Cdc2: A monopotent or pluripotent CDK?
Open accessAbstract
Cell cycle progression is controlled by both extracellular and intracellular signalling molecules. It has been generally believed that cdc2/CDK1 only control G(2)-M transition in mammalian and many other higher eukaryotic cells. Accumulating evidence shows that cdc2 not only promotes G(2)-M transition but is also capable of regulating G(1) progress and G(1)-S transition via association with multiple interphase cyclins; cdc2 activity can be inhibited by p21 and p27, two traditional G(1) CDK inhibitors. In addition, cdc2-cyclin B controls pronuclear union in interphase fertilized eggs. These data suggest that cdc2 may be a pluripotent CDK. Although mechanisms responsible for the multiple functions of cdc2 remain to be further investigated, interactions of cdc2 with pRb and with several important transcription factors may provide a clue to the pluripotent role of cdc2.
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Mangiferin triggers G2/M phase cell cycle arrest via regulation of the CDK1-cyclin B1 signaling pathway.
“Notably, mangiferin has been validated to trigger G2/M phase cell cycle arrest via regulation of the CDK1-cyclin B1 signaling pathway (49)(50)(51).”
From Mangiferin: An effective therapeutic agent against several disorders (Review) (2018) · cites this paper as [49]
The section on cell-cycle progression states that cdc2 (CDK1) interacts with cyclin B to regulate the G2–M transition. It does not mention mangiferin or show that mangiferin causes G2/M arrest through this pathway (searched: mangiferin, cyclin B1, G2/M arrest). (LLM, conf=0.86)
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p130/E2F4 Binds to and Represses the cdc2 Promoter in Response to p53
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Mangiferin: An effective therapeutic agent against several disorders (Review)
Du, S., Liu, H., Lei, T., Xie, X., Wang, H., He, X., Tong, R., & Wang, Y. (2018) · Molecular Medicine Reports · doi:10.3892/mmr.2018.9529 · Cited by 139 · see citing works
“Notably, mangiferin has been validated to trigger G2/M phase cell cycle arrest via regulation of the CDK1-cyclin B1 signaling pathway (49-51).”
Morozkina, S. N., Nhung Vu, T. H., Generalova, Y. E., Snetkov, P. P., & Uspenskaya, M. V. (2021) · Biomolecules · doi:10.3390/biom11010079 · Cited by 82 · see citing works
SAHA and/or MG132 reverse the aggressive phenotypes of glioma cells: An<i>in vitro</i>and vivo study
Yang, X.-F., Zhao, Z.-J., Liu, J.-J., Yang, X.-H., Gao, Y., Zhao, S., Shi, S., Huang, K.-Q., & Zheng, H.-C. (2017) · Oncotarget · doi:10.18632/oncotarget.13680 · Cited by 15 · see citing works
- Authors
- Hu, X., & Moscinski, L. C.
- Affiliations
- Barry University (US)
- ORCID
- Moscinski, L. C.
- Venue
- Cell Proliferation
- Publisher
- Wiley
- Published
- 2011-04-28
- Volume
- 44
- Issue
- 3
- Pages
- 205-211
- ISSN
- 0960-7722 (ISSN-L)
- PMC
- PMC6496858
- OpenAlex
- W1962995704
- Cited by
- 69
- References
- 3
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 2 · 2023: 4 · 2022: 3 · 2021: 6 · 2020: 5 · 2019: 4 · 2018: 4 · 2017: 4 · 2016: 5 · 2015: 9 · 2014: 9 · 2013: 5 · 2012: 5
- FWCI
- 0.56
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cell Proliferation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- cdc2, CDK1, cyclin-dependent kinases, cell cycle regulation, G2/M transition, G1/S transition, p21, p27, Cdc2/cyclin B, pronuclear fusion, zygote, retinoblastoma protein, transcription factors
- MeSH terms
- Animals, Cell Cycle, Gene Expression Regulation, Humans, Models, Biological, Phosphorylation, CDC2 Protein Kinase, Mice, Knockout, Cyclin-Dependent Kinases, Cyclin B, CDC2-CDC28 Kinases, Cyclin-Dependent Kinase Inhibitor p27, Cyclin-Dependent Kinase 4, Cyclin-Dependent Kinase 6, Mice, p21-Activated Kinases
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