ArticleeLife2019
Cdc7 activates replication checkpoint by phosphorylating the Chk1-binding domain of Claspin in human cells.
Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 47 citations in OpenAlex.
- Exploring the multifaceted Dbf4-dependent kinase from temporal, spatial, and substrate repertoire perspectives.Communications biology · 2026Review
- Cyclin E modulates vulnerability to CDC7 kinase inhibition.Oncogenesis · 2026Article
- Fibrillarin and fibrillarin-like their role in cancer progression: new approaches and perspectives.Molecular biology reports · 2026Review
- Claspin and Cancer: Where Are We Now?International journal of molecular sciences · 2025Review
- Chromatin Licensing and DNA Replication Factor 1 (CDT1) Is a Potential Prognostic Biomarker Involved in the Malignant Biological Behavior of Glioma.ACS pharmacology & translational science · 2024Article
- Review
- DBF4, not DRF1, is the crucial regulator of CDC7 kinase at replication forks.The Journal of cell biology · 2024Article
- Nanosystem Delivers Senescence Activators and Immunomodulators to Combat Liver Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The RNA binding proteins LARP4A and LARP4B promote sarcoma and carcinoma growth and metastasis.iScience · 2024Article
- The Interaction between CLSPN Gene Polymorphisms and Alcohol Consumption Contributes to Oral Cancer Progression.International journal of molecular sciences · 2024Article
- Protein kinase Cdc7 supports viral replication by phosphorylatingJournal of virology · 2023Article
- The TIMELESS effort for timely DNA replication and protection.Cellular and molecular life sciences : CMLS · 2023Review
- Claspin-Dependent and -Independent Chk1 Activation by a Panel of Biological Stresses.Biomolecules · 2023Article
- Claspin is Required for Growth Recovery from Serum Starvation through Regulating the PI3K-PDK1-mTOR Pathway in Mammalian Cells.Molecular and cellular biology · 2023Article
- Identification of CDT1 as a prognostic marker in human lung adenocarcinoma using bioinformatics approaches.PeerJ · 2023Article
- CDC7 as a novel biomarker and druggable target in cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Review
- DDK: The Outsourced Kinase of Chromosome Maintenance.Biology · 2022Review
- A rethink about enzymes that drive DNA replication.Nature · 2022Article
- Article
- CHK1 phosphorylates PRIMPOL to promote replication stress tolerance.Science advances · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Replication checkpoint is essential for maintaining genome integrity in response to various replication stresses as well as during the normal growth. The evolutionally conserved ATR-Claspin-Chk1 pathway is induced during replication checkpoint activation. Cdc7 kinase, required for initiation of DNA replication at replication origins, has been implicated in checkpoint activation but how it is involved in this pathway has not been known. Here, we show that Cdc7 is required for Claspin-Chk1 interaction in human cancer cells by phosphorylating CKBD (Chk1-binding-domain) of Claspin. The residual Chk1 activation in Cdc7-depleted cells is lost upon further depletion of casein kinase1 (CK1γ1), previously reported to phosphorylate CKBD. Thus, Cdc7, in conjunction with CK1γ1, facilitates the interaction between Claspin and Chk1 through phosphorylating CKBD. We also show that, whereas Cdc7 is predominantly responsible for CKBD phosphorylation in cancer cells, CK1γ1 plays a major role in non-cancer cells, providing rationale for targeting Cdc7 for cancer cell-specific cell killing.
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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.