ArticleAging cell2024
A defective splicing machinery promotes senescence through MDM4 alternative splicing.
Article in Aging cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Alternative Splicing Constitutes a Transcription-independent Regulatory Layer in Replicative Senescence of Human Umbilical Cord Mesenchymal Stem Cells.Stem cell reviews and reports · 2026Article
- Senescent cells cluster CTCF on nuclear speckles to instruct an alternative splicing program.Nature aging · 2026Article
- Pharmacological targeting of SF3a1-MDM4 splicing vulnerability in ovarian cancer with rifaximin and antisense oligonucleotide.Journal of translational medicine · 2026Article
- LMO7-mediated POLR2A degradation promotes cellular senescence through the MDM4/p53/p21 axis.Cell death & disease · 2026Article
- New evidence for the protective effect of gut microbiota regulation of ferroptosis-related proteins against osteoporosis.World journal of microbiology & biotechnology · 2025Article
- A defective splicing machinery promotes senescence through MDM4 alternative splicing.Aging cell · 2024Article
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Authors and funding
6 authors.
Funding
Abstract
Defects in the splicing machinery are implicated in various diseases, including cancer. We observed a general reduction in the expression of spliceosome components and splicing regulators in human cell lines undergoing replicative, stress-induced, and telomere uncapping-induced senescence. Supporting the view that defective splicing contributes to senescence, splicing inhibitors herboxidiene, and pladienolide B induced senescence in normal and cancer cell lines. Furthermore, depleting individual spliceosome components also promoted senescence. All senescence types were associated with an alternative splicing transition from the MDM4-FL variant to MDM4-S. The MDM4 splicing shift was reproduced when splicing was inhibited, and spliceosome components were depleted. While decreasing the level of endogenous MDM4 promoted senescence and cell survival independently of the MDM4-S expression status, cell survival was also improved by increasing MDM4-S. Overall, our work establishes that splicing defects modulate the alternative splicing of MDM4 to promote senescence and cell survival.
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Registered trials
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