ArticleMolecular cell2008
Quantitative analysis of pathways controlling extrinsic apoptosis in single cells.
Article in Molecular cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 209 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
209 citing papers in PubMed, 382 citations in OpenAlex.
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- Understanding cell fate decisions with temporal attention.PLoS computational biology · 2026Article
- Short-term memory of past caspase activity biases cell elimination in vivo.Nature communications · 2026Article
- Evasion of cell death despite mitochondrial outer membrane permeabilization: an oncogenic outcome of apoptosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Regulated cell death plasticity in cancer: thresholds, reversibility, and therapeutic failure.Journal of translational medicine · 2026Review
- Decoding necrosome assembly: harmonizing signal amplification and attenuation through optimal RIP3 stoichiometry.Nature communications · 2025Article
- Transition between cell states of sensitivity reveals molecular vulnerability of drug-tolerant cells.Molecular systems biology · 2025Article
- Review
- Mitochondrial orchestration of PANoptosis: mechanisms, disease pathogenesis, and emerging therapeutic frontiers.Cell death discovery · 2025Review
- Gradient matching accelerates mixed-effects inference for biochemical networks.Bioinformatics (Oxford, England) · 2025Article
- Factors that determine cell fate in mitotically arrested cancer cells.Frontiers in cell and developmental biology · 2025Article
- RUCova: Removal of Unwanted Covariance in mass cytometry data.Bioinformatics (Oxford, England) · 2024Article
- Tipping-point transition from transient to persistent inflammation in pancreatic islets.NPJ systems biology and applications · 2024Article
- Measuring Drug Response with Single-Cell Growth Rate Quantification.Analytical chemistry · 2023Article
- Drug-tolerant persister cells in cancer: the cutting edges and future directions.Nature reviews. Clinical oncology · 2023Review
- Stressed neuronal cells can recover from profound membrane blebbing, nuclear condensation and mitochondrial fragmentation, but not from cytochrome c release.Scientific reports · 2023Article
- To eat or not to eat mitochondria? How do host cells cope with mitophagy upon bacterial infection?PLoS pathogens · 2023Review
- Model certainty in cellular network-driven processes with missing data.PLoS computational biology · 2023Article
- Cell survival following direct executioner-caspase activation.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- A review on cell damage, viability, and functionality during 3D bioprinting.Military Medical Research · 2022Review
149 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
6 authors at 3 institutions in 1 country.
Funding
Abstract
Apoptosis in response to TRAIL or TNF requires the activation of initiator caspases, which then activate the effector caspases that dismantle cells and cause death. However, little is known about the dynamics and regulatory logic linking initiators and effectors. Using a combination of live-cell reporters, flow cytometry, and immunoblotting, we find that initiator caspases are active during the long and variable delay that precedes mitochondrial outer membrane permeabilization (MOMP) and effector caspase activation. When combined with a mathematical model of core apoptosis pathways, experimental perturbation of regulatory links between initiator and effector caspases reveals that XIAP and proteasome-dependent degradation of effector caspases are important in restraining activity during the pre-MOMP delay. We identify conditions in which restraint is impaired, creating a physiologically indeterminate state of partial cell death with the potential to generate genomic instability. Together, these findings provide a quantitative picture of caspase regulatory networks and their failure modes.
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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.