The gasdermin E (GSDME) protein, also known as DFNA5. is a member of the gasdermin family implicated in inflammatory cell death (pyroptosis) and apoptosis. GSDME contains an N-terminal pore-forming domain and a C-terminal repressor domain connected by a flexible linker. Upon cleavage by caspase-3 or granzyme B, the N-terminal fragment oligomerizes to form plasma membrane pores, triggering pyroptosis, while the C-terminal fragment is released. Unlike other gasdermins, GSDME is expressed in specific tissues, including the brain, testes, and intestines, but is epigenetically silenced in many cancers.
Research links GSDME to tumor suppression, inflammation regulation, and chemotherapy-induced cytotoxicity. Its inactivation via promoter methylation is associated with poor prognosis in cancers like gastric and colorectal. Conversely, GSDME activation amplifies antitumor immunity by releasing pro-inflammatory cytokines. Mutations in GSDME are also linked to autosomal dominant hearing loss (DFNA5 syndrome).
GSDME antibodies are critical tools for detecting full-length or cleaved forms in studies exploring pyroptosis mechanisms, cancer biology, and inflammatory diseases. They help assess GSDME expression levels in tissues or cell lines, monitor caspase-mediated cleavage during apoptosis/pyroptosis transitions, and evaluate its role in therapeutic responses. These antibodies support both basic research and drug development targeting gasdermin pathways.