ArticleThe Journal of biological chemistry2009
MAPK pathway activation delays G2/M progression by destabilizing Cdc25B.
Article in The Journal of biological chemistry, 2009. 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, 36 citations in OpenAlex.
- Erythropoiesis-Stimulating Agent Protects Against Kidney Fibrosis by Inhibiting G2/M Cell Cycle Arrest.Cells · 2025Article
- IER5 Negatively Regulates Cdc25B Expression in HeLa Cells After Gamma Ray Irradiation.BioMed research international · 2025Article
- Catalytic Subunit of Protein Phosphatase 2A (PP2Ac) Influences the Meiosis Initiation During Spermatocyte Meiosis Prophase I.Reproductive sciences (Thousand Oaks, Calif.) · 2022Article
- From AKI to CKD: Maladaptive Repair and the Underlying Mechanisms.International journal of molecular sciences · 2022Review
- Review
- The Connection Between Cell Fate and Telomere.Advances in experimental medicine and biology · 2021Review
- Understanding MAPK Signaling Pathways in Apoptosis.International journal of molecular sciences · 2020Review
- Epithelial Cell Cycle Behaviour in the Injured Kidney.International journal of molecular sciences · 2018Review
- Oxidative stress preconditioning of mouse perivascular myogenic progenitors selects a subpopulation of cells with a distinct survival advantage in vitro and in vivo.Cell death & disease · 2018Article
- Phosphatases and kinases regulating CDC25 activity in the cell cycle: clinical implications of CDC25 overexpression and potential treatment strategies.Molecular and cellular biochemistry · 2016Review
- Effect of lentivirus-mediated survivin transfection on the morphology and apoptosis of nucleus pulposus cells derived from degenerative human disc in vitro.International journal of molecular medicine · 2015Article
- Cell cycle arrest and the evolution of chronic kidney disease from acute kidney injury.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2015Review
- A small molecule, MTBT, prevents cancer cell growth by activating p38 MAPK.Anti-cancer drugs · 2014Article
- ATM/ATR-dependent Tyr15 phosphorylation of cyclin-dependent kinases in response to hydroxyurea in Vicia faba root meristem cells.Protoplasma · 2013Article
- MC1R and cAMP signaling inhibit cdc25B activity and delay cell cycle progression in melanoma cells.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Transcript and protein profiling identifies signaling, growth arrest, apoptosis, and NF-κB survival signatures following GNRH receptor activation.Endocrine-related cancer · 2013Article
- Growth inhibition of human hepatocellular carcinoma cells by overexpression of G-protein-coupled receptor kinase 2.Journal of cellular physiology · 2012Article
- Expanding applications of chemical genetics in signal transduction.Cell cycle (Georgetown, Tex.) · 2012Article
- Cascades of transcription regulation during liver regeneration.The international journal of biochemistry & cell biology · 2011Review
- Mitotic phosphorylation of Cdc25B Ser321 disrupts 14-3-3 binding to the high affinity Ser323 site.The Journal of biological chemistry · 2010Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of the mitogen-activated protein kinase (MAPK) pathway by growth factors or phorbol esters during G(2) phase delays entry into mitosis; however, the role of the MAPK pathway during G(2)/M progression remains controversial. Here, we demonstrate that activation of the MAPK pathway with either epidermal growth factor or 12-O-tetradecanoylphorbol-13-acetate induces a G(2) phase delay independent of known G(2) phase checkpoint pathways but was specifically dependent on MAPK/extracellular signal-regulated kinase kinase (MEK1). Activation of MAPK signaling also blocked exit from a G(2) phase checkpoint arrest. Both the G(2) phase delay and blocked exit from the G(2) checkpoint arrest were mediated by the MEK1-dependent destabilization of the critical G(2)/M regulator cdc25B. Reintroduction of cdc25B overcame the MEK1-dependent G(2) phase delay. Thus, we have demonstrated a new function for MEK1 that controls G(2)/M progression by regulating the stability of cdc25B. This represents a novel mechanism by which factors that activate MAPK signaling can influence the timing of entry into mitosis, particularly exit from a G(2) phase checkpoint arrest.
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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.