ArticleProceedings of the National Academy of Sciences of the United States of America2013
Essential role for Cdk2 inhibitory phosphorylation during replication stress revealed by a human Cdk2 knockin mutation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
42 citing papers in PubMed, 76 citations in OpenAlex.
- WEE1 opposes APC/CNature · 2026Article
- Illuminating the Co-Phosphoregulatory Network of the Dark Kinase STK10 by Omics Approaches.BioMed research international · 2026Article
- A high-resolution, nanopore-based artificial intelligence assay for DNA replication stress in human cancer cells.Nature communications · 2025Article
- Genetic modeling of ELP1-associated Sonic hedgehog medulloblastoma identifies MDM2 as a selective therapeutic target.Cancer cell · 2025Article
- The S-Phase Arrest of Host Cells Caused by an Alpha-Herpesvirus Genome Replication Facilitates Viral Recruitment of RNA Polymerase II to Transcribe Viral Genes.Cell proliferation · 2025Article
- Article
- Identification of CDKN3 overexpression as a marker of poor prognosis and potential therapeutic target in low-grade glioma.Scientific reports · 2025Article
- Multi-proteomics and interactome dataset of tick-borne encephalitis virus infected host cells.Scientific data · 2024Article
- Comprehensive proteogenomic characterization of rare kidney tumors.Cell reports. Medicine · 2024Article
- Ki-67 is necessary during DNA replication for fork protection and genome stability.Genome biology · 2024Article
- The dimeric deubiquitinase USP28 integrates 53BP1 and MYC functions to limit DNA damage.Nucleic acids research · 2024Article
- CDK4/6 inhibitor-induced bone marrow micronuclei might be caused by cell cycle arrest during erythropoiesis.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2024Article
- Cyclin A-CDK1 suppresses the expression of the CDK1 activator CDC25A to safeguard timely mitotic entry.The Journal of biological chemistry · 2023Article
- ABRO1 arrests cardiomyocyte proliferation and myocardial repair by suppressing PSPH.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Identification of a Molecularly-Defined Subset of Breast and Ovarian Cancer Models that Respond to WEE1 or ATR Inhibition, Overcoming PARP Inhibitor Resistance.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Human DDK rescues stalled forks and counteracts checkpoint inhibition at unfired origins to complete DNA replication.Molecular cell · 2021Article
- Cyclin E/CDK2: DNA Replication, Replication Stress and Genomic Instability.Frontiers in cell and developmental biology · 2021Review
- PTEN and DNA-PK determine sensitivity and recovery in response to WEE1 inhibition in human breast cancer.eLife · 2020Article
- Proteogenomic Characterization of Ovarian HGSC Implicates Mitotic Kinases, Replication Stress in Observed Chromosomal Instability.Cell reports. Medicine · 2020Article
- Inhibition of the ATR-CHK1 Pathway in Ewing Sarcoma Cells Causes DNA Damage and Apoptosis via the CDK2-Mediated Degradation of RRM2.Molecular cancer research : MCR · 2020Article
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 2 institutions in 1 country.
Funding
Abstract
Cyclin-dependent kinases (Cdks) coordinate cell division, and their activities are tightly controlled. Phosphorylation of threonine 14 (T14) and tyrosine 15 (Y15) inhibits Cdks and regulates their activities in numerous physiologic contexts. Although the roles of Cdk1 inhibitory phosphorylation during mitosis are well described, studies of Cdk2 inhibitory phosphorylation during S phrase have largely been indirect. To specifically study the functions of Cdk2 inhibitory phosphorylation, we used gene targeting to make an endogenous Cdk2 knockin allele in human cells, termed Cdk2AF, which prevents Cdk2 T14 and Y15 phosphorylation. Cdk2AF caused premature S-phase entry, rapid cyclin E degradation, abnormal DNA replication, and genome instability. Cdk2AF cells also exhibited strikingly abnormal responses to replication stress, accumulated irreparable DNA damage, and permanently exited the cell cycle after transient exposure to S-phase inhibitors. Our results reveal the specific and essential roles of Cdk2 inhibitory phosphorylation in the successful execution of the replication stress checkpoint response and in maintaining genome integrity.
Indexed as
Identifiers
What OpenQuestion holds
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.