Evidence map›Paper›PMID 30153076›Full record

ArticleAutophagy2019

Transcriptional and epigenetic profiling of nutrient-deprived cells to identify novel regulators of autophagy.

J G C Peeters, L W Picavet, S G J M Coenen, M Mauthe, S J Vervoort, E Mocholi, C de Heus, J Klumperman, S J Vastert, F Reggiori and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Autophagy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 8% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Guideline
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  12. mCell · 2025
    Article
  13. Article
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  15. Review
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  19. Article
  20. Modulation ofAutophagy · 2023
    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 2 institutions in 1 country.

J G C Peetersa Center for Molecular Medicine , University Medical Center Utrecht, Utrecht University , Utrecht , The Netherlands.
L W Picavetb Laboratory of Translational Immunology , University Medical Center Utrecht, Utrecht University , Utrecht , The Netherlands.
S G J M Coenenb Laboratory of Translational Immunology , University Medical Center Utrecht, Utrecht University , Utrecht , The Netherlands.
M Mauthed Department of Cell Biology , University Medical Center Groningen, University of Groningen , Groningen , The Netherlands.
S J Vervoorta Center for Molecular Medicine , University Medical Center Utrecht, Utrecht University , Utrecht , The Netherlands.
E Mocholia Center for Molecular Medicine , University Medical Center Utrecht, Utrecht University , Utrecht , The Netherlands.
C de Heusa Center for Molecular Medicine , University Medical Center Utrecht, Utrecht University , Utrecht , The Netherlands.ORCID 0000-0001-8618-8451
J Klumpermana Center for Molecular Medicine , University Medical Center Utrecht, Utrecht University , Utrecht , The Netherlands.
S J Vastertb Laboratory of Translational Immunology , University Medical Center Utrecht, Utrecht University , Utrecht , The Netherlands.
F Reggiorid Department of Cell Biology , University Medical Center Groningen, University of Groningen , Groningen , The Netherlands.
P J Coffera Center for Molecular Medicine , University Medical Center Utrecht, Utrecht University , Utrecht , The Netherlands.
M Mokryc Division of Pediatrics , Wilhelmina Children's Hospital, University Medical Center Utrecht, Utrecht University , Utrecht , The Netherlands.
J van Loosdregta Center for Molecular Medicine , University Medical Center Utrecht, Utrecht University , Utrecht , The Netherlands.
Utrecht University · NLUniversity Medical Center Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macroautophagy (hereafter autophagy) is a lysosomal degradation pathway critical for maintaining cellular homeostasis and viability, and is predominantly regarded as a rapid and dynamic cytoplasmic process. To increase our understanding of the transcriptional and epigenetic events associated with autophagy, we performed extensive genome-wide transcriptomic and epigenomic profiling after nutrient deprivation in human autophagy-proficient and autophagy-deficient cells. We observed that nutrient deprivation leads to the transcriptional induction of numerous autophagy-associated genes. These transcriptional changes are reflected at the epigenetic level (H3K4me3, H3K27ac, and H3K56ac) and are independent of autophagic flux. As a proof of principle that this resource can be used to identify novel autophagy regulators, we followed up on one identified target: EGR1 (early growth response 1), which indeed appears to be a central transcriptional regulator of autophagy by affecting autophagy-associated gene expression and autophagic flux. Taken together, these data stress the relevance of transcriptional and epigenetic regulation of autophagy and can be used as a resource to identify (novel) factors involved in autophagy regulation.

Indexed as

Epigenesis, GeneticGene Expression ProfilingAutophagyEarly Growth Response Protein 1Gene Expression RegulationHEK293 CellsHumansLysosomesNutrientsEarly Growth Response Protein 1NutrientsAutophagyChIP-seqEGR1nutrient-deprivationRNA-seq

Identifiers

PMID30153076
PMCPMC6287694
OpenAlexW2889269873

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.