MAGE-A4 (E7O1U) XP® Rabbit mAb (BSA and Azide Free) #31135
- WB
- IHC
- IF
- F
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 40-50 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IHC-Immunohistochemistry
- IF-Immunofluorescence
- F-Flow Cytometry
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
This product is the carrier-free version of product #82491. 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.
BSA and Azide Free antibodies are quality control tested by size exclusion chromatography (SEC) to determine antibody integrity.Formulation
For standard formulation of this product see product #82491.
Storage
Specificity / Sensitivity
Species Reactivity:
Source / Purification
Background
Melanoma-associated antigen-A4 (MAGE-A4) is a cancer testis antigen that belongs to the type I MAGE family of proteins. MAGE-A4 is often overexpressed and mutated in several types of cancer (4-8). Research shows MAGE-A4 promotes aberrant cell growth by preventing p53-dependent cell cycle arrest and apoptosis in normal oral keratinocyte (9). However, MAGE-A4 was also found to interact with the liver oncoprotein gankyrin, suppressing its tumorigenic activity (10). The diverse roles of MAGE-A4 in tumor development may be dependent upon sub-cellular localization (nuclear or cytosolic) and p53 status (6). Due to its upregulated expression in human tumors and high degree of immunogenicity, MAGE-A4 has received significant attention as an immunotherapy target through the use of vaccines and adoptive cell therapy (11-14).
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- De Smet, C. et al. (1999) Mol Cell Biol 19, 7327-35.
- Gjerstorff, M.F. et al. (2015) Oncotarget 6, 15772-87.
- Iura, K. et al. (2017) Virchows Arch 471, 383-392.
- Sani, S.A. et al. (2018) J Cancer Res Ther 14, 1059-1064.
- Fujiwara-Kuroda, A. et al. (2018) Int J Oncol 53, 713-724.
- Iura, K. et al. (2017) Hum Pathol 61, 130-139.
- Caballero, O.L. et al. (2010) PLoS One 5, e12773. doi: 10.1371/journal.pone.0012773.
- Bhan, S. et al. (2012) Oncol Rep 28, 1498-502.
- Nagao, T. et al. (2003) J Biol Chem 278, 10668-74.
- Saito, T. et al. (2014) Vaccine 32, 5901-7.
- Kageyama, S. et al. (2015) Clin Cancer Res 21, 2268-77.
- Ueda, S. et al. (2018) Oncotarget 9, 35997-36011.
- Cruz, C.R. et al. (2011) Clin Cancer Res 17, 7058-66.
Limited Uses
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