ArticleCell host & microbe2012
Phospholipid scramblase 1 mediates type i interferon-induced protection against staphylococcal α-toxin.
Article in Cell host & microbe, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
38 citing papers in PubMed, 59 citations in OpenAlex.
- Extracellular vesicle proteomics in staphylococcus aureus-treated blood and sepsis reveals coordinated complement, acute phase, neutrophil, and exocytosis responses.Scientific reports · 2026Article
- Unraveling the Biology of Interferon-Stimulated Genes: Mechanisms, Functions, and Clinical Implications.Infection and drug resistance · 2026Review
- Article
- Phospholipid Scramblase 1 (PLSCR1) Regulates Interferon-Lambda Receptor 1 (IFN-λR1) and IFN-λ Signaling in Influenza A Virus (IAV) Infection.bioRxiv : the preprint server for biology · 2025Article
- PLSCR1 suppresses SARS-CoV-2 infection by downregulating cell surface ACE2.Journal of virology · 2025Article
- zDHHC-Mediated S-Palmitoylation in Skin Health and Its Targeting as a Treatment Perspective.International journal of molecular sciences · 2025Review
- The epsilon toxin from Clostridium perfringens stimulates calcium-activated chloride channels, generating extracellular vesicles in Xenopus oocytes.Pharmacology research & perspectives · 2024Article
- Type 1 interferons promote Staphylococcus aureus nasal colonization by inducing phagocyte apoptosis.Cell death discovery · 2024Article
- Machine learning framework develops neutrophil extracellular traps model for clinical outcome and immunotherapy response in lung adenocarcinoma.Apoptosis : an international journal on programmed cell death · 2024Article
- Molecular Characteristics and Pathogenicity ofInternational journal of molecular sciences · 2023Review
- Phospholipid scramblase-1 regulates innate type 2 inflammation in mouse lungs via CRTH2-dependent mechanisms.The Journal of clinical investigation · 2023Article
- Exploring the Role ofToxins · 2022Review
- Scramblases as Regulators of ProteolyticMembranes · 2022Review
- Planarians (Platyhelminthes)-An Emerging Model Organism for Investigating Innate Immune Mechanisms.Frontiers in cellular and infection microbiology · 2021Review
- Two gene set variation indexes as potential diagnostic tool for sepsis.American journal of translational research · 2020Article
- Toll-like receptor 2-dependent endosomal signaling byThe Journal of biological chemistry · 2019Article
- Staphylococcus aureus modulation of innate immune responses through Toll-like (TLR), (NOD)-like (NLR) and C-type lectin (CLR) receptors.FEMS microbiology reviews · 2018Article
- Review
- Phospholipid scramblase 1 interacts with influenza A virus NP, impairing its nuclear import and thereby suppressing virus replication.PLoS pathogens · 2018Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The opportunistic gram-positive pathogen Staphylococcus aureus is a leading cause of pneumonia and sepsis. Staphylococcal α-toxin, a prototypical pore-forming toxin, is a major virulence factor of S. aureus clinical isolates, and lung epithelial cells are highly sensitive to α-toxin's cytolytic activity. Type I interferon (IFN) signaling activated in response to S. aureus increases pulmonary cell resistance to α-toxin, but the underlying mechanisms are uncharacterized. We show that IFNα protects human lung epithelial cells from α-toxin-induced intracellular ATP depletion and cell death by reducing extracellular ATP leakage. This effect depends on protein palmitoylation and induction of phospholipid scramblase 1 (PLSCR1). IFNα-induced PLSCR1 associates with the cytoskeleton after exposure to α-toxin, and cellular depletion of PLSCR1 negates IFN-induced protection from α-toxin. PLSCR1-deficient mice display enhanced sensitivity to inhaled α-toxin and an α-toxin-producing S. aureus strain. These results uncover PLSCR1 activity as part of an innate protective mechanism to a bacterial pore-forming toxin.
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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.