Evidence map›Paper›PMID 32516305›Full record

ArticlePLoS biology2020

Mitotic phosphorylation of the ULK complex regulates cell cycle progression.

Akinori Yamasaki, Yui Jin, Yoshinori Ohsumi

Open access · goldAbstract readComment
In one paragraph

Article in PLoS biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Physiological functions of ULK1/2.Journal of molecular biology · 2024
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Akinori YamasakiCell Biology Center, Institute of Innovative Research, Tokyo Institute of Technology, Yokohama, Japan.ORCID 0000-0002-5820-5549
Yui JinCell Biology Center, Institute of Innovative Research, Tokyo Institute of Technology, Yokohama, Japan.ORCID 0000-0001-6551-5775
Yoshinori OhsumiCell Biology Center, Institute of Innovative Research, Tokyo Institute of Technology, Yokohama, Japan.
Tokyo Institute of Technology · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is an intracellular degradation pathway targeting organelles and macromolecules, thereby regulating various cellular functions. Phosphorylation is a key posttranscriptional protein modification implicated in the regulation of biological function including autophagy. Under asynchronous conditions, autophagy activity is predominantly suppressed by mechanistic target of rapamycin (mTOR) kinase, but whether autophagy-related genes (ATG) proteins are phosphorylated differentially throughout the sequential phases of the cell cycle remains unclear. In this issue, Li and colleagues report that cyclin-dependent kinase 1 (CDK1) phosphorylates the ULK complex during mitosis. This phosphorylation induces autophagy and, surprisingly, is shown to drive cell cycle progression. This work reveals a yet-unappreciated role for autophagy in cell cycle progression and enhances our understanding of the specific phase-dependent autophagy regulation during cellular growth and proliferation.

Indexed as

AutophagyCDC2 Protein KinaseMechanistic Target of Rapamycin Complex 1MitosisPhosphorylationTOR Serine-Threonine KinasesCDC2 Protein KinaseMechanistic Target of Rapamycin Complex 1TOR Serine-Threonine Kinases

Identifiers

PMID32516305
PMCPMC7282621
OpenAlexW3033358956

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.