ArticleAging2019
A large-scale CRISPR screen and identification of essential genes in cellular senescence bypass.
Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- MORF4L1 regulation and its role in chromatin remodeling, DNA damage, cellular senescence, and cardiometabolic disease.Vascular pharmacology · 2026Review
- Replicative senescence induction in single cells is not predicted by telomere length, dysfunction, or oxidation.iScience · 2026Article
- Identification of replicative aging and inflammatory aging signatures via whole-genome CRISPRi screens.Genome biology · 2025Article
- MRG15 alternative splicing regulates CDK1 transcriptional activity in mouse cell senescence and myocardial regeneration.Communications biology · 2025Article
- Fibromodulin selectively accelerates myofibroblast apoptosis in cutaneous wounds by enhancing interleukin 1β signaling.Nature communications · 2025Article
- CAP superfamily proteins in human: a new target for cancer therapy.Medical oncology (Northwood, London, England) · 2024Review
- Structural and functional insights into the epigenetic regulator MRG15.Acta pharmacologica Sinica · 2024Review
- Cellular senescence: Neither irreversible nor reversible.The Journal of experimental medicine · 2024Article
- CRISPR screen identifies CEBPB as contributor to dyskeratosis congenita fibroblast senescence via augmented inflammatory gene response.G3 (Bethesda, Md.) · 2023Article
- Bioinformatics analysis to identify potential biomarkers and therapeutic targets for ST-segment-elevation myocardial infarction-related ischemic stroke.Frontiers in neurology · 2022Article
- Stem Cells of the Aging Brain.Frontiers in aging neuroscience · 2020Review
- The Signaling of Cellular Senescence in Diabetic Nephropathy.Oxidative medicine and cellular longevity · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence is an important mechanism of autonomous tumor suppression, while its consequence such as the senescence-associated secretory phenotype (SASP) may drive tumorigenesis and age-related diseases. Therefore, controlling the cell fate optimally when encountering senescence stress is helpful for anti-cancer or anti-aging treatments. To identify genes essential for senescence establishment or maintenance, we carried out a CRISPR-based screen with a deliberately designed single-guide RNA (sgRNA) library. The library comprised of about 12,000 kinds of sgRNAs targeting 1378 senescence-associated genes selected by integrating the information of literature mining, protein-protein interaction network, and differential gene expression. We successfully detected a dozen gene deficiencies potentially causing senescence bypass, and their phenotypes were further validated with a high true positive rate. RNA-seq analysis showed distinct transcriptome patterns of these bypass cells. Interestingly, in the bypass cells, the expression of SASP genes was maintained or elevated with CHEK2, HAS1, or MDK deficiency; but neutralized with MTOR, CRISPLD2, or MORF4L1 deficiency. Pathways of some age-related neurodegenerative disorders were also downregulated with MTOR, CRISPLD2, or MORF4L1 deficiency. The results demonstrated that disturbing these genes could lead to distinct cell fates as a consequence of senescence bypass, suggesting that they may play essential roles in cellular senescence.
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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.