TIM-3 (D3M9R) XP® Rabbit mAb (BSA and Azide Free) #72911
- WB
- IHC
Supporting Data
| REACTIVITY | M |
| SENSITIVITY | Endogenous |
| MW (kDa) | 45-80 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IHC-Immunohistochemistry
Species Cross-Reactivity Key:
- M-Mouse
Product Information
Product Usage Information
This product is the carrier free version of product #83882. All data were generated using the same antibody clone in the standard formulation which contains BSA and glycerol.
This formulation is ideal for use with technologies requiring specialized or custom antibody labeling, including fluorophores, metals, lanthanides, and oligonucleotides. It is not recommended for ChIP, ChIP-seq, CUT&RUN, or CUT&Tag assays. If you require a carrier-free formulation for chromatin profiling, please contact us. Optimal dilutions/concentrations should be determined by the end user.
Formulation
Storage
Specificity / Sensitivity
TIM-3 (D3M9R) XP® Rabbit mAb (BSA and Azide Free) recognizes endogenous levels of total TIM-3 protein.
Species Reactivity:
Mouse
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro137 of mouse 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.
Limited Uses
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