[Gasdermin-D]: Precursor of a pore-forming protein that plays a key role in host defense against pathogen infection and danger signals . This form constitutes the precursor of the pore-forming protein: upon cleavage, the released N-terminal moiety binds to membranes and forms pores, triggering pyroptosis . ; [Gasdermin-D, N-terminal]: Promotes pyroptosis in response to microbial infection and danger signals . Produced by the cleavage of gasdermin-D by inflammatory caspases CASP1, CASP4 or CASP5 in response to canonical, as well as non-canonical inflammasome activators . After cleavage, moves to the plasma membrane where it strongly binds to inner leaflet lipids, including monophosphorylated phosphatidylinositols, such as phosphatidylinositol 4-phosphate, bisphosphorylated phosphatidylinositols, such as phosphatidylinositol -bisphosphate, as well as phosphatidylinositol -bisphosphate, and more weakly to phosphatidic acid and phosphatidylserine . Homooligomerizes within the membrane and forms pores of 10-15 nanometers of inner diameter, allowing the release of mature interleukin-1 and triggering pyroptosis . Gasdermin pores also allow the release of mature caspase-7 . In some, but not all, cells types, pyroptosis is followed by pyroptotic cell death, which is caused by downstream activation of ninjurin-1 , which mediates membrane rupture . Also forms pores in the mitochondrial membrane, resulting in release of mitochondrial DNA into the cytosol . Gasdermin-D, N-terminal released from pyroptotic cells into the extracellular milieu rapidly binds to and kills both Gram-negative and Gram-positive bacteria, without harming neighboring mammalian cells, as it does not disrupt the plasma membrane from the outside due to lipid-binding specificity . Under cell culture conditions, also active against intracellular bacteria, such as Listeria monocytogenes . Also active in response to MAP3K7/TAK1 inactivation by Yersinia toxin YopJ, which triggers cleavage by CASP8 and subsequent activation . Required for mucosal tissue defense against enteric pathogens . Activation of the non-canonical inflammasome in brain endothelial cells can lead to excessive pyroptosis, leading to blood-brain barrier breakdown . Strongly binds to bacterial and mitochondrial lipids, including cardiolipin . Does not bind to unphosphorylated phosphatidylinositol, phosphatidylethanolamine nor phosphatidylcholine . ; [Gasdermin-D, p13]: Transcription coactivator produced by the cleavage by CASP3 or CASP7 in the upper small intestine in response to dietary antigens . Required to maintain food tolerance in small intestine: translocates to the nucleus and acts as a coactivator for STAT1 to induce the transcription of CIITA and MHC class II molecules, which in turn induce type 1 regulatory T cells in upper small intestine . ; [Gasdermin-D, p40]: Produced by the cleavage by papain allergen . After cleavage, moves to the plasma membrane and homooligomerizes within the membrane and forms pores of 10-15 nanometers of inner diameter, allowing the specific release of mature interleukin-33 , promoting type 2 inflammatory immune response .

Gasdermin-D (Gasdermin domain-containing protein 1) [Cleaved into: Gasdermin-D, N-terminal (GSDMD-NT) (hGSDMD-NTD); Gasdermin-D, C-terminal (GSDMD-CT) (hGSDMD-CTD); Gasdermin-D, p13 (Gasdermin-D, 13 kDa) (13 kDa GSDMD); Gasdermin-D, p40]

p57764

Human

WB

WB 1:1000

~53 kD

Rabbit

50mM Tris-Glycine(pH 7.4), 0.15M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.

Store at -20°C. Stable for 12 months from date of receipt.