ArticleMolecular biology of the cell2005
Changes in regulatory phosphorylation of Cdc25C Ser287 and Wee1 Ser549 during normal cell cycle progression and checkpoint arrests.
Article in Molecular biology of the cell, 2005. 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.
- Compound C Inhibits Renca Renal Epithelial Carcinoma Growth in Syngeneic Mouse Models by Blocking Cell Cycle Progression, Adhesion and Invasion.International journal of molecular sciences · 2022Article
- The role of CDC25C in cell cycle regulation and clinical cancer therapy: a systematic review.Cancer cell international · 2020Review
- Vertebrate Reproduction.Cold Spring Harbor perspectives in biology · 2015Review
- Transmembrane signal transduction in oocyte maturation and fertilization: focusing on Xenopus laevis as a model animal.International journal of molecular sciences · 2014Review
- Changes in oscillatory dynamics in the cell cycle of early Xenopus laevis embryos.PLoS biology · 2014Article
- Molecular mechanisms of garlic-derived allyl sulfides in the inhibition of skin cancer progression.Annals of the New York Academy of Sciences · 2012Review
- The M phase kinase Greatwall (Gwl) promotes inactivation of PP2A/B55delta, a phosphatase directed against CDK phosphosites.Molecular biology of the cell · 2009Article
- Estrogen inhibits ATR signaling to cell cycle checkpoints and DNA repair.Molecular biology of the cell · 2009Article
- Discovery of gene expression-based pharmacodynamic biomarker for a p53 context-specific anti-tumor drug Wee1 inhibitor.Molecular cancer · 2009Article
- Aven-dependent activation of ATM following DNA damage.Current biology : CB · 2008Article
- Roles of Greatwall kinase in the regulation of cdc25 phosphatase.Molecular biology of the cell · 2008Article
- Human immunodeficiency virus type 1 Vpr induces cell cycle G2 arrest through Srk1/MK2-mediated phosphorylation of Cdc25.Journal of virology · 2008Article
- Control of mitotic exit by PP2A regulation of Cdc25C and Cdk1.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Cdc25 and Wee1: analogous opposites?Cell division · 2007Article
- Role for non-proteolytic control of M-phase-promoting factor activity at M-phase exit.PloS one · 2007Article
- Role for the PP2A/B56delta phosphatase in regulating 14-3-3 release from Cdc25 to control mitosis.Cell · 2006Article
- Antagonism of Chk1 signaling in the G2 DNA damage checkpoint by dominant alleles of Cdr1.Genetics · 2006Article
- Ubiquitin and SUMO systems in the regulation of mitotic checkpoints.Trends in biochemical sciences · 2006Review
- Aurora A, mitotic entry, and spindle bipolarity.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- A role for PP1 in the Cdc2/Cyclin B-mediated positive feedback activation of Cdc25.Molecular biology of the cell · 2006Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Entry into mitosis is catalyzed by cdc2 kinase. Previous work identified the cdc2-activating phosphatase cdc25C and the cdc2-inhibitory kinase wee1 as targets of the incomplete replication-induced kinase Chk1. Further work led to the model that checkpoint kinases block mitotic entry by inhibiting cdc25C through phosphorylation on Ser287 and activating wee1 through phosphorylation on Ser549. However, almost all conclusions underlying this idea were drawn from work using recombinant proteins. Here, we report that in the early Xenopus egg cell cycles, phosphorylation of endogenous cdc25C Ser287 is normally high during interphase and shows no obvious increase after checkpoint activation. By contrast, endogenous wee1 Ser549 phosphorylation is low during interphase and increases after activation of either the DNA damage or replication checkpoints; this is accompanied by a slight increase in wee1 kinase activity. Blocking mitotic entry by adding the catalytic subunit of PKA also results in increased wee1 Ser549 phosphorylation and maintenance of cdc25C Ser287 phosphorylation. These results argue that in response to checkpoint activation, endogenous wee1 is indeed a critical responder that functions by repressing the cdc2-cdc25C positive feedback loop. Surprisingly, endogenous wee1 Ser549 phosphorylation is highest during mitosis just after the peak of cdc2 activity. Treatments that block inactivation of cdc2 result in further increases in wee1 Ser549 phosphorylation, suggesting a previously unsuspected role for wee1 in mitosis.
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