ArticleProceedings of the National Academy of Sciences of the United States of America2014
Caspase-1 autoproteolysis is differentially required for NLRP1b and NLRP3 inflammasome function.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.
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Who cites it
83 citing papers in PubMed, 1 synthesis or guideline pooled it, 121 citations in OpenAlex.
- The role of CD36 in immune function: bridging innate and adaptive responses.Frontiers in immunology · 2026Pooled it
- Spatial control of NLRP3 inflammasome assembly by membrane lipid composition.Communications biology · 2026Review
- Article
- Streptococcus pyogenes EVs induce the alternative inflammasome via caspase-4/-5 in human monocytes.EMBO reports · 2025Article
- A comprehensive analysis of the relationship between inflammasomes and autophagy in human tumors: Recent developments.Journal of cell communication and signaling · 2025Review
- Unleashing the potential of exercise: conquering cardiovascular disease by targeting inflammasome activation.European journal of medical research · 2025Review
- Nlrc4 Inflammasome Expression After Acute Myocardial Infarction in Rats.International journal of molecular sciences · 2025Article
- The molecular mechanism of berberine affecting psoriasis skin inflammation by regulating keratinocyte pyroptosis via the p38 MAPK/NF-κB pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- ATG16L1 restrains macrophage NLRP3 activation and alveolar epithelial cell injury during septic lung injury.Clinical and translational medicine · 2025Article
- Article
- Targeting PANoptosis in Bacterial-Induced Inflammatory Diseases: Mechanisms and Therapeutic Interventions.Journal of inflammation research · 2025Review
- Review
- Tonabersat suppresses priming/activation of the NOD-like receptor protein-3 (NLRP3) inflammasome and decreases renal tubular epithelial-to-macrophage crosstalk in a model of diabetic kidney disease.Cell communication and signaling : CCS · 2024Article
- Unanticipated Loss of Inflammasomes in Birds.Genome biology and evolution · 2024Article
- Harnessing Pyroptosis for Cancer Immunotherapy.Cells · 2024Review
- Hope for vascular cognitive impairment: Ac-YVAD-cmk as a novel treatment against white matter rarefaction.PloS one · 2024Article
- The non-pathogenic protozoonFrontiers in immunology · 2024Article
- The tetrapeptide sequence of IL-18 and IL-1β regulates their recruitment and activation by inflammatory caspases.Cell reports · 2023Article
- Review
- Tripping the wire: sensing of viral protease activity by CARD8 and NLRP1 inflammasomes.Current opinion in immunology · 2023Review
23 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammasomes are caspase-1-activating multiprotein complexes. The mouse nucleotide-binding domain and leucine rich repeat pyrin containing 1b (NLRP1b) inflammasome was identified as the sensor of Bacillus anthracis lethal toxin (LT) in mouse macrophages from sensitive strains such as BALB/c. Upon exposure to LT, the NLRP1b inflammasome activates caspase-1 to produce mature IL-1β and induce pyroptosis. Both processes are believed to depend on autoproteolysed caspase-1. In contrast to human NLRP1, mouse NLRP1b lacks an N-terminal pyrin domain (PYD), indicating that the assembly of the NLRP1b inflammasome does not require the adaptor apoptosis-associated speck-like protein containing a CARD (ASC). LT-induced NLRP1b inflammasome activation was shown to be impaired upon inhibition of potassium efflux, which is known to play a major role in NLRP3 inflammasome formation and ASC dimerization. We investigated whether NLRP3 and/or ASC were required for caspase-1 activation upon LT stimulation in the BALB/c background. The NLRP1b inflammasome activation was assessed in both macrophages and dendritic cells lacking either ASC or NLRP3. Upon LT treatment, the absence of NLRP3 did not alter the NLRP1b inflammasome activity. Surprisingly, the absence of ASC resulted in IL-1β cleavage and pyroptosis, despite the absence of caspase-1 autoprocessing activity. By reconstituting caspase-1/caspase-11(-/-) cells with a noncleavable or catalytically inactive mutant version of caspase-1, we directly demonstrated that noncleavable caspase-1 is fully active in response to the NLRP1b activator LT, whereas it is nonfunctional in response to the NLRP3 activator nigericin. Taken together, these results establish variable requirements for caspase-1 cleavage depending on the pathogen and the responding NLR.
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