ArticleMolecular and cellular biology2001
Absence of apparent phenotype in mice lacking Cdc25C protein phosphatase.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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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.
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Who cites it
55 citing papers in PubMed, 188 citations in OpenAlex.
- Targeting KIFC1 to disrupt centrosome clustering and trigger anaphase catastrophe in small-cell lung cancer.JCI insight · 2026Article
- The subcortical maternal complex modulates the cell cycle during early mammalian embryogenesis via 14-3-3.Nature communications · 2024Article
- CHK1-CDC25A-CDK1 regulate cell cycle progression and protect genome integrity in early mouse embryos.EMBO reports · 2023Article
- Article
- Downregulation of CDC25C in NPCs Disturbed Cortical Neurogenesis.International journal of molecular sciences · 2023Article
- Mechanisms of Oocyte Maturation and Related Epigenetic Regulation.Frontiers in cell and developmental biology · 2021Review
- YWHA (14-3-3) protein isoforms and their interactions with CDC25B phosphatase in mouse oogenesis and oocyte maturation.BMC developmental biology · 2019Article
- The subcellular location of cyclin B1 and CDC25 associated with the formation of polyploid giant cancer cells and their clinicopathological significance.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Review
- Human TRIB2 Oscillates during the Cell Cycle and Promotes Ubiquitination and Degradation of CDC25C.International journal of molecular sciences · 2016Article
- Acetylation and deacetylation of Cdc25A constitutes a novel mechanism for modulating Cdc25A functions with implications for cancer.Oncotarget · 2016Article
- WNT/β-Catenin Signaling Regulates Multiple Steps of Myogenesis by Regulating Step-Specific Targets.Molecular and cellular biology · 2015Article
- The biochemistry of mitosis.Cold Spring Harbor perspectives in biology · 2015Review
- Therapeutic targeting the cell division cycle 25 (CDC25) phosphatases in human acute myeloid leukemia--the possibility to target several kinases through inhibition of the various CDC25 isoforms.Molecules (Basel, Switzerland) · 2014Review
- A PREVIOUSLY UNKNOWN UNIQUE CHALLENGE FOR INHIBITORS OF SYK ATP-BINDING SITE: ROLE OF SYK AS A CELL CYCLE CHECKPOINT REGULATOR.EBioMedicine · 2014Article
- Coordination of cell proliferation and cell fate determination by CES-1 snail.PLoS genetics · 2013Article
- Cdc25B phosphatase participates in maintaining metaphase II arrest in mouse oocytes.Molecules and cells · 2013Article
- Gain-of-function mutations of PPM1D/Wip1 impair the p53-dependent G1 checkpoint.The Journal of cell biology · 2013Article
- Cdc25A activity is required for the metaphase II arrest in mouse oocytes.Journal of cell science · 2013Article
- The role of 14-3-3ε interaction with phosphorylated Cdc25B at its Ser321 in the release of the mouse oocyte from prophase I arrest.PloS one · 2013Article
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
The Cdc25 family of protein phosphatases positively regulate the cell division cycle by activating cyclin-dependent protein kinases. In humans and rodents, three Cdc25 family members denoted Cdc25A, -B, and -C have been identified. The murine forms of Cdc25 exhibit distinct patterns of expression both during development and in adult mouse tissues. In order to determine unique contributions made by the Cdc25C protein phosphatase to embryonic and adult cell cycles, mice lacking Cdc25C were generated. We report that Cdc25C(-/-) mice are viable and do not display any obvious abnormalities. Among adult tissues in which Cdc25C is detected, its transcripts are most abundant in testis, followed by thymus, ovary, spleen, and intestine. Mice lacking Cdc25C were fertile, indicating that Cdc25C does not contribute an essential function during spermatogenesis or oogenesis in the mouse. T- and B-cell development was also found to be normal in Cdc25C(-/-) mice, and Cdc25C(-/-) mouse splenic T and B cells exhibited normal proliferative responses in vitro. Finally, the phosphorylation status of Cdc2, the timing of entry into mitosis, and the cellular response to DNA damage were unperturbed in mouse embryo fibroblasts lacking Cdc25C. These findings indicate that Cdc25A and/or Cdc25B may compensate for loss of Cdc25C in the mouse.
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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.