Evidence map›Paper›PMID 42337302›Full record

ReviewCommunications biology2026

Exploring the multifaceted Dbf4-dependent kinase from temporal, spatial, and substrate repertoire perspectives.

Lorenzo Galanti, Boris Pfander

Abstract readReview
In one paragraph

Review in Communications biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Lorenzo GalantiCell Biology, TU Dortmund Life Science Center (DOLCE), Department of Chemistry and Chemical Biology, TU Dortmund University, Dortmund, Germany.ORCID 0000-0003-2538-3581
Boris PfanderCell Biology, TU Dortmund Life Science Center (DOLCE), Department of Chemistry and Chemical Biology, TU Dortmund University, Dortmund, Germany. boris.pfander@tu-dortmund.de.ORCID 0000-0003-2180-5054

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) 466479039
6 · The paper itself

Abstract

The Dbf4‑dependent kinase (DDK), composed of the catalytic subunit Cdc7 and the regulatory subunit Dbf4, is a serine/threonine kinase traditionally defined as an essential activator of DNA replication. Here, we review DDK function from three complementary perspectives: its temporal regulation during the cell cycle, its spatial organization on chromosomes, and its expanding substrate repertoire. These perspectives reveal that DDK acts beyond DNA replication, targeting proteins involved in chromosome segregation, DNA damage responses and homologous recombination. Together, they redefine DDK as multifunctional genome integrity kinase which coordinates cell cycle progression and genome stability offering a unique therapeutic potential in cancer therapy.

Indexed as

Cell Cycle ProteinsProtein Serine-Threonine KinasesAnimalsCell CycleDNA DamageDNA ReplicationGenomic InstabilityHumansSubstrate SpecificityCDC7 protein, humanCell Cycle ProteinsDBF4 protein, humanProtein Serine-Threonine Kinases

Identifiers

PMID42337302
PMCPMC13291351

What OpenQuestion holds

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Registered trials

None linked

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.