ArticleThe Journal of experimental medicine1998
Inhibition of caspases increases the sensitivity of L929 cells to necrosis mediated by tumor necrosis factor.
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 368 papers.
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Who cites it
368 citing papers in PubMed, 911 citations in OpenAlex.
- The rise of reducing reagent-resistant TfR1 dimer marks ferroptosis.Nature cell biology · 2026Article
- Integrated Necroptosis Within Programmed Cell Death in Traumatic Brain Injury.Molecular neurobiology · 2026Review
- Reprogramming gut microenvironment for the treatment of acute severe ulcerative colitis via a synergistic therapy of necroptosis blockade and organoid transplantation.Nature communications · 2026Article
- Organoid phenotypic screening identified glycyrrhizin that confers protection against tumor necrosis factor-induced cell death.Stem cell reports · 2026Article
- A century of cell death research.Journal of cell science · 2026Review
- Bilirubin directly activates RIPK3 to induce non-classical necroptosis.Cell discovery · 2026Article
- Targeting MLKL-Driven Necroptosis: A Therapeutic Target in Inflammation and Host Defense.Biomolecules · 2026Review
- A viable kinase-inactive RIPK3 D143N mouse model reveals its scaffold function in driving TNF-induced inflammatory disorder.Cell death discovery · 2026Article
- Radionuclide-stimulated dynamic therapy induces complementary immunogenic necroptosis and apoptosis cancer cell death pathways.Communications biology · 2026Article
- Activation of RIPK3 drives PANoptosis in human cells and inflammatory apoptosis in canine cells dependent on RIPK1, FADD and caspases.Apoptosis : an international journal on programmed cell death · 2026Article
- Bidirectional Crosstalk Between cGAS-STING and Necroptosis: From Mitochondrial DNA Release to Inflammatory Disease.Drug design, development and therapy · 2026Review
- The Protective Effect of Vitamin D Against Necroptosis in Preeclampsia.Journal of pregnancy · 2026Article
- Resident alveolar macrophages are highly susceptible to the induction of RIPK1/RIPK3-mediated necroptosis which promote efficient pulmonary immune response.Cell death & disease · 2025Article
- Caspase 6 deficiency exacerbates inflammatory bowel disease via enterocyte necroptosis and bacterial translocation.Cell death discovery · 2025Article
- Trigger Points of Necroptosis (RIPK1, RIPK3, and MLKL)-Promising Horizon or Blind Alley in Therapy of Colorectal Cancer?International journal of molecular sciences · 2025Review
- Necroptotic cell death consequences and disease relevance.Nature immunology · 2025Review
- The Multifaceted Role of Calcium Signaling in Regulated Necrosis.Biomolecules · 2025Review
- Role of oxeiptosis in disease mechanisms and therapeutic opportunities.Apoptosis : an international journal on programmed cell death · 2025Review
- Caspases: structural and molecular mechanisms and functions in cell death, innate immunity, and disease.Cell discovery · 2025Review
- Exploring necroptosis: mechanistic analysis and antitumor potential of nanomaterials.Cell death discovery · 2025Review
308 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
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Murine L929 fibrosarcoma cells treated with tumor necrosis factor (TNF) rapidly die in a necrotic way, due to excessive formation of reactive oxygen intermediates. We investigated the role of caspases in the necrotic cell death pathway. When the cytokine response modifier A (CrmA), a serpin-like caspase inhibitor of viral origin, was stably overexpressed in L929 cells, the latter became 1,000-fold more sensitive to TNF-mediated cell death. In addition, TNF sensitization was also observed when the cells were pretreated with Ac-YVAD-cmk or zDEVD-fmk, which inhibits caspase-1- and caspase-3-like proteases, respectively. zVAD-fmk and zD-fmk, two broad-spectrum inhibitors of caspases, also rendered the cells more sensitive, since the half-maximal dose for TNF-mediated necrosis decreased by a factor of 1,000. The presence of zVAD-fmk also resulted in a more rapid increase of TNF-mediated production of oxygen radicals. zVAD-fmk-dependent sensitization of TNF cytotoxicity could be completely inhibited by the oxygen radical scavenger butylated hydroxyanisole. These results indicate an involvement of caspases in protection against TNF-induced formation of oxygen radicals and necrosis.
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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.