ArticleJournal of cell science2016
Two new competing pathways establish the threshold for cyclin-B-Cdk1 activation at the meiotic G2/M transition.
Article in Journal of cell science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
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- Recycling of Uridylated mRNAs in Starfish Embryos.Biomolecules · 2024Article
- An Update on Physiopathological Roles of Akt in the ReprodAKTive Mammalian Ovary.Life (Basel, Switzerland) · 2024Review
- Design, synthesis and anticancer evaluation of polymethoxy aurones as potential cell cycle inhibitors.Heliyon · 2023Article
- Review
- Integration of metabolomics and transcriptomics provides insights into enhanced osteogenesis inFrontiers in endocrinology · 2023Article
- Network topology-directed design of molecular CPU for cell-like dynamic information processing.Science advances · 2022Article
- SGK1 is essential for meiotic resumption in mammalian oocytes.European journal of cell biology · 2022Article
- Hormesis of low-dose inhibition of pAkt1 (Ser473) followed by a great increase of proline-rich inositol polyphosphate 5-phosphatase (PIPP) level in oocytes.In vitro cellular & developmental biology. Animal · 2021Article
- CDK1 serves as a novel therapeutic target for endometrioid endometrial cancer.Journal of Cancer · 2021Article
- Anticancer Activities of Meroterpenoids Isolated from the Brown AlgaFoods (Basel, Switzerland) · 2020Article
- Oocyte Maturation in Starfish.Cells · 2020Review
- A novel topoisomerase I inhibitor DIA-001 induces DNA damage mediated cell cycle arrest and apoptosis in cancer cell.Annals of translational medicine · 2020Article
- Trib1 Contributes to Recovery From Ischemia/Reperfusion-Induced Acute Kidney Injury by Regulating the Polarization of Renal Macrophages.Frontiers in immunology · 2020Article
- SGK phosphorylates Cdc25 and Myt1 to trigger cyclin B-Cdk1 activation at the meiotic G2/M transition.The Journal of cell biology · 2019Article
- SGK regulates pH increase and cyclin B-Cdk1 activation to resume meiosis in starfish ovarian oocytes.The Journal of cell biology · 2019Article
- Deciphering therapeutic potential of PEGylated recombinant PTEN-silver nanoclusters ensemble on 3D spheroids.Molecular biology reports · 2019Article
- MUS81 Inhibition Increases the Sensitivity to Therapy Effect in Epithelial Ovarian Cancer via Regulating CyclinB Pathway.Journal of Cancer · 2019Article
- Resveratrol suppresses human cervical carcinoma cell proliferation and elevates apoptosis via the mitochondrial and p53 signaling pathways.Oncology letters · 2018Article
- MPF-based meiotic cell cycle control: Half a century of lessons from starfish oocytes.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2018Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Extracellular ligands control biological phenomena. Cells distinguish physiological stimuli from weak noise stimuli by establishing a ligand-concentration threshold. Hormonal control of the meiotic G2/M transition in oocytes is essential for reproduction. However, the mechanism for threshold establishment is unclear. In starfish oocytes, maturation-inducing hormones activate the PI3K-Akt pathway through the Gβγ complex of heterotrimeric G-proteins. Akt directly phosphorylates both Cdc25 phosphatase and Myt1 kinase, resulting in activation of cyclin-B-Cdk1, which then induces meiotic G2/M transition. Here, we show that cyclin-B-Cdk1 is partially activated after subthreshold hormonal stimuli, but this triggers negative feedback, resulting in dephosphorylation of Akt sites on Cdc25 and Myt1, thereby canceling the signal. We also identified phosphatase activity towards Akt substrates that exists independent of stimuli. In contrast to these negative regulatory activities, an atypical Gβγ-dependent pathway enhances PI3K-Akt-dependent phosphorylation. Based on these findings, we propose a model for threshold establishment in which hormonal dose-dependent competition between these new pathways establishes a threshold; the atypical Gβγ-pathway becomes predominant over Cdk-dependent negative feedback when the stimulus exceeds this threshold. Our findings provide a regulatory connection between cell cycle and signal transduction machineries.
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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.