ArticleOncogene2007
Differential mitotic degradation of the CDC25B phosphatase variants.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 27 citations in OpenAlex.
- Revealing β-TrCP activity dynamics in live cells with a genetically encoded biosensor.Nature communications · 2022Article
- Phosphatases in Mitosis: Roles and Regulation.Biomolecules · 2019Review
- Neurogenic decisions require a cell cycle independent function of the CDC25B phosphatase.eLife · 2018Article
- Tripartite degrons confer diversity and specificity on regulated protein degradation in the ubiquitin-proteasome system.Nature communications · 2016Article
- LSD1 is essential for oocyte meiotic progression by regulating CDC25B expression in mice.Nature communications · 2015Article
- Overexpression of mutant cell division cycle 25 homolog B (CDC25B) enhances the efficiency of selection in Chinese hamster ovary cells.Cytotechnology · 2013Article
- Genotoxic stress modulates CDC25C phosphatase alternative splicing in human breast cancer cell lines.Molecular oncology · 2012Article
- Unscheduled expression of CDC25B in S-phase leads to replicative stress and DNA damage.Molecular cancer · 2010Article
- CDC25A phosphatase controls meiosis I progression in mouse oocytes.Developmental biology · 2008Article
- Small interfering RNA targeting CDC25B inhibits liver tumor growth in vitro and in vivo.Molecular cancer · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CDC25 phosphatases control cell-cycle progression by dephosphorylating and activating cyclin-dependent kinases. CDC25B, one of the three members of this family in human cells, is thought to regulate initial mitotic events. CDC25B is an unstable protein whose proteasomal degradation is proposed to be controlled by beta-TrCP. Here, we have investigated the regulation of CDC25B during mitosis, using time-lapse video microscopy. We found that CDC25B expression is high during early mitosis, and that its degradation occurs after the metaphase-anaphase transition and cyclin B1 destruction. We also show that CDC25B degradation after metaphase is dependent on the integrity of the KEN-box and RRKSE motifs that are located within the alternatively spliced B domain, and that the CDC25B2 splice variant, that lacks this domain, is stable during mitosis. Furthermore, we show that the N-terminal region of CDC25B, encompassing the B domain, undergoes major conformational changes during mitosis that can be monitored by intramolecular fluorescence resonance energy transfer variation of specific CDC25B biosensors. This study demonstrates that CDC25B splice variants have differential mitotic stabilities, a feature that is likely to have major consequences on the local control of cyclin-dependent kinase-cyclin activities during mitotic progression.
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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.