ArticleProceedings of the National Academy of Sciences of the United States of America2021
The chromatin-binding domain of Ki-67 together with p53 protects human chromosomes from mitotic damage.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Ki-67 shapes the nucleolus by anchoring chromatin via its amphiphilic properties.The EMBO journal · 2026Article
- Liquid-Liquid Phase Separation in Cancer Drug Resistance: Mechanisms and Therapeutic Opportunities.Oncology research · 2026Review
- Applying a Conservation-Based Approach for Predicting Novel Phosphorylation Sites in Eukaryotes and Evaluating Their Functional Relevance.Journal of proteome research · 2025Article
- The mitotic chromosome periphery modulates chromosome mechanics.Nature communications · 2025Article
- The role of MKI67 in the regulation of 60S pre-ribosome nucleolar export, transcripts, energy supply, and apoptosis.bioRxiv : the preprint server for biology · 2025Article
- Ki-67 and CDK1 control the dynamic association of nuclear lipids with mitotic chromosomes.Journal of lipid research · 2025Article
- Ki67 deficiency impedes chromatin accessibility and BCR gene rearrangement.The Journal of experimental medicine · 2024Article
- Gastroenteropancreatic neuroendocrine neoplasms: current development, challenges, and clinical perspectives.Military Medical Research · 2024Review
- Ki-67 is necessary during DNA replication for fork protection and genome stability.Genome biology · 2024Article
- Bulk RNA-seq analyses of mandibular condylar cartilage in a post-traumatic TMJ osteoarthritis rabbit model.Orthodontics & craniofacial research · 2023Article
- Liver Organoids as an In Vitro Model to Study Primary Liver Cancer.International journal of molecular sciences · 2023Review
- Dynamic chromosomal interactions and control of heterochromatin positioning by Ki-67.EMBO reports · 2022Article
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Authors and funding
6 authors.
Funding
Abstract
Vertebrate mammals express a protein called Ki-67 which is most widely known as a clinically useful marker of highly proliferative cells. Previous studies of human cells indicated that acute depletion of Ki-67 can elicit a delay at the G1/S boundary of the cell cycle, dependent on induction of the checkpoint protein p21. Consistent with those observations, we show here that acute Ki-67 depletion causes hallmarks of DNA damage, and the damage occurs even in the absence of checkpoint signaling. This damage is not observed in cells traversing S phase but is instead robustly detected in mitotic cells. The C-terminal chromatin-binding domain of Ki-67 is necessary and sufficient to protect cells from this damage. We also observe synergistic effects when Ki-67 and p53 are simultaneously depleted, resulting in increased levels of chromosome bridges at anaphase, followed by the appearance of micronuclei. Therefore, these studies identify the C terminus of Ki-67 as an important module for genome stability.
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