LIGHT/TNFSF14 (E1Y2S) Rabbit mAb #53373
- WB
- IP
Supporting Data
| REACTIVITY | H M |
| SENSITIVITY | Endogenous |
| MW (kDa) | 28 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:100 |
Storage
Protocol
Specificity / Sensitivity
LIGHT/TNFSF14 (E1Y2S) Rabbit mAb recognizes endogenous levels of total LIGHT/TNFSF14 protein.
Species Reactivity:
Human, Mouse
Source / Purification
Monoclonal antibody is produced by immunizing animals with recombinant protein specific to the extracellular domain of human LIGHT/TNFSF14 protein.
Background
Tumor necrosis factor superfamily member 14 (TNFSF14), also known as CD258 and LIGHT, is a cell surface type II transmembrane protein that is expressed as a homotrimer (1). The extracellular region can be cleaved to generate a soluble cytokine (2). TNFSF14 is a ligand for the receptors herpesvirus entry mediator (HVEM) and lymphotoxin receptor (LTR) (1). TNFSF14 is expressed on activated NK cells, activated T cells, activated monocytes, immature DCs, and mast cells (1,3,4). TNFSF14 interactions with HVEM induce potent co-stimulatory signaling in T cells and trigger NK cells to produce IFN-γ via NF-κB RelA/p50 pathway signaling (5,6). TNFRSF14 produced by tumor-sensing NK cells aids in DC maturation, enabling de novo anti-tumor adaptive immune responses (7). TNFSF14-HVEM interactions are considered the main drivers of anti-tumor immune responses, whereas TNFSF14-LTR interactions have been characterized as maintaining the infrastructure that supports the anti-tumor response via lymphoid development and cancer cells’ susceptibility to the immune response (8,9). TNFSF14 induces the normalization of tumor vasculature, sensitizes tumor cells to IFN-γ-mediated apoptosis, and results in a more inflamed tumor microenvironment (TME) (6,8,10,11). Due to its effects on the TME and anti-tumor immune cell responses, TNFSF14 is being investigated as a target for immunotherapeutic intervention in cancer (9). TNFSF14 has also been implicated in the development and pathogenesis of inflammatory bowel disease and airway remodeling leading to asthma (12,13).
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- Granger, S.W. et al. (2001) J Immunol 167, 5122-8.
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- Sibilano, R. et al. (2016) Nat Commun 7, 13696.
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- Fan, Z. et al. (2006) Blood 107, 1342-51.
- Holmes, T.D. et al. (2014) Proc Natl Acad Sci U S A 111, E5688-96.
- Lu, T.T. and Browning, J.L. (2014) Front Immunol 5, 47.
- Skeate, J.G. et al. (2020) Front Immunol 11, 922.
- Zhang, M. et al. (2003) Cancer Lett 195, 201-10.
- Kanodia, S. et al. (2010) Cancer Res 70, 3955-64.
- Cohavy, O. et al. (2004) J Immunol 173, 251-8.
- Doherty, T.A. et al. (2011) Nat Med 17, 596-603.
Limited Uses
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