CST, 55879T, Cleaved Gasdermin E (Asp270) (E8G4U) Rabbit Monoclonal Antibody

Monoclonal Antibody for studying DFNA5 (Asp270) cleaved. Validated for Western Blotting,Immunofluorescence (Immunocytochemistry). Available in 2 sizes. Highly specific and rigorously validated in-house, Cleaved Gasdermin E (Asp270) (E8G4U) Rabbit Monoclonal Antibody (CST #55879) is ready to ship. Product Usage Information Western Blotting: 1:1000 Immunofluorescence (Immunocytochemistry): 1:100 - 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. For a carrier free (BSA and azide free) version of this product see product # 89929 . Protocol Available protocols: Western Blotting, Immunofluorescence (Immunocytochemistry) Specificity / Sensitivity Cleaved Gasdermin E (Asp270) (E8G4U) Rabbit Monoclonal Antibody recognizes endogenous levels of Gasdermin E protein only when cleaved at Asp270. A band of unknown origin is detected at around 25 kDa. Species Reactivity: Human Source / Purification Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Asp270 of human Gasdermin E protein. 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). Alternate Names deafness, autosomal dominant 5; DFNA5; DFNA5, deafness associated tumor suppressor; gasdermin E; Gasdermin-E; Gasdermin-E, C-terminal; Gasdermin-E, N-terminal; GSDME; GSDME-CT; GSDME-NT; ICERE-1; ICERE1; Inversely correlated with estrogen receptor expression 1; Non-syndromic hearing impairment protein 5; nonsyndromic hearing impairment protein Specification REACTIVITY: H SENSITIVITY: Endogenous MW (kDa): 30 Source/Isotype: Rabbit IgG