ArticleOncogene2010
p53- and p21-dependent premature APC/C-Cdh1 activation in G2 is part of the long-term response to genotoxic stress.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
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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
43 citing papers in PubMed, 72 citations in OpenAlex.
- E2F3 amplification primes bladder cancer cells for premature mitosis.Cancer gene therapy · 2026Article
- APC/C-CDH1 suppresses AROS-mediated protection against DNA damage-induced senescence by ubiquitination.BMB reports · 2026Article
- Targeting EphA2 under DNA damage causes mitotic bypass via p21 induction.The Journal of biological chemistry · 2026Article
- Understanding cellular senescence: pathways involved, therapeutics and longevity aiding.Cell cycle (Georgetown, Tex.) · 2023Review
- Article
- SIRT1 ubiquitination is regulated by opposing activities of APC/C-Cdh1 and AROS during stress-induced premature senescence.Experimental & molecular medicine · 2023Article
- The molecular architecture of cell cycle arrest.Molecular systems biology · 2022Article
- MDC1 is essential for G2/M transition and spindle assembly in mouse oocytes.Cellular and molecular life sciences : CMLS · 2022Article
- Cell Cycle Commitment and the Origins of Cell Cycle Variability.Frontiers in cell and developmental biology · 2021Review
- Cell cycle inertia underlies a bifurcation in cell fates after DNA damage.Science advances · 2021Article
- SCFCell death & disease · 2020Article
- Kaposi's Sarcoma-Associated Herpesvirus Lytic Replication Is Independent of Anaphase-Promoting Complex Activity.Journal of virology · 2020Article
- Oocytes mount a noncanonical DNA damage response involving APC-Cdh1-mediated proteolysis.The Journal of cell biology · 2020Article
- The cGAS/STING/TBK1/IRF3 innate immunity pathway maintains chromosomal stability through regulation of p21 levels.Experimental & molecular medicine · 2020Article
- P53 suppresses SENP3 phosphorylation to mediate G2 checkpoint.Cell discovery · 2020Article
- From Oxidative Stress Damage to Pathways, Networks, and Autophagy via MicroRNAs.Oxidative medicine and cellular longevity · 2018Article
- miR-300 regulates cellular radiosensitivity through targeting p53 and apaf1 in human lung cancer cells.Cell cycle (Georgetown, Tex.) · 2017Article
- ATRX is a regulator of therapy induced senescence in human cells.Nature communications · 2017Article
- The anaphase promoting complex impacts repair choice by protecting ubiquitin signalling at DNA damage sites.Nature communications · 2017Article
- Residual Cdk1/2 activity after DNA damage promotes senescence.Aging cell · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The long-term cellular response to DNA damage is controlled by the tumor suppressor p53. It results in cell-cycle arrest followed by DNA repair and, depending on the degree of damage inflicted, premature senescence or apoptotic cell death. Here we show that in normal diploid fibroblasts the ubiquitin ligase anaphase-promoting complex or cyclosome (APC/C)-Cdh1 becomes prematurely activated in G2 as part of the sustained long-term but not the rapid short-term response to genotoxic stress and results in the degradation of numerous APC/C substrates. Using HCT116 somatic knockout cells we show that mechanistically premature APC/C activation depends on p53 and its transcriptional target p21 that mediates the signal through downregulation of the APC/C inhibitor Emi1. Cdc14B is dispensable in this setting but might function redundantly. Our data suggest an unexpected role for the APC/C in executing a part of the p53-dependent DNA damage response that leads to premature 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.