ArticleProceedings of the National Academy of Sciences of the United States of America2011
Fas-mediated neutrophil apoptosis is accelerated by Bid, Bak, and Bax and inhibited by Bcl-2 and Mcl-1.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.
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Who cites it
61 citing papers in PubMed, 1 synthesis or guideline pooled it, 114 citations in OpenAlex.
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- Assessment of DNA damage and repair in adults consuming allyl isothiocyanate or Brassica vegetables.The Journal of nutritional biochemistry · 2013Trial
- Neutrophil-derived apoptotic bodies function as decoy signals to preserve bone integrity during infectious osteomyelitis.Bone research · 2026Article
- Immunosenescence: signaling pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2025Review
- The context-dependent effect of cellular senescence: From embryogenesis and wound healing to aging.Ageing research reviews · 2025Review
- Drug repurposing of cyclin-dependent kinase inhibitors for neutrophilic acute respiratory distress syndrome and psoriasis.Journal of advanced research · 2025Review
- New insights into constitutive neutrophil death.Cell death discovery · 2025Review
- Oral Spore-Based Probiotic Supplementation Alters Post-Prandial Expression of mRNA Associated with Gastrointestinal Health.Biomedicines · 2024Article
- Integrative analysis reveals novel insights into juvenile idiopathic arthritis pathogenesis and shared molecular pathways with associated traits.Frontiers in genetics · 2024Article
- Regulated cell death in neutrophils: From apoptosis to NETosis and pyroptosis.Seminars in immunology · 2023Review
- Article
- Possible mechanisms associated with immune escape and apoptosis on anti-hepatocellular carcinoma effect of Mu Ji Fang granules.World journal of gastrointestinal oncology · 2023Article
- Lactoferrin modification of berberine nanoliposomes enhances the neuroprotective effects in a mouse model of Alzheimer's disease.Neural regeneration research · 2023Article
- Cellular senescence: a key therapeutic target in aging and diseases.The Journal of clinical investigation · 2022Review
- Hybrid Biomaterial Initiates Refractory Wound Healing via Inducing Transiently Heightened Inflammatory Responses.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- FTO protects human granulosa cells from chemotherapy-induced cytotoxicity.Reproductive biology and endocrinology : RB&E · 2022Article
- How sphingolipids affect T cells in the resolution of inflammation.Frontiers in pharmacology · 2022Review
- Prime, shock and kill: BCL-2 inhibition for HIV cure.Frontiers in immunology · 2022Review
- Effects of low intensity pulsed ultrasound on expression of B-cell lymphoma-2 and BCL2-Associated X in premature ovarian failure mice induced by 4-vinylcyclohexene diepoxide.Reproductive biology and endocrinology : RB&E · 2021Article
- Conditions Mimicking the Cancer Microenvironment Modulate the Functional Outcome of Human Chorionic Villus Mesenchymal Stem/Stromal CellsFrontiers in cell and developmental biology · 2021Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
18 authors at 3 institutions in 1 country.
Funding
Abstract
During immune responses, neutrophils must integrate survival and death signals from multiple sources to regulate their lifespan. Signals that activate either the Bcl-2- or death receptor-regulated apoptosis pathways can provide powerful stimuli for neutrophils to undergo cell death, but whether they act cooperatively in parallel or directly cross-talk in neutrophils is not known. Previous studies suggested that Bcl-2 family proteins are not required for Fas-induced cell death in neutrophils, but did not examine whether they could modulate its rapid onset. By monitoring the rate of change in neutrophil viability associated with activation of the Fas-triggered death receptor pathway using real-time cell imaging, we show that the Bcl-2-related proteins Bid, Bax, and Bak accelerate neutrophil apoptosis but are not essential for cell death. Increased Bcl-2 or Mcl-1 expression prevents efficient induction of apoptosis by Fas stimulation indicating that the Bcl-2-regulated apoptosis pathway can directly interfere with Fas-triggered apoptosis. Fas has been shown to initiate NFκB activation and gene transcription in cell lines, however gene transcription is not altered in Fas-activated Bid(-/-) neutrophils, indicating that apoptosis occurs independently of gene transcription in neutrophils. The specification of kinetics of neutrophil apoptosis by Bid impacts on the magnitude of neutrophil IL-1β production, implicating a functional role for the Bcl-2-regulated pathway in controlling neutrophil responses to FasL. These data demonstrate that the intrinsic apoptosis pathway directly controls the kinetics of Fas-triggered apoptosis in neutrophils.
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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.