ReviewCellular and molecular life sciences : CMLS2010
Tumor necrosis factor-mediated cell death: to break or to burst, that's the question.
Review in Cellular and molecular life sciences : CMLS, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
94 citing papers in PubMed, 211 citations in OpenAlex.
- Molecular Mechanisms Underlying Reproductive Dysfunction in Polycystic Ovary Syndrome.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Exploring Gene Expression Patterns in Alzheimer's Disease Using a Human Microarray Data Meta-Analysis.Biology · 2026Article
- Cell death in glioblastoma and the central nervous system.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- The multiple biological activities of hyperoside: from molecular mechanisms to therapeutic perspectives in neoplastic and non-neoplastic diseases.Frontiers in pharmacology · 2025Review
- Insights into the Emerging Therapeutic Targets of Triple-negative Breast Cancer.Current cancer drug targets · 2025Review
- The Role of Necroptosis in Cerebral Ischemic Stroke.Molecular neurobiology · 2024Review
- The mechanistic functional landscape of retinitis pigmentosa: a machine learning-driven approach to therapeutic target discovery.Journal of translational medicine · 2024Article
- Anti-Necroptotic Effects of Itaconate and its Derivatives.Inflammation · 2024Article
- The fate and function of non-coding RNAs during necroptosis.Epigenomics · 2024Review
- The roles of long non-coding RNAs in the necroptotic signaling of colon cancer cells.Molecular biology reports · 2023Article
- Spleen Toxicity of Organophosphorus Flame Retardant TDCPP in Mice and the Related Mechanisms.Toxics · 2023Article
- Harnessing TRAIL-induced cell death for cancer therapy: a long walk with thrilling discoveries.Cell death and differentiation · 2023Review
- The regulation of necroptosis by ubiquitylation.Apoptosis : an international journal on programmed cell death · 2022Review
- Non-apoptotic cell death-based cancer therapy: Molecular mechanism, pharmacological modulators, and nanomedicine.Acta pharmaceutica Sinica. B · 2022Review
- Multi-omics analysis reveals the panoramic picture of necroptosis-related regulators in pan-cancer.Aging · 2022Article
- Ripk3 signaling regulates HSCs during stress and represses radiation-induced leukemia in mice.Stem cell reports · 2022Article
- Sensitivity, specificity of biochemical markers for early prediction of endothelial dysfunction in atherosclerotic obese subjects.African health sciences · 2022Article
- Review
- Hepatoprotective effect of diallyl trisulfide against lipopolysaccharide and D-galactosamine induced acute liver failure in mice via suppressing inflammation and apoptosis.Toxicology research · 2022Article
- RIP3 knockdown inhibits necroptosis of human intestinal epithelial cells via TLR4/MyD88/NF-κB signaling and ameliorates murine colitis.BMC gastroenterology · 2022Article
34 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
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this review, we discuss the signal-transduction pathways of three major cellular responses induced by tumor necrosis factor (TNF): cell survival through NF-kappaB activation, apoptosis, and necrosis. Recruitment and activation of caspases plays a crucial role in the initiation and execution of TNF-induced apoptosis. However, experimental inhibition of caspases reveals an alternative cell death pathway, namely necrosis, also called necroptosis, suggesting that caspases actively suppress the latter outcome. TNF-induced necrotic cell death crucially depends on the kinase activity of receptor interacting protein serine-threonine kinase 1 (RIP1) and RIP3. It was recently demonstrated that ubiquitination of RIP1 determines whether it will function as a pro-survival or pro-cell death molecule. Deeper insight into the mechanisms that control the molecular switches between cell survival and cell death will help us to understand why TNF can exert so many different biological functions in the etiology and pathogenesis of human diseases.
Indexed as
Identifiers
What OpenQuestion holds
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.