| 别名 | GSDMD |
| 基因名称 | GSDMD |
| 蛋白名称 | Gasdermin domain-containing protein 1,Gasdermin-D,GSDMD,GSDMD-CT,GSDMD-NT,GSDMD_HUMAN |
| 推荐应用 | |
| 反应物种 | Human |
| 存储缓冲液 | PBS, 50% glycerol, 0.05% Proclin 300, 0.05%BSA |
| Human Gene Link | 79792 |
| Human Swissprot No. | P57764 |
| 特异性 | endogenous |
| 稀释度 | WB 1:1000-1:5000； |
| 参考分子量 | MW(Observed):35kD |
| 预测分子量 | MW(Calculated):53kD |
| 运输及保存条件 | -15°C to -25°C/1 year(Do not lower than -25°C) |
| 宿主 | Rabbit |
| 同种型 | IgG,Kappa |
| 背景介绍 | The protein encoded by the GSDMD gene is a member of the gasdermin family and the key executioner of pyroptosis, a pro-inflammatory form of programmed cell death. Full-length GSDMD exists in an autoinhibited state through intramolecular interactions between its N-terminal pore-forming domain and C-terminal inhibitory domain. Upon activation by inflammatory caspases (caspase-1 in canonical inflammasomes and caspase-4/5/11 in non-canonical inflammasomes), GSDMD is cleaved at the interdomain linker, releasing the cytotoxic N-terminal fragment. This cleaved N-terminal domain translocates to the plasma membrane, forms large oligomeric pores, and mediates the release of pro-inflammatory cytokines (IL-1尾, IL-18) and cellular contents, leading to pyroptotic cell death. Dysregulation of GSDMD-mediated pyroptosis is associated with various human diseases, including sepsis, infectious diseases, autoimmune disorders, inflammatory bowel disease, neurodegenerative diseases, and cancer. This antibody specifically recognizes the cleaved N-terminal fragment of GSDMD, but not the full-length inactive protein. |
| 细胞定位 | [Gasdermin-D]: Cytoplasm, cytosol . Inflammasome . In response to a canonical inflammasome stimulus, such as nigericin, recruited to NLRP3 inflammasone with similar kinetics to that of uncleaved CASP1 precursor. .; [Gasdermin-D, N-terminal]: Cell membrane ; Multi-pass membrane protein . Secreted . Released in the extracellular milieu following pyroptosis. .; [Gasdermin-D, C-terminal]: Cytoplasm, cytosol . |
| 功能 | Cleavage at Asp-275 by CASP1 (mature and uncleaved precursor forms), CASP4, CASP5 or CASP8 relieves autoinhibition and is sufficient to initiate pyroptosis (PubMed:26375003, PubMed:29898893, PubMed:32109412). Cleavage by CASP1 and CASP4 is not strictly dependent on the consensus cleavage site on GSDMD but depends on an exosite interface on CASP1 that recognizes and binds the Gasdermin-D, C-terminal (GSDMD-CT) part (PubMed:32109412). Cleavage by CASP8 takes place following inactivation of MAP3K7/TAK1 by Yersinia toxin YopJ (By similarity). Cleavage at Asp-87 by CASP3 or CAPS7 inactivates the ability to mediate pyroptosis (PubMed:28392147, PubMed:28045099). |
| 纯化 | Protein A |
| Clonality | Monoclonal |
| 修饰类型 | Unmodified |
| 细胞定位 | [Gasdermin-D]: Cytoplasm, cytosol . Inflammasome . In response to a canonical inflammasome stimulus, such as nigericin, recruited to NLRP3 inflammasone with similar kinetics to that of uncleaved CASP1 precursor. .; [Gasdermin-D, N-terminal]: Cell membrane ; Multi-pass membrane protein . Secreted . Released in the extracellular milieu following pyroptosis. .; [Gasdermin-D, C-terminal]: Cytoplasm, cytosol . |
| 组织表达 | Expressed in the suprabasal cells of esophagus, as well as in the isthmus/neck, pit, and gland of the stomach, suggesting preferential expression in differentiating cells. |
| 研究领域 | >>Neutrophil extracellular trap formation;>>NOD-like receptor signaling pathway;>>Salmonella infection |
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