Precursor of a pore-forming protein involved in the transition from catagen to telogen at the end of hair follicle morphogenesis (PubMed:15475261, PubMed:26375003, PubMed:27281216). This form constitutes the precursor of the pore: upon cleavage, the released N-terminal moiety (Gasdermin-A3, N-terminal) binds to membranes and forms pores, triggering cell death (PubMed:26375003, PubMed:27281216). Pore-forming protein that causes membrane permeabilization and pyroptosis (PubMed:26375003, PubMed:27281216). Released upon cleavage in vitro of genetically engineered Gsdma3, and binds to membrane inner leaflet lipids (PubMed:27281216). Homooligomerizes within the membrane and forms pores of 10-15 nanometers (nm) of inner diameter, allowing the release of mature interleukin-1 (IL1B and IL18) and triggering pyroptosis (PubMed:27281216, PubMed:33883744). Binds to membrane inner leaflet lipids, including bisphosphorylated phosphatidylinositols, such as phosphatidylinositol (4,5)-bisphosphate, as well as phosphatidylinositol (3,4,5)-bisphosphate, and more weakly to monophosphorylated phosphatidylinositols (PubMed:27281216). Also binds to bacterial and mitochondrial lipids, including cardiolipin, and exhibits bactericidal activity (PubMed:27281216, PubMed:29695864). The functional mechanisms and physiological proteases that cleave and activate this pore-forming protein are unknown (Probable). Plays a role in the transition from catagen to telogen at the end of hair follicle morphogenesis, possibly by regulating hair follicle stem cell niche maintenance (PubMed:15475261, PubMed:15737203, PubMed:17572385, PubMed:22155111, PubMed:32302611). Also required for mammary gland development (PubMed:28168650). The full-length protein before cleavage is inactive: intramolecular interactions between N- and C-terminal domains mediate autoinhibition in the absence of activation signal (PubMed:25825937, PubMed:26100518, PubMed:26375003). The intrinsic pyroptosis-inducing activity is carried by the released N-terminal moiety (Gasdermin-A3, N-terminal) (PubMed:26100518, PubMed:26375003). Homooligomer; homooligomeric ring-shaped pore complex containing 27-28 subunits when inserted in the membrane. Highest levels in skin with weak expression in placenta and testis. Not detected in the gastrointestinal tract. In skin, expressed in postnatal hair follicles and epidermis as well as sebaceous gland basal cells. Not detected at postnatal day 1. Expressed on subsequent postnatal days up to day 20 and throughout adulthood. Intramolecular interactions between N- and C-terminal domains are important for autoinhibition in the absence of activation signal (PubMed:26375003). The intrinsic pyroptosis-inducing activity is carried by the N-terminal domain (PubMed:26375003). Forms a ring-shaped pore complex containing 27-28 subunits that inserts into the membrane (PubMed:33883744). The pore conduit is predominantly negatively charged, facilitating the release of mature interleukin-1 (IL1B and IL18). In contrast interleukin-1 precursors are not released, due to the presence of an acidic region that is proteolytically removed by CASP1 during maturation (PubMed:33883744). Cleavage relieves autoinhibition by releasing the N-terminal moiety (Gasdermin-A3, N-terminal) that initiates pyroptosis. No visible phenotype (PubMed:25825937). A number of gain-of-function mutations, such as alopecia and excoriation (AE), bareskin (Bsk), defolliculated (Dfl), finnegan (Fgn) reduced coat 2 (Rco2), Rex-denuded (Re-den) and recombination induced mutation 3 (Rim3), have been identified: they cause progressive hair loss (alopecia) accompanied with hyperkeratosis and chronic skin inflammation (PubMed:15475261, PubMed:15737203, PubMed:17572385, PubMed:22155111). Gain-of-function mutations cause bulge stem cell depletion, leading to skin inflammation and alopecia (PubMed:22155111). Pyroptosis-induced inflammation mediated by Gsdma3 triggers robust anti-tumor immunity and may be used in therapies to suppress tumor growth (PubMed:32188939). Use of a nanoparticle-mediated delivery system that selectively directs release of N-terminal moiety (Gasdermin-A3, N-terminal) into tumor cells, triggers pyroptosis and robust anti-tumor immunity (PubMed:32188939). Pyroptosis of less than 15% of tumor cells is sufficient to clear the entire tumor in a mammary tumor graft (PubMed:32188939). Belongs to the gasdermin family.