Evidence map›Paper›PMID 34923909›Full record

ArticleAutophagy2022

Autophagy modulates cell fate decisions during lineage commitment.

Kulbhushan Sharma, Nagham T Asp, Sean Harrison, Richard Siller, Saphira F Baumgarten, Swapnil Gupta, Maria E Chollet, Elisabeth Andersen, Gareth J Sullivan, Anne Simonsen

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Autophagy-mediated ID1 turnover dictates chemo-resistant fate in ovarian cancer stem cells.Journal of experimental & clinical cancer research : CR · 2024
    Article
  6. Article
  7. Article
  8. Review
  9. Autophagy-related gene and protein expressions during blastocyst development.Journal of assisted reproduction and genetics · 2023
    Article
  10. Article
  11. 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

10 authors at 2 institutions in 2 countries.

Kulbhushan SharmaDepartment of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.ORCID 0000-0001-5226-4209
Nagham T AspDepartment of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.ORCID 0000-0002-2143-1470
Sean HarrisonDepartment of Pediatric Research, Oslo University Hospital, Oslo, Norway.ORCID 0000-0001-9399-9631
Richard SillerDepartment of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.ORCID 0000-0001-6691-9261
Saphira F BaumgartenHybrid Technology Hub, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Swapnil GuptaDepartment of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.ORCID 0000-0003-1902-7441
Maria E CholletResearch Institute of Internal Medicine, Oslo University Hospital, Oslo, Norway.
Elisabeth AndersenResearch Institute of Internal Medicine, Oslo University Hospital, Oslo, Norway.
Gareth J SullivanDepartment of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.ORCID 0000-0001-8718-7944
Anne SimonsenDepartment of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.ORCID 0000-0003-4711-7057
Oslo University Hospital · NOUniversity of Oslo · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Early events during development leading to exit from a pluripotent state and commitment toward a specific germ layer still need in-depth understanding. Autophagy has been shown to play a crucial role in both development and differentiation. This study employs human embryonic and induced pluripotent stem cells to understand the early events of lineage commitment with respect to the role of autophagy in this process. Our data indicate that a dip in autophagy facilitates exit from pluripotency. Upon exit, we demonstrate that the modulation of autophagy affects SOX2 levels and lineage commitment, with induction of autophagy promoting SOX2 degradation and mesendoderm formation, whereas inhibition of autophagy causes SOX2 accumulation and neuroectoderm formation. Thus, our results indicate that autophagy-mediated SOX2 turnover is a determining factor for lineage commitment. These findings will deepen our understanding of development and lead to improved methods to derive different lineages and cell types.

Indexed as

AutophagyInduced Pluripotent Stem CellsCell DifferentiationHeLa CellsHumansAutophagosomedifferentiationectodermendodermmesodermpluripotent stem cellsSOX2

Identifiers

PMID34923909
PMCPMC9450964
OpenAlexW4200138381

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.