R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
EI24 (D3F6Z) Rabbit mAb #42328
Filter:
- WB
- IP
Supporting Data
| REACTIVITY | H M R |
| SENSITIVITY | Endogenous |
| MW (kDa) | 30 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:200 |
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.
Protocol
Specificity / Sensitivity
EI24 (D3F6Z) Rabbit mAb recognizes endogenous levels of total EI24 protein.
Species Reactivity:
Human, Mouse, Rat
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ala31 of human EI24 protein.
Background
Etoposide-induced 2.4 mRNA (EI24)/p53-induced gene 8 (PIG8) was identified as a DNA damage response gene induced by etoposide in a p53 dependent manner with roles in growth suppression and apoptosis (1-3). As a pro-apoptotic gene, some evidence suggests that EI24 functions as a tumor suppressor gene in cases such as breast and cervical cancer (4-6). The mechanism of EI24 is still unclear, but studies have shown that it can localize to the endoplasmic reticulum and associate with Bcl-2 and could regulate apoptosis through regulation of Bcl-2 function (7). Liver-specific deletions of EI24 in mice show impaired autophagic flux, suggesting that it may also play a role in regulating basal autophagy (8). EI24 was shown to be involved in the autophagic degradation of many RING E3 ligases (9). In addition, decreased expression of EI24 in epithelial tumor cells induced epithelial-to-mesenchymal transition (EMT) (10). Together these studies suggest multiple mechanisms for EI24 to regulate tumor progression that includes regulation of apoptosis, autophagy, and EMT.
- Polyak, K. et al. (1997) Nature 389, 300-5.
- Lehar, S.M. et al. (1996) Oncogene 12, 1181-7.
- Gu, Z. et al. (2000) Mol Cell Biol 20, 233-41.
- Gentile, M. et al. (2001) Oncogene 20, 7753-60.
- Sinha, S. et al. (2011) Mol Oncol 5, 454-64.
- Mazumder Indra, D. et al. (2011) Int J Cancer 129, 1859-71.
- Zhao, X. et al. (2005) Cancer Res 65, 2125-9.
- Zhao, Y.G. et al. (2012) J Biol Chem 287, 42053-63.
- Devkota, S. et al. (2016) Autophagy 12, 2038-2053.
- Choi, J.M. et al. (2013) Oncotarget 4, 2383-96.
限制使用
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For Research Use Only. Not For Use In Diagnostic Procedures.
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