ArticleNeoplasia (New York, N.Y.)2018
DDK Has a Primary Role in Processing Stalled Replication Forks to Initiate Downstream Checkpoint Signaling.
Article in Neoplasia (New York, N.Y.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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Who cites it
16 citing papers in PubMed.
- 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
- ATR and TopBP1 oppose to control dormant origin activity and global replication dynamics, providing a first defense against replication stress.Nucleic acids research · 2026Article
- CDC7 is a targetable regulator of advanced prostate cancer.Scientific reports · 2025Article
- Dbf4-dependent kinase promotes cell cycle controlled resection of DNA double-strand breaks and repair by homologous recombination.Nature communications · 2024Article
- The nucleolar protein GNL3 prevents resection of stalled replication forks.EMBO reports · 2023Article
- DDK: The Outsourced Kinase of Chromosome Maintenance.Biology · 2022Review
- Rad51-mediated replication of damaged templates relies on monoSUMOylated DDK kinase.Nature communications · 2022Article
- Article
- The yeast Dbf4 ZnCurrent genetics · 2022Article
- CDC7 kinase (DDK) inhibition disrupts DNA replication leading to mitotic catastrophe in Ewing sarcoma.Cell death discovery · 2022Article
- Lactate induces aberration in the miR-30a-DBF4 axis to promote the development of gastric cancer and weakens the sensitivity to 5-Fu.Cancer cell international · 2021Article
- Dbf4-Dependent Kinase: DDK-ated to post-initiation events in DNA replication.Cell cycle (Georgetown, Tex.) · 2021Review
- Article
- Human DDK rescues stalled forks and counteracts checkpoint inhibition at unfired origins to complete DNA replication.Molecular cell · 2021Article
- CDC7 kinase promotes MRE11 fork processing, modulating fork speed and chromosomal breakage.EMBO reports · 2020Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
CDC7-DBF4 kinase (DDK) initiates DNA replication in eukaryotes by activating the replicative MCM helicase. DDK has diverse and apparently conflicting roles in the replication checkpoint response in various organisms, but the underlying mechanisms are far from settled. We show that human DDK promotes limited resection of newly synthesized DNA at stalled replication forks or sites of DNA damage to initiate replication checkpoint signaling. DDK is also required for efficient fork restart and G2/M cell cycle arrest. DDK exhibits genetic interactions with the ssDNA exonuclease EXO1 and phosphorylates EXO1 in vitro. EXO1 is also required for nascent strand degradation following exposure to HU, so DDK might regulate EXO1 directly. Lastly, sublethal DDK inhibition causes various mitotic abnormalities, which is consistent with a checkpoint deficiency. In summary, DDK has a primary and previously undescribed role in the replication checkpoint to promote ssDNA accumulation at stalled forks, which is required to initiate a robust checkpoint response and cell cycle arrest to maintain genome integrity.
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