ArticleCell metabolism2023
Death-seq identifies regulators of cell death and senolytic therapies.
Article in Cell metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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.
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
- Inducible CRISPR-Cas9 screening platform to interrogate non-proliferative cellular states.Nature protocols · 2026Review
- IAP Antagonists Selectively Eliminate Therapy-Induced Senescent Cancer Cells via TNFα-Independent Apoptosis.Cancer science · 2026Article
- Recycling senescent cell lipids for targeted senotherapy.Nature communications · 2026Article
- Parabiosis, Assembloids, Organoids (PAO).Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- CBX8 suppresses autophagy-dependent senescence in colorectal cancer by modulating the mTOR signaling pathway.International journal of biological sciences · 2026Article
- Lipofuscin accumulation in aging and neurodegeneration: a potential "timebomb" overlooked in Alzheimer's disease.Translational neurodegeneration · 2025Review
- The drug discovery and therapeutic nano-strategies targeting cellular senescence.Materials today. Bio · 2025Review
- Article
- The Mechanism and Potential Therapeutic Strategies of Vascular Aging.Aging medicine (Milton (N.S.W)) · 2025Review
- Programmed Cell Death in Cancer.MedComm · 2025Review
- Identification of replicative aging and inflammatory aging signatures via whole-genome CRISPRi screens.Genome biology · 2025Article
- High-content screening identifies ganoderic acid A as a senotherapeutic to prevent cellular senescence and extend healthspan in preclinical models.Nature communications · 2025Article
- Senolysis by GLS1 Inhibition Ameliorates Kidney Aging by Inducing Excessive mPTP Opening Through MFN1.The journals of gerontology. Series A, Biological sciences and medical sciences · 2025Article
- MEDUSA for Identifying Death Regulatory Genes in Chemo-genetic Profiling Data.Journal of visualized experiments : JoVE · 2025Article
- Immune therapeutic strategies for the senescent tumor microenvironment.British journal of cancer · 2025Review
- Functional genomic screens with death rate analyses reveal mechanisms of drug action.Nature chemical biology · 2024Article
- The paradox of senescent-marker positive cancer cells: challenges and opportunities.npj aging · 2024Review
- A nutrigeroscience approach: Dietary macronutrients and cellular senescence.Cell metabolism · 2024Review
- Targeting Cellular Senescence in Aging and Age-Related Diseases: Challenges, Considerations, and the Emerging Role of Senolytic and Senomorphic Therapies.Aging and disease · 2024Review
- Article
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Authors and funding
19 authors at 3 institutions in 1 country.
Funding
Abstract
Selectively ablating damaged cells is an evolving therapeutic approach for age-related disease. Current methods for genome-wide screens to identify genes whose deletion might promote the death of damaged or senescent cells are generally underpowered because of the short timescales of cell death as well as the difficulty of scaling non-dividing cells. Here, we establish "Death-seq," a positive-selection CRISPR screen optimized to identify enhancers and mechanisms of cell death. Our screens identified synergistic enhancers of cell death induced by the known senolytic ABT-263. The screen also identified inducers of cell death and senescent cell clearance in models of age-related diseases by a related compound, ABT-199, which alone is not senolytic but exhibits less toxicity than ABT-263. Death-seq enables the systematic screening of cell death pathways to uncover molecular mechanisms of regulated cell death subroutines and identifies drug targets for the treatment of diverse pathological states such as senescence, cancer, and fibrosis.
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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.