ArticleCancer research2007
Cyclin-dependent kinase 2 dependent phosphorylation of ATRIP regulates the G2-M checkpoint response to DNA damage.
Article in Cancer research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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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
40 citing papers in PubMed, 65 citations in OpenAlex.
- Phosphorylation-dependent regulation of Eleven Lysine Rich Leukemia (ELL) uncovered by quantitative global phosphoproteomic analysis.Molecular genetics and genomics : MGG · 2026Article
- Phosphoproteome Remodeling upon CDK1 Inhibition Restricts HSV-1 IE Gene Transcription and Replication.Cells · 2026Article
- UHRF1 Controls the Timing of RAD51 Removal During DNA Damage Repair Through Suppressing RFWD3.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- ATR-CHK1 Axis Inhibitors in Gastric Cancer Treatment.International journal of molecular sciences · 2025Review
- Molecular subtyping of endometrial carcinoma cell lines uncovers subtype-specific targetable vulnerabilities.NPJ precision oncology · 2025Article
- CDK2 regulates collapsed replication fork repair in CCNE1-amplified ovarian cancer cells via homologous recombination.NAR cancer · 2023Article
- A DNA damage-induced phosphorylation circuit enhances Mec1Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Cell cycle regulators and bone: development and regeneration.Cell & bioscience · 2023Review
- PARP1 Inhibitor Combined With Oxaliplatin Efficiently Suppresses Oxaliplatin Resistance in Gastric Cancer-Derived Organoids via Homologous Recombination and the Base Excision Repair Pathway.Frontiers in cell and developmental biology · 2021Article
- Deciphering MET-dependent modulation of global cellular responses to DNA damage by quantitative phosphoproteomics.Molecular oncology · 2020Article
- Review
- Persistent repair intermediates induce senescence.Nature communications · 2018Article
- Cdk2 strengthens the intra-S checkpoint and counteracts cell cycle exit induced by DNA damage.Scientific reports · 2017Article
- The essential kinase ATR: ensuring faithful duplication of a challenging genome.Nature reviews. Molecular cell biology · 2017Review
- Residual Cdk1/2 activity after DNA damage promotes senescence.Aging cell · 2017Article
- Structural prediction of the interaction of the tumor suppressor p27BMC bioinformatics · 2017Article
- CDK-mediated RNF4 phosphorylation regulates homologous recombination in S-phase.Nucleic acids research · 2015Article
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Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
The ATR-ATRIP kinase complex regulates cellular responses to DNA damage and replication stress. Mass spectrometry was used to identify phosphorylation sites on ATR and ATRIP to understand how the kinase complex is regulated by post-translational modifications. Two novel phosphorylation sites on ATRIP were identified, S224 and S239. Phosphopeptide-specific antibodies to S224 indicate that it is phosphorylated in a cell cycle-dependent manner. S224 matches a consensus site for cyclin-dependent kinase (CDK) phosphorylation and is phosphorylated by CDK2-cyclin A in vitro. S224 phosphorylation in cells is sensitive to CDK2 inhibitors. Mutation of S224 to alanine causes a defect in the ATR-ATRIP-dependent maintenance of the G(2)-M checkpoint to ionizing and UV radiation. Thus, ATRIP is a CDK2 substrate, and CDK2-dependent phosphorylation of S224 regulates the ability of ATR-ATRIP to promote cell cycle arrest in response to DNA damage.
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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.