ArticleCellular microbiology2008
Killing of macrophages by anthrax lethal toxin: involvement of the N-end rule pathway.
Article in Cellular microbiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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Who cites it
37 citing papers in PubMed, 83 citations in OpenAlex.
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- Protein folding stress potentiates NLRP1 and CARD8 inflammasome activation.Cell reports · 2023Article
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- Innate Sensors Trigger Regulated Cell Death to Combat Intracellular Infection.Annual review of immunology · 2022Review
- CARD8 is an inflammasome sensor for HIV-1 protease activity.Science (New York, N.Y.) · 2021Article
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- Phosphoproteomics identifies microglial Siglec-F inflammatory response during neurodegeneration.Molecular systems biology · 2020Article
- A comprehensive guide to studying inflammasome activation and cell death.Nature protocols · 2020Article
- The NLRP1 and CARD8 inflammasomes.Immunological reviews · 2020Review
- The NLRP1 Inflammasome in Human Skin and Beyond.International journal of molecular sciences · 2020Review
- Programmed Cell Death in the Evolutionary Race against Bacterial Virulence Factors.Cold Spring Harbor perspectives in biology · 2020Review
- The NLRP1 inflammasome: new mechanistic insights and unresolved mysteries.Current opinion in immunology · 2019Review
- DPP8/9 inhibitors are universal activators of functional NLRP1 alleles.Cell death & disease · 2019Article
- The N-end rule ubiquitin ligase UBR2 mediates NLRP1B inflammasome activation by anthrax lethal toxin.The EMBO journal · 2019Article
- NLRP1 - One NLR to guard them all.The EMBO journal · 2019Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Macrophages from certain inbred mouse strains are rapidly killed (< 90 min) by anthrax lethal toxin (LT). LT cleaves cytoplasmic MEK proteins at 20 min and induces caspase-1 activation in sensitive macrophages at 50-60 min, but the mechanism of LT-induced death is unknown. Proteasome inhibitors block LT-mediated caspase-1 activation and can protect against cell death, indicating that the degradation of at least one cellular protein is required for LT-mediated cell death. Proteins can be degraded by the proteasome via the N-end rule, in which a protein's stability is determined by its N-terminal residue. Using amino acid derivatives that act as inhibitors of this pathway, we show that the N-end rule is required for LT-mediated caspase-1 activation and cell death. We also found that bestatin methyl ester, an aminopeptidase inhibitor protects against LT in vitro and in vivo and that the different inhibitors of the protein degradation pathway act synergistically in protecting against LT. We identify c-IAP1, a mammalian member of the inhibitor of apoptosis protein (IAP) family, as a novel N-end rule substrate degraded in macrophages treated with LT. We also show that LT-induced c-IAP1 degradation is independent of the IAP-antagonizing proteins Smac/DIABLO and Omi/HtrA2, but dependent on caspases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.