ArticleCell cycle (Georgetown, Tex.)2010
Putting one step before the other: distinct activation pathways for Cdk1 and Cdk2 bring order to the mammalian cell cycle.
Article in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The trial behind it
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Integrated DFT, molecular docking, and molecular dynamics investigation of some novel 2-thiohydantoin analogues as potent CDK2 inhibitors for anticancer therapy.Scientific reports · 2026Article
- Dual treatment with Val-083 and AZD1775 shows potent anti-tumor activity in diffuse midline glioma models.NPJ precision oncology · 2025Article
- Preparation for DNA replication: the key to a successful S phase.FEBS letters · 2019Review
- Neuronal cell cycle: the neuron itself and its circumstances.Cell cycle (Georgetown, Tex.) · 2015Review
- The CDK Network: Linking Cycles of Cell Division and Gene Expression.Genes & cancer · 2012Article
- Mammalian interphase cdks: dispensable master regulators of the cell cycle.Genes & cancer · 2012Article
- Why minimal is not optimal: driving the mammalian cell cycle--and drug discovery--with a physiologic CDK control network.Cell cycle (Georgetown, Tex.) · 2012Article
- Switching Cdk2 on or off with small molecules to reveal requirements in human cell proliferation.Molecular cell · 2011Article
- Fluorescent peptide biosensor for probing the relative abundance of cyclin-dependent kinases in living cells.PloS one · 2011Article
- Coordinate regulation of histone mRNA metabolism and DNA replication: cyclin A/cdk1 is involved in inactivation of histone mRNA metabolism and DNA replication at the end of S phase.Cell cycle (Georgetown, Tex.) · 2010Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Eukaryotic cell division is controlled by the activity of cyclin-dependent kinases (CDKs). Cdk1 and Cdk2, which function at different stages of the mammalian cell cycle, both require cyclin-binding and phosphorylation of the activation (T-) loop for full activity, but differ with respect to the order in which the two steps occur in vivo. To form stable complexes with either of its partners-cyclins A and B-Cdk1 must be phosphorylated on its T-loop, but that phosphorylation in turn depends on the presence of cyclin. Cdk2 can follow a kinetically distinct path to activation in which T-loop phosphorylation precedes cyclin-binding, and thereby out-compete the more abundant Cdk1 for limiting amounts of cyclin A. Mathematical modeling suggests this could be a principal basis for the temporal ordering of CDK activation during S phase, which may dictate the sequence in which replication origins fire. Still to be determined are how: (1) the activation machinery discriminates between closely related CDKs, and (2) coordination of the cell cycle is affected when this mechanism of pathway insulation breaks down.
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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.