Evidence map›Paper›PMID 29950310›Full record

ArticleThe EMBO journal2018

Cdc48/p97 segregase is modulated by cyclin-dependent kinase to determine cyclin fate during G1 progression.

Eva Parisi, Galal Yahya, Alba Flores, Martí Aldea

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Mad3 modulates the GScience advances · 2022
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. An intrinsically disordered motif regulates the interaction between the p47 adaptor and the p97 AAA+ ATPase.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Golgi Structure and Function in Health, Stress, and Diseases.Results and problems in cell differentiation · 2019
    Review
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.

Eva ParisiMolecular Biology Institute of Barcelona IBMB-CSIC, Barcelona, Catalonia, Spain.
Galal YahyaMolecular Biology Institute of Barcelona IBMB-CSIC, Barcelona, Catalonia, Spain.
Alba FloresMolecular Biology Institute of Barcelona IBMB-CSIC, Barcelona, Catalonia, Spain.
Martí AldeaMolecular Biology Institute of Barcelona IBMB-CSIC, Barcelona, Catalonia, Spain mambmc@ibmb.csic.es.ORCID 0000-0002-8710-5336
Institut de Biologia Molecular de Barcelona · ESUniversitat Internacional de Catalunya · ESZagazig University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cells sense myriad signals during G1, and a rapid response to prevent cell cycle entry is of crucial importance for proper development and adaptation. Cln3, the most upstream G1 cyclin in budding yeast, is an extremely short-lived protein subject to ubiquitination and proteasomal degradation. On the other hand, nuclear accumulation of Cln3 depends on chaperones that are also important for its degradation. However, how these processes are intertwined to control G1-cyclin fate is not well understood. Here, we show that Cln3 undergoes a challenging ubiquitination step required for both degradation and full activation. Segregase Cdc48/p97 prevents degradation of ubiquitinated Cln3, and concurrently stimulates its ER release and nuclear accumulation to trigger Start. Cdc48/p97 phosphorylation at conserved Cdk-target sites is important for recruitment of specific cofactors and, in both yeast and mammalian cells, to attain proper G1-cyclin levels and activity. Cdk-dependent modulation of Cdc48 would subjugate G1 cyclins to fast and reversible state switching, thus arresting cells promptly in G1 at developmental or environmental checkpoints, but also resuming G1 progression immediately after proliferative signals reappear.

Indexed as

Proteolysis3T3 CellsAnimalsCyclinsG1 PhaseHEK293 CellsHumansMembrane GlycoproteinsMiceMolecular ChaperonesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsValosin Containing ProteinCDC48 protein, S cerevisiaeCLN3 protein, humanCLN3 protein, mouseCLN3 protein, S cerevisiaeCyclinsMembrane GlycoproteinsMolecular ChaperonesSaccharomyces cerevisiae ProteinsValosin Containing ProteinVCP protein, humanVcp protein, mouseCdc48cell cycleCln3ER releaseStart

Identifiers

PMID29950310
PMCPMC6092614
OpenAlexW2810619040

What OpenQuestion holds

Textmetadata
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.