本条款不同的客书条款和条件，除非书 CST 的合法授书代表以书面形式书独接受， 否书均被拒书，并且无效。
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For Research Use Only. Not For Use In Diagnostic Procedures.
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