ArticleMolecular cell2011
Switching Cdk2 on or off with small molecules to reveal requirements in human cell proliferation.
Article in Molecular cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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
57 citing papers in PubMed, 84 citations in OpenAlex.
- Adaptive Replication Fork Acceleration by CDK1-Cyclin B1 Sustains Genome Duplication despite Impaired Origin Firing.bioRxiv : the preprint server for biology · 2026Article
- Identification and inhibition of the Cyclin D Rb-docking interface that drives cell division.bioRxiv : the preprint server for biology · 2026Article
- Targeted Immunotherapies for Cancers.Cancers · 2023Article
- Cyclin-dependent kinases: Masters of the eukaryotic universe.Wiley interdisciplinary reviews. RNA · 2023Review
- CDK2 regulates collapsed replication fork repair in CCNE1-amplified ovarian cancer cells via homologous recombination.NAR cancer · 2023Article
- Development of allosteric and selective CDK2 inhibitors for contraception with negative cooperativity to cyclin binding.Nature communications · 2023Article
- CDK4/6 initiates Rb inactivation and CDK2 activity coordinates cell-cycle commitment and G1/S transition.Scientific reports · 2022Article
- A ROS-dependent mechanism promotes CDK2 phosphorylation to drive progression through S phase.Developmental cell · 2022Article
- Degron Tagging Using mAID and SMASh Tags in RPE-1 Cells.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Integrating Old and New Paradigms of G1/S Control.Molecular cell · 2020Review
- Release from cell cycle arrest with Cdk4/6 inhibitors generates highly synchronized cell cycle progression in human cell culture.Open biology · 2020Article
- A novel landscape of nuclear human CDK2 substrates revealed by in situ phosphorylation.Science advances · 2020Article
- Article
- Induction of G0/G1 phase arrest and apoptosis by CRISPR/Cas9-mediated knockout of CDK2 in A375 melanocytes.Molecular and clinical oncology · 2020Article
- Transient Hysteresis in CDK4/6 Activity Underlies Passage of the Restriction Point in G1.Molecular cell · 2019Article
- Cyclin D-Cdk4,6 Drives Cell-Cycle Progression via the Retinoblastoma Protein's C-Terminal Helix.Molecular cell · 2019Article
- Phosphoregulation of the oncogenic protein regulator of cytokinesis 1 (PRC1) by the atypical CDK16/CCNY complex.Experimental & molecular medicine · 2019Article
- Regulation of the initiation of DNA replication in human cells.DNA repair · 2018Review
- NOP14 inhibits melanoma proliferation and metastasis by regulating Wnt/β-catenin signaling pathway.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · 2018Article
- A Precise Cdk Activity Threshold Determines Passage through the Restriction Point.Molecular cell · 2018Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Multiple cyclin-dependent kinases (CDKs) control eukaryotic cell division, but assigning specific functions to individual CDKs remains a challenge. During the mammalian cell cycle, Cdk2 forms active complexes before Cdk1, but lack of Cdk2 protein does not block cell-cycle progression. To detect requirements and define functions for Cdk2 activity in human cells when normal expression levels are preserved, and nonphysiologic compensation by other CDKs is prevented, we replaced the wild-type kinase with a version sensitized to specific inhibition by bulky adenine analogs. The sensitizing mutation also impaired a noncatalytic function of Cdk2 in restricting assembly of cyclin A with Cdk1, but this defect could be corrected by both inhibitory and noninhibitory analogs. This allowed either chemical rescue or selective antagonism of Cdk2 activity in vivo, to uncover a requirement in cell proliferation, and nonredundant, rate-limiting roles in restriction point passage and S phase entry.
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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.