Gasdermin E Antibody #40618
- WB
Supporting Data
| REACTIVITY | M R |
| SENSITIVITY | Endogenous |
| MW (kDa) | 57, 33 |
| SOURCE | Rabbit |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- M-Mouse
- R-Rat
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
Storage
Protocol
Specificity / Sensitivity
Gasdermin E Antibody recognizes endogenous levels of total Gasdermin E protein. This antibody can also detect the amino-terminal cleavage fragment associated with pyroptosis.
Species Reactivity:
Mouse, Rat
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding His112 of mouse Gasdermin E protein. Antibodies are purified by peptide affinity chromatography.
Background
The gasdermin family, which includes GSDMA, GSDMB, GSDMC, GSDMD, and GSDME, has been shown to play a role in inflammation and cell death. Gasdermin D has been reported to have a critical role as a downstream effector of pyroptosis (1,2). Pyroptosis is a lytic type of cell death triggered by inflammasomes, multiprotein complexes assembled in response to pathogen-associated molecular patterns (PAMPs) or danger-associated molecular patterns (DAMPs) that result in the activation of caspase-1 and subsequent cleavage of pro-inflammatory cytokines IL-1β and IL-18 (3). Gasdermin D was identified by two independent groups as a substrate of inflammatory caspases, caspase-1 and caspase-11/4/5, producing two fragments: GSDMD-N and GSDMD-C. Cleavage results in release of an intramolecular inhibitory interaction between the N- and C-terminal domains, allowing the N-terminal fragment GSDMD-N to initiate pyroptosis through the formation of pores on the plasma membrane (4-7).
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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- 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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