Galectin-9 (D9R4A) XP® Rabbit mAb #54330
- WB
- IHC
- F
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 9-40 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IHC-Immunohistochemistry
- F-Flow Cytometry
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| IHC Leica Bond | 1:800 |
| Immunohistochemistry (Paraffin) | 1:800 |
| Flow Cytometry (Fixed/Permeabilized) | 1:1600 |
Storage
For a carrier free (BSA and azide free) version of this product see product #71325.
Protocol
Specificity / Sensitivity
Species Reactivity:
Source / Purification
Monoclonal antibody is produced by immunizing animals with recombinant human galectin-9 protein.
Background
Galectins are a family of β-galactose binding proteins that are characterized by an affinity for poly-N-acetyllactosamine-enriched glycoconjugates and a carbohydrate-binding site (1,2). Members of the galectin family have been implicated in a variety of biological functions, including cell adhesion (3), growth regulation (4), cytokine production (5), T-cell apoptosis (6), and immune responses (7).
Galectin-9 is induced by proinflammatory stimuli, including IFN-γ, TNF-α, and TLR ligands, and regulates various immune responses through interaction with its ligand TIM-3 (8, 9). Binding of galectin-9 to TIM-3 expressed by Th1 CD4 T cells resulted in T cell death (9). On the other hand, galectin-9 treatment of tumor-bearing mice increased the number of IFN-γ-producing TIM-3+ CD8 T cells and TIM-3+ dendritic cells (10). Transgenic overexpression of either TIM-3 or galectin-9 in mice led to an increase in cells with a myeloid-derived suppressor cell phenotype and inhibition of immune responses (11). CD44 is also proposed to be a receptor for galectin-9, and interaction of galectin-9 with CD44 expressed by induced regulatory T (iTreg) cells enhanced the stability of function of iTreg cells. In addition, galectin-9 was recently demonstrated to bind Dectin-1 expressed by pancreatic ductal adenocarcinoma-infiltrating macrophages, resulting in tolerogenic macrophage reprogramming and suppression of anti-tumor immunity. Increased galectin-9 expression has been observed in several cancer types, including lung, liver, breast, and kidney (12). Alternative splicing of the galectin-9 transcript leads to several isoforms (13).
- Barondes, S.H. et al. (1994) Cell 76, 597-8.
- Barondes, S.H. et al. (1994) J Biol Chem 269, 20807-10.
- Offner, H. et al. (1990) J Neuroimmunol 28, 177-84.
- Wells, V. and Mallucci, L. (1991) Cell 64, 91-7.
- Filer, A. et al. (2009) Arthritis Rheum 60, 1604-14.
- Perillo, N.L. et al. (1995) Nature 378, 736-9.
- Cooper, D.N. et al. (1991) J Cell Biol 115, 1437-48.
- Gieseke, F. et al. (2013) Eur J Immunol 43, 2741-9.
- Zhu, C. et al. (2005) Nat Immunol 6, 1245-52.
- Nagahara, K. et al. (2008) J Immunol 181, 7660-9.
- Dardalhon, V. et al. (2010) J Immunol 185, 1383-92.
- Heusschen, R. et al. (2014) Biochim Biophys Acta 1842, 284-92.
- Heusschen, R. et al. (2013) Biol Reprod 88, 22.
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