Cleaved Gasdermin E (Asp270) (E8G4U) Rabbit mAb #55879
- WB
- IF
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 30 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IF-Immunofluorescence
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunofluorescence (Immunocytochemistry) | 1:100 - 1:200 |
Storage
Protocol
Specificity / Sensitivity
Species Reactivity:
Source / Purification
Background
Gasdermin E (GSDME), also known as DFNA5, was originally identified as a genetic cause of nonsyndromic hearing loss (8). Like other gasdermin family members, Gasdermin E contains an amino-terminal pore forming domain that triggers pyroptosis. Cleavage of Gasdermin E at Asp270 is induced by apoptotic-associated Caspase-3, converting apoptotic signals to pyroptosis (9). In addition, cleavage of Gasdermin E can be induced by Granzyme B secreted by NK cells and contributes to tumor suppressive activity (10). Gasdermin E expression is suppressed in several types of cancer including gastric, colorectal, and breast carcinoma, and may be associated with decreased survival (11-13). In contrast, an increase in Gasdermin E, including the amino-terminal pore-forming fragment, is associated with conditions of excessive inflammation (14-16).
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- Liu, X. et al. (2016) Nature 535, 153-8.
- Sborgi, L. et al. (2016) EMBO J 35, 1766-78.
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- Rogers, C. et al. (2017) Nat Commun 8, 14128.
- Zhang, Z. et al. (2020) Nature 579, 415-420.
- Kim, M.S. et al. (2008) Oncogene 27, 3624-34.
- Kim, M.S. et al. (2008) Biochem Biophys Res Commun 370, 38-43.
- Yokomizo, K. et al. (2012) Anticancer Res 32, 1319-22.
- Tan, G. et al. (2021) Cell Rep 35, 109265.
- Li, Y. et al. (2021) Cell Death Differ 28, 2333-2350.
- Shi, H. et al. (2021) Circ Res 129, 383-396.
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