ArticleMolecular and cellular biology2009
TTK/hMps1 mediates the p53-dependent postmitotic checkpoint by phosphorylating p53 at Thr18.
Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 65 citations in OpenAlex.
- MPS1 inhibition as an anticancer strategy: where do we stand?Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2026Review
- Rewiring mitotic checkpoint control via Mps1 inhibition overcomes DNA repair-mediated resistance in glioblastoma.The Journal of biological chemistry · 2026Article
- Stratified signaling network remodeling of kinase-transcription factors' interactions in Parkinson's disease.Bioinformatics advances · 2026Article
- Doxycycline Enhances Anticancer Activity of Zoledronic Acid via Inducing ROS and Autophagy in Osteosarcoma Cell Lines.International journal of medical sciences · 2025Article
- Cancer testis antigens: Emerging therapeutic targets leveraging genomic instability in cancer.Molecular therapy. Oncology · 2024Review
- Comprehensive analysis of the expression and prognosis for RAI2: A promising biomarker in breast cancer.Frontiers in oncology · 2023Article
- Different Cell Responses to Hinokitiol Treatment Result in Senescence or Apoptosis in Human Osteosarcoma Cell Lines.International journal of molecular sciences · 2022Article
- Phosphotyrosine picked threonine kinase stimulates proliferation of human osteosarcoma cellsArchives of medical science : AMS · 2022Article
- The essential roles of Mps1 in spermatogenesis and fertility in mice.Cell death & disease · 2021Article
- Mitotic and DNA Damage Response Proteins: Maintaining the Genome Stability and Working for the Common Good.Frontiers in cell and developmental biology · 2021Review
- TC Mps1 12, a novel Mps1 inhibitor, suppresses the growth of hepatocellular carcinoma cells via the accumulation of chromosomal instability.British journal of pharmacology · 2017Article
- Article
- Genetic and pharmacological inhibition of TTK impairs pancreatic cancer cell line growth by inducing lethal chromosomal instability.PloS one · 2017Article
- Identification of important long non-coding RNAs and highly recurrent aberrant alternative splicing events in hepatocellular carcinoma through integrative analysis of multiple RNA-Seq datasets.Molecular genetics and genomics : MGG · 2016Article
- Mitotic Protein Kinase 1: Role in Spindle Assembly Checkpoint Revisited.Journal of cancer clinical trials · 2016Article
- Requirement for human Mps1/TTK in oxidative DNA damage repair and cell survival through MDM2 phosphorylation.Nucleic acids research · 2016Article
- Article
- Functional Significance of Aurora Kinases-p53 Protein Family Interactions in Cancer.Frontiers in oncology · 2016Review
- A putative N-terminal nuclear export sequence is sufficient for Mps1 nuclear exclusion during interphase.BMC cell biology · 2015Article
- Candidate tumor suppressor B-cell translocation gene 3 impedes neoplastic progression by suppression of AKT.Cell death & disease · 2015Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Upon prolonged arrest in mitosis, cells undergo adaptation and exit mitosis without cell division. These tetraploid cells are either eliminated by apoptosis or arrested in the subsequent G(1) phase in a spindle checkpoint- and p53-dependent manner. p53 has long been known to be activated by spindle poisons, such as nocodazole and Taxol, although the underlying mechanism remains elusive. Here we present evidence that stabilization and activation of p53 by spindle disruption requires the spindle checkpoint kinase TTK/hMps1. TTK/hMps1 phoshorylates the N-terminal domain of p53 at Thr18, and this phosphorylation disrupts the interaction with MDM2 and abrogates MDM2-mediated p53 ubiquitination. Phosphorylation at Thr18 enhances p53-dependent activation of not only p21 but also Lats2, two mediators of the postmitotic checkpoint. Furthermore, a phospho-mimicking substitution at Thr18 (T18D) is more competent than the phospho-deficient mutant (T18A) in rescuing the tetraploid checkpoint defect of p53-depleted cells. Our findings therefore provide a mechanism connecting the spindle checkpoint with p53 in the maintenance of genome stability.
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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.