Evidence map›Paper›PMID 35119917›Full record

ArticleScience advances2022

The CDK1-TOPBP1-PLK1 axis regulates the Bloom's syndrome helicase BLM to suppress crossover recombination in somatic cells.

Chiara Balbo Pogliano, Ilaria Ceppi, Sara Giovannini, Vasiliki Petroulaki, Nathan Palmer, Federico Uliana, Marco Gatti, Kristina Kasaciunaite, Raimundo Freire, Ralf Seidel and 3 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. 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

13 authors at 6 institutions in 4 countries.

Chiara Balbo PoglianoInstitute of Biochemistry, ETH Zürich, Otto-Stern-Weg 3, 8093 Zürich, Switzerland.ORCID 0000-0001-9192-7773
Ilaria CeppiInstitute for Research in Biomedicine, Faculty of Biomedical Sciences, Università della Svizzera italiana (USI), 6500 Bellinzona, Switzerland.ORCID 0000-0001-6496-8983
Sara GiovanniniInstitute of Biochemistry, ETH Zürich, Otto-Stern-Weg 3, 8093 Zürich, Switzerland.ORCID 0000-0002-8916-476X
Vasiliki PetroulakiDepartment of Chromosome Biology, Max Perutz Labs, University of Vienna, Vienna Biocenter, Vienna, Austria.ORCID 0000-0002-3249-2893
Nathan PalmerDepartment of Chromosome Biology, Max Perutz Labs, University of Vienna, Vienna Biocenter, Vienna, Austria.ORCID 0000-0002-1913-9454
Federico UlianaInstitute of Biochemistry, ETH Zürich, Otto-Stern-Weg 3, 8093 Zürich, Switzerland.
Marco GattiDepartment of Molecular Mechanisms of Disease, University of Zurich, Winterthurerstrasse 190, 8057 Zürich, Switzerland.ORCID 0000-0001-5307-0123
Kristina KasaciunaitePeter Debye Institute for Soft Matter Physics, Universität Leipzig, 04103 Leipzig, Germany.
Raimundo FreireUnidad de Investigación, Hospital Universitario de Canarias-FIISC, Ofra s/n, 38320 La Laguna, Tenerife, Spain.ORCID 0000-0003-4473-8894
Ralf SeidelPeter Debye Institute for Soft Matter Physics, Universität Leipzig, 04103 Leipzig, Germany.
Matthias AltmeyerDepartment of Molecular Mechanisms of Disease, University of Zurich, Winterthurerstrasse 190, 8057 Zürich, Switzerland.
Petr CejkaInstitute of Biochemistry, ETH Zürich, Otto-Stern-Weg 3, 8093 Zürich, Switzerland.ORCID 0000-0002-9087-032X
Joao MatosInstitute of Biochemistry, ETH Zürich, Otto-Stern-Weg 3, 8093 Zürich, Switzerland.ORCID 0000-0002-3754-3709
ETH Zurich · CHUniversity of Vienna · ATLeipzig University · DEZHAW Zurich University of Applied Sciences · CHUniversidad de La Laguna · ESUniversità della Svizzera italiana · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bloom's syndrome is caused by inactivation of the BLM helicase, which functions with TOP3A and RMI1-2 (BTR complex) to dissolve recombination intermediates and avoid somatic crossing-over. We show here that crossover avoidance by BTR further requires the activity of cyclin-dependent kinase-1 (CDK1), Polo-like kinase-1 (PLK1), and the DDR mediator protein TOPBP1, which act in the same pathway. Mechanistically, CDK1 phosphorylates BLM and TOPBP1 and promotes the interaction of both proteins with PLK1. This is amplified by the ability of TOPBP1 to facilitate phosphorylation of BLM at sites that stimulate both BLM-PLK1 and BLM-TOPBP1 binding, creating a positive feedback loop that drives rapid BLM phosphorylation at the G

Indexed as

Bloom SyndromeCarrier ProteinsCDC2 Protein KinaseCell Cycle ProteinsDNA-Binding ProteinsGenomic InstabilityHumansNuclear ProteinsPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsRecombination, GeneticRecQ HelicasesCarrier ProteinsCDC2 Protein KinaseCDK1 protein, humanCell Cycle ProteinsDNA-Binding ProteinsNuclear ProteinsPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsRecQ HelicasesTOPBP1 protein, human

Identifiers

PMID35119917
PMCPMC8816346
OpenAlexW4210646538

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.