ArticleMolecular biology of the cell2012
Human Cdc14A regulates Wee1 stability by counteracting CDK-mediated phosphorylation.
Article in Molecular biology of the cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 37 citations in OpenAlex.
- Wee Kinases, Big Impact: Wee and Myt Kinases as Critical Regulators of Meiotic Progression.Journal of developmental biology · 2026Review
- First-in-class ultralong-target-residence-time p38α inhibitors as a mitosis-targeted therapy for colorectal cancer.Nature cancer · 2025Article
- Article
- Maintaining Genome Integrity: Protein Kinases and Phosphatases Orchestrate the Balancing Act of DNA Double-Strand Breaks Repair in Cancer.International journal of molecular sciences · 2023Review
- Combined inhibition of Wee1 and Chk1 as a therapeutic strategy in multiple myeloma.Frontiers in oncology · 2023Article
- SFPQ-ABL1 and BCR-ABL1 use different signaling networks to drive B-cell acute lymphoblastic leukemia.Blood advances · 2022Article
- ATR and CDK4/6 inhibition target the growth of methotrexate-resistant choriocarcinoma.Oncogene · 2022Article
- DNA damage checkpoint execution and the rules of its disengagement.Frontiers in cell and developmental biology · 2022Review
- UNC5B mediates G2/M phase arrest of bladder cancer cells by binding to CDC14A and P53.Cancer gene therapy · 2020Article
- Network mechanisms and dysfunction within an integrated computational model of progression through mitosis in the human cell cycle.PLoS computational biology · 2020Article
- Insights into antitrypanosomal drug mode-of-action from cytology-based profiling.PLoS neglected tropical diseases · 2018Article
- Biochemical analyses reveal amino acid residues critical for cell cycle-dependent phosphorylation of human Cdc14A phosphatase by cyclin-dependent kinase 1.Scientific reports · 2018Article
- The G2 checkpoint-a node-based molecular switch.FEBS open bio · 2017Article
- Opposing post-translational modifications regulate Cep76 function to suppress centriole amplification.Oncogene · 2016Article
- Human phosphatase CDC14A is recruited to the cell leading edge to regulate cell migration and adhesion.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
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- Article
- HuR posttranscriptionally regulates WEE1: implications for the DNA damage response in pancreatic cancer cells.Cancer research · 2014Article
- Overexpression of DOC-1R inhibits cell cycle G1/S transition by repressing CDK2 expression and activation.International journal of biological sciences · 2013Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The activity of Cdk1-cyclin B1 mitotic complexes is regulated by the balance between the counteracting activities of Wee1/Myt1 kinases and Cdc25 phosphatases. These kinases and phosphatases must be strictly regulated to ensure proper mitotic timing. One masterpiece of this regulatory network is Cdk1, which promotes Cdc25 activity and suppresses inhibitory Wee1/Myt1 kinases through direct phosphorylation. The Cdk1-dependent phosphorylation of Wee1 primes phosphorylation by additional kinases such as Plk1, triggering Wee1 degradation at the onset of mitosis. Here we report that Cdc14A plays an important role in the regulation of Wee1 stability. Depletion of Cdc14A results in a significant reduction in Wee1 protein levels. Cdc14A binds to Wee1 at its amino-terminal domain and reverses CDK-mediated Wee1 phosphorylation. In particular, we found that Cdc14A inhibits Wee1 degradation through the dephosphorylation of Ser-123 and Ser-139 residues. Thus the lack of phosphorylation of these two residues prevents the interaction with Plk1 and the consequent efficient Wee1 degradation at the onset of mitosis. These data support the hypothesis that Cdc14A counteracts Cdk1-cyclin B1 activity through Wee1 dephosphorylation.
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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.