ArticleMolecular and cellular biology2012
Loss of cyclin-dependent kinase 2 (CDK2) inhibitory phosphorylation in a CDK2AF knock-in mouse causes misregulation of DNA replication and centrosome duplication.
Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Review
- Cyclin E/CDK2: DNA Replication, Replication Stress and Genomic Instability.Frontiers in cell and developmental biology · 2021Review
- A novel function for CDK2 activity at meiotic crossover sites.PLoS biology · 2020Article
- CDK2 kinase activity is a regulator of male germ cell fate.Development (Cambridge, England) · 2019Article
- Oligodendrocyte Intrinsic miR-27a Controls Myelination and Remyelination.Cell reports · 2019Article
- Diverse roles for CDK-associated activity during spermatogenesis.FEBS letters · 2019Review
- Cell cycle regulation and hematologic malignancies.Blood science (Baltimore, Md.) · 2019Review
- Premature activation of Cdk1 leads to mitotic events in S phase and embryonic lethality.Oncogene · 2019Article
- Article
- The genetics of human infertility by functional interrogation of SNPs in mice.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Essential role for Cdk2 inhibitory phosphorylation during replication stress revealed by a human Cdk2 knockin mutation.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Signaling pathways that control cell proliferation.Cold Spring Harbor perspectives in biology · 2013Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Cyclin-dependent kinase 1 (CDK1) inhibitory phosphorylation controls the onset of mitosis and is essential for the checkpoint pathways that prevent the G(2)- to M-phase transition in cells with unreplicated or damaged DNA. To address whether CDK2 inhibitory phosphorylation plays a similar role in cell cycle regulation and checkpoint responses at the start of the S phase, we constructed a mouse strain in which the two CDK2 inhibitory phosphorylation sites, threonine 14 and tyrosine 15, were changed to alanine and phenylalanine, respectively (CDK2AF). This approach showed that inhibitory phosphorylation of CDK2 had a major role in controlling cyclin E-associated kinase activity and thus both determined the timing of DNA replication in a normal cell cycle and regulated centrosome duplication. Further, DNA damage in G(1) CDK2AF cells did not downregulate cyclin E-CDK2 activity when the CDK inhibitor p21 was also knocked down. We were surprised to find that this was insufficient to cause cells to bypass the checkpoint and enter the S phase. This led to the discovery of two previously unrecognized pathways that control the activity of cyclin A at the G(1) DNA damage checkpoint and may thereby prevent S-phase entry even when cyclin E-CDK2 activity is deregulated.
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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.