R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
IL-13RA2/CD213a2 (E7U7B) Rabbit mAb #85677
Filter:
- WB
- IP
- IHC
- F
Supporting Data
REACTIVITY | H |
SENSITIVITY | Endogenous |
MW (kDa) | 55, 65 |
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) | 1:100 - 1:400 |
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 #68588.
For a carrier free (BSA and azide free) version of this product see product #68588.
Protocol
Specificity / Sensitivity
IL-13RA2/CD213a2 (E7U7B) Rabbit mAb recognizes endogenous levels of total IL-13RA2/CD213a2 protein. This antibody does not cross-react with IL-13RA1 protein.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of human IL-13RA2/CD213a2 protein.
Background
Cancer/testis antigens (CTAs) are a family of more than 100 proteins whose normal expression is largely restricted to immune privileged germ cells of the testis, ovary, and trophoblast cells of the placenta. Although most normal somatic tissues are void of CTA expression, due to epigenetic silencing of gene expression, their expression is upregulated in a wide variety of human solid and liquid tumors (1,2). As such, CTAs have garnered much attention as attractive targets for a variety of immunotherapy-based approaches to selectively attack tumors (3).
IL-13 receptor alpha-2 (IL-13RA2/CD213a2) is a type-I monomeric transmembrane glycoprotein and component of the IL-4/IL-13 receptor system. Research studies have shown that IL-13RA2 controls IL-13 signaling by serving as a high affinity decoy receptor for IL-13, but not IL-4, in a variety of cellular contexts (4,5). Some studies, however, have suggested that signaling through IL-13RA2 expressed on immunosuppressive myeloid cells facilitates tumor immune evasion through the production of TGF-β (6,7).
IL-13RA2 displays a highly restricted expression pattern in normal human tissues, which positions this receptor as a potentially novel therapeutic target for multiple types of solid tumors (8-10). Indeed, research studies have shown that IL-13RA2 is highly over expressed in glioblastomas (11), which has prompted investigation of different IL-13RA2-directed immunotherapies to treat this cancer (12-14).
IL-13 receptor alpha-2 (IL-13RA2/CD213a2) is a type-I monomeric transmembrane glycoprotein and component of the IL-4/IL-13 receptor system. Research studies have shown that IL-13RA2 controls IL-13 signaling by serving as a high affinity decoy receptor for IL-13, but not IL-4, in a variety of cellular contexts (4,5). Some studies, however, have suggested that signaling through IL-13RA2 expressed on immunosuppressive myeloid cells facilitates tumor immune evasion through the production of TGF-β (6,7).
IL-13RA2 displays a highly restricted expression pattern in normal human tissues, which positions this receptor as a potentially novel therapeutic target for multiple types of solid tumors (8-10). Indeed, research studies have shown that IL-13RA2 is highly over expressed in glioblastomas (11), which has prompted investigation of different IL-13RA2-directed immunotherapies to treat this cancer (12-14).
- Caballero, O.L. and Chen, Y.T. (2009) Cancer Sci 100, 2014-21.
- De Smet, C. et al. (1999) Mol Cell Biol 19, 7327-35.
- Gjerstorff, M.F. et al. (2015) Oncotarget 6, 15772-87.
- Yoshikawa, M. et al. (2003) Biochem Biophys Res Commun 312, 1248-55.
- Bernard, J. et al. (2001) Lab Invest 81, 1223-31.
- Fichtner-Feigl, S. et al. (2006) Nat Med 12, 99-106.
- Fichtner-Feigl, S. et al. (2008) Cancer Res 68, 3467-75.
- Debinski, W. and Gibo, D.M. (2000) Mol Med 6, 440-9.
- Taguchi, A. et al. (2014) Cancer Res 74, 4694-705.
- Beard, R.E. et al. (2013) Clin Cancer Res 19, 4941-50.
- Jarboe, J.S. et al. (2007) Cancer Res 67, 7983-6.
- Brown, C.E. et al. (2015) Clin Cancer Res 21, 4062-72.
- Brown, C.E. et al. (2012) Clin Cancer Res 18, 2199-209.
- Mintz, A. et al. (2008) Cancer Biother Radiopharm 23, 581-9.
限制使用
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