Cleavage of GSDMD by inflammatory caspases determines pyroptotic cell death

By Jianjin Shi, Yue Zhao, Kun Wang, Xuyan Shi, Yue Wang, Huanwei Huang, Yinghua Zhuang, T. Cai, Fengchao Wang, F. Shao. Nature, 2015

5,789 citations recorded by the source corpus.

Subfields: Hematology, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/0d1a6cc8871ed500d9e4cbbc07cb08e3e15a93db

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Citations in the corpus

A guide to cell death pathways (2023, neutral): “Activated caspase-1 and caspase-11 can mediate the cleavage of gasdermin D (GSDMD) to remove an autoinhibitory carboxy-terminal domain from GSDMD, enabling the N-terminal fragment to form pores on the plasma membrane and resulting in pyroptosis 101,106–108 .”
Synergism of TNF-α and IFN-γ Triggers Inflammatory Cell Death, Tissue Damage, and Mortality in SARS-CoV-2 Infection and Cytokine Shock Syndromes (2020, neutral): “Granzyme A from cytotoxic lymphocytes cleaves GSDMB to trigger pyroptosis in target cells.”
Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018 (2018, background): “Cleaved GSDMD-N acquires the ability to translocate to the inner leaflet of the plasma membrane (or the bacterial plasma membrane), where it binds with high specificity to selected phosphoinositides (or cardiolipin) [629, 630].”
Pyroptosis in inflammatory diseases and cancer (2022, background): “showed that GSDMD participates in both canonical and non-canonical pyroptosis [8, 36].”
Autophagy in inflammation, infection, and immunometabolism (2021, background): “, 2017) before GSDMD-pores and pyroptosis start to dominate in their release (Broz et al., 2020; Kayagaki et al., 2015; Shi et al., 2015), which appears to be a preferred way for IL-1β release by neutrophils (Karmakar et al.”
Structural Mechanism for GSDMD Targeting by Autoprocessed Caspases in Pyroptosis. (2020, methodology): “Cell Viability and Death Assays Cell viability and cytotoxicity assays were performed as previous described (Shi et al., 2015; Wang et al., 2017).”
Gasdermins: Effectors of pyroptosis (2017, methodology): “Upon activation, this domain forms a pore in the plasma membrane (this activity has not been studied for DFNB59 at this time).”
Pseudomonas aeruginosa: pathogenesis, virulence factors, antibiotic resistance, interaction with host, technology advances and emerging therapeutics (2022, background): “Recent work reveals that inflammasome is involved in pyroptosis dependent on the cleavage of Gasdermin D, which contributed to the formation of plasma membrane pores, and in turn promoting the release of inflammatory cytokines and pyroptosis.(288,289) Typically, inflammasome consists of cytosolic PR”
An update on the regulatory mechanisms of NLRP3 inflammasome activation (2021, background): “In macrophages, N-GSDMD oligomerizes in the plasma membrane to form pores that promote NLRP3 inflammasome-associated pyroptosis.(27) In contrast, N-GSDMD does not localize to the plasma membrane or mediate pyroptosis in NLRP3-activated neutrophils, although it is required for IL-1β secretion.”
Inflammasomes: mechanism of assembly, regulation and signalling (2016, background): “These dominant mutations map to the C-terminal domain, and Shi et al.(4) recently demonstrated that they”