Evidence map›Paper›PMID 34445496›Full record

ReviewInternational journal of molecular sciences2021

Coordinating DNA Replication and Mitosis through Ubiquitin/SUMO and CDK1.

Antonio Galarreta, Pablo Valledor, Oscar Fernandez-Capetillo, Emilio Lecona

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 2 pooled it
0.7field-weighted citation impact, top 31% of its field
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

8 citing papers in PubMed, 2 syntheses or guidelines pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Multifaceted roles of SUMO in DNA metabolism.Nucleus (Austin, Tex.) · 2024
    Review
  6. Review
  7. Review
  8. Article
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

4 authors at 3 institutions in 2 countries.

Antonio GalarretaGenomic Instability Group, Spanish National Cancer Research Centre (CNIO), 28029 Madrid, Spain.ORCID 0000-0003-2358-7927
Pablo ValledorGenomic Instability Group, Spanish National Cancer Research Centre (CNIO), 28029 Madrid, Spain.
Oscar Fernandez-CapetilloGenomic Instability Group, Spanish National Cancer Research Centre (CNIO), 28029 Madrid, Spain.
Emilio LeconaCentre for Molecular Biology Severo Ochoa (CBMSO, CSIC-UAM), Chromatin, Cancer and the Ubiquitin System Lab, Department of Genome Dynamics and Function, 28049 Madrid, Spain.ORCID 0000-0002-1687-2562
Spanish National Cancer Research Centre · ESCentro de Biología Molecular Severo Ochoa · ESScience for Life Laboratory · SE

Funding

European Research Council ERC-617840Ministerio de Ciencia e Innovación BFU2014-55168-JINMinisterio de Ciencia e Innovación RTI2018-093485-B-I00Ministerio de Ciencia e Innovación RTI2018-102204-B-I00
6 · The paper itself

Abstract

Post-translational modification of the DNA replication machinery by ubiquitin and SUMO plays key roles in the faithful duplication of the genetic information. Among other functions, ubiquitination and SUMOylation serve as signals for the extraction of factors from chromatin by the AAA ATPase VCP. In addition to the regulation of DNA replication initiation and elongation, we now know that ubiquitination mediates the disassembly of the replisome after DNA replication termination, a process that is essential to preserve genomic stability. Here, we review the recent evidence showing how active DNA replication restricts replisome ubiquitination to prevent the premature disassembly of the DNA replication machinery. Ubiquitination also mediates the removal of the replisome to allow DNA repair. Further, we discuss the interplay between ubiquitin-mediated replisome disassembly and the activation of CDK1 that is required to set up the transition from the S phase to mitosis. We propose the existence of a ubiquitin-CDK1 relay, where the disassembly of terminated replisomes increases CDK1 activity that, in turn, favors the ubiquitination and disassembly of more replisomes. This model has important implications for the mechanism of action of cancer therapies that induce the untimely activation of CDK1, thereby triggering premature replisome disassembly and DNA damage.

Indexed as

AnimalsCDC2 Protein KinaseDNA ReplicationHumansMitosisProtein Processing, Post-TranslationalSmall Ubiquitin-Related Modifier ProteinsUbiquitinCDC2 Protein KinaseSmall Ubiquitin-Related Modifier ProteinsUbiquitinCDK1DNA replicationmitosisSUMOubiquitinUSP7

Identifiers

PMID34445496
PMCPMC8395760
OpenAlexW3194191517

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.