ArticleThe Journal of experimental medicine1998
Dual signaling of the Fas receptor: initiation of both apoptotic and necrotic cell death pathways.
Article in The Journal of experimental medicine, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 176 papers.
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Who cites it
176 citing papers in PubMed, 552 citations in OpenAlex.
- Macrophages and the Survival of Cardiomyocytes After Myocardial Infarction.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Bidirectional Crosstalk Between cGAS-STING and Necroptosis: From Mitochondrial DNA Release to Inflammatory Disease.Drug design, development and therapy · 2026Review
- PANoptosis: potential new targets and therapeutic prospects in digestive diseases.Apoptosis : an international journal on programmed cell death · 2025Review
- Necroptotic cell death consequences and disease relevance.Nature immunology · 2025Review
- Dual role mechanisms of regulated cell death in apical periodontitis: from pathogenic destruction to therapeutic potential.Cell death discovery · 2025Review
- Polymorphisms in Necroptosis Pathway Genes: Novel Prognostic Markers for Multiple Myeloma Treatment Outcomes.International journal of molecular sciences · 2025Article
- Deciphering Necroptosis-Associated Molecular Subtypes in Acute Ischemic Stroke Through Bioinformatics and Machine Learning Analysis.Journal of molecular neuroscience : MN · 2025Article
- For Better or Worse: The Impact of Necrotic Cell Death Modalities.Advances in experimental medicine and biology · 2025Review
- Necroptosis-based glioblastoma prognostic subtypes: implications for TME remodeling and therapy response.Annals of medicine · 2024Article
- The importance of murine phospho-MLKL-S345 in situ detection for necroptosis assessment in vivo.Cell death and differentiation · 2024Article
- ZBP1 and TRIF trigger lethal necroptosis in mice lacking caspase-8 and TNFR1.Cell death and differentiation · 2024Article
- Immunogenic cell death in cancer: targeting necroptosis to induce antitumour immunity.Nature reviews. Cancer · 2024Review
- RIPK3 cleavage is dispensable for necroptosis inhibition but restricts NLRP3 inflammasome activation.Cell death and differentiation · 2024Article
- The lipid basis of cell death and autophagy.Autophagy · 2024Review
- Necroptosis does not drive disease pathogenesis in a mouse infective model of SARS-CoV-2 in vivo.Cell death & disease · 2024Article
- Perish in the Attempt: Regulated Cell Death in Regenerative and Nonregenerative Tissue.Antioxidants & redox signaling · 2023Review
- PANoptosis: Mechanism and Role in Pulmonary Diseases.International journal of molecular sciences · 2023Review
- Different types of cell death and their shift in shaping disease.Cell death discovery · 2023Review
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Caspase Inhibition Modulates Monocyte-Derived Macrophage Polarization in Damaged Tissues.International journal of molecular sciences · 2023Article
116 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Murine L929 fibrosarcoma cells were transfected with the human Fas (APO-1/CD95) receptor, and the role of various caspases in Fas-mediated cell death was assessed. Proteolytic activation of procaspase-3 and -7 was shown by Western analysis. Acetyl-Tyr-Val-Ala-Asp-chloromethylketone and benzyloxycarbonyl-Asp(OMe)-Glu(OMe)-Val-Asp(OMe)-fluoromethylketone++ +, tetrapeptide inhibitors of caspase-1- and caspase-3-like proteases, respectively, failed to block Fas-induced apoptosis. Unexpectedly, the broad-spectrum caspase inhibitors benzyloxycarbonyl-Val-Ala-Asp(OMe)-fluoromethylketone and benzyloxycarbonyl-Asp(OMe)-fluoromethylketone rendered the cells even more sensitive to Fas-mediated cell death, as measured after 18 h incubation. However, when the process was followed microscopically, it became clear that anti-Fas-induced apoptosis of Fas-transfected L929 cells was blocked during the first 3 h, and subsequently the cells died by necrosis. As in tumor necrosis factor (TNF)-induced necrosis, Fas treatment led to accumulation of reactive oxygen radicals, and Fas-mediated necrosis was inhibited by the oxygen radical scavenger butylated hydroxyanisole. However, in contrast to TNF, anti-Fas did not activate the nuclear factor kappaB under these necrotic conditions. These results demonstrate the existence of two different pathways originating from the Fas receptor, one rapidly leading to apoptosis, and, if this apoptotic pathway is blocked by caspase inhibitors, a second directing the cells to necrosis and involving oxygen radical production.
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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.