ArticleScientific reports2016
MASTL(Greatwall) regulates DNA damage responses by coordinating mitotic entry after checkpoint recovery and APC/C activation.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 44 citations in OpenAlex.
- Greatwall kinase regulates acute myeloid leukaemia cell division through a non-canonical mechanism.EMBO reports · 2026Article
- MASTL Promotes Hepatocellular Carcinoma Progression and Paclitaxel Resistance Through Mitotic Catastrophe.Cancer science · 2026Article
- Hypoxia inducible factor 1α-driven steroidogenesis impacts systemic hematopoiesis.Cellular & molecular biology letters · 2025Article
- IL-22 regulates MASTL expression in intestinal epithelial cells.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Article
- The ATM-E6AP-MASTL axis mediates DNA damage checkpoint recovery.bioRxiv : the preprint server for biology · 2023Article
- SILAC kinase screen identifies potential MASTL substrates.Scientific reports · 2022Article
- DNA damage checkpoint execution and the rules of its disengagement.Frontiers in cell and developmental biology · 2022Review
- The MASTL-ENSA-PP2A/B55 axis modulates cisplatin resistance in oral squamous cell carcinoma.Frontiers in cell and developmental biology · 2022Article
- Host Genome-Wide Association Study of Infant Susceptibility toInfection and immunity · 2021Article
- Dysregulated G2 phase checkpoint recovery pathway reduces DNA repair efficiency and increases chromosomal instability in a wide range of tumours.Oncogenesis · 2021Article
- Knockdown of Microtubule Associated Serine/threonine Kinase Like Expression Inhibits Gastric Cancer Cell Growth and Induces Apoptosis by Activation of ERK1/2 and Inactivation of NF-κB Signaling.Current medical science · 2021Article
- MASTL: A novel therapeutic target for Cancer Malignancy.Cancer medicine · 2020Review
- MASTL promotes cell contractility and motility through kinase-independent signaling.The Journal of cell biology · 2020Article
- AKT Regulates Mitotic Progression of Mammalian Cells by Phosphorylating MASTL, Leading to Protein Phosphatase 2A Inactivation.Molecular and cellular biology · 2020Article
- Mitotic slippage is determined by p31Oncogene · 2020Article
- Molecular Basis of the Mechanisms Controlling MASTL.Molecular & cellular proteomics : MCP · 2020Article
- Cell Cycle and DNA Repair Regulation in the Damage Response: Protein Phosphatases Take Over the Reins.International journal of molecular sciences · 2020Review
- Review
- Multiple interaction nodes define the postreplication repair response to UV-induced DNA damage that is defective in melanomas and correlated with UV signature mutation load.Molecular oncology · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The G2 DNA damage checkpoint is one of the most important mechanisms controlling G2-mitosis transition. The kinase Greatwall (MASTL in human) promotes normal G2-mitosis transition by inhibiting PP2A via ARPP19 and ENSA. In this study, we demonstrate that MASTL is critical for maintaining genome integrity after DNA damage. Although MASTL did not affect the activation of DNA damage responses and subsequent repair, it determined the timing of entry into mitosis and the subsequent fate of the recovering cells. Constitutively active MASTL promoted dephosphorylation of CDK1(Tyr15) and accelerated mitotic entry after DNA damage. Conversely, downregulation of MASTL or ARPP19/ENSA delayed mitotic entry. Remarkably, APC/C was activated precociously, resulting in the damaged cells progressing from G2 directly to G1 and skipping mitosis all together. Collectively, these results established that precise control of MASTL is essential to couple DNA damage to mitosis through the rate of mitotic entry and APC/C activation.
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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.