Evidence map›Paper›PMID 29465287›Full record

ArticleAutophagy2018

The exoribonuclease Xrn1 is a post-transcriptional negative regulator of autophagy.

Elizabeth Delorme-Axford, Emma Abernathy, Nicholas J Lennemann, Amélie Bernard, Aileen Ariosa, Carolyn B Coyne, Karla Kirkegaard, Daniel J Klionsky

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
3.1field-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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

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  16. Adaptive Response ofJournal of fungi (Basel, Switzerland) · 2022
    Article
  17. Processing body (P-body) and its mediators in cancer.Molecular and cellular biochemistry · 2022
    Review
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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

8 authors at 3 institutions in 1 country.

Elizabeth Delorme-Axforda Life Sciences Institute, University of Michigan , Ann Arbor , MI , USA.
Emma Abernathyb Department of Genetics , Stanford University School of Medicine , Stanford , CA , USA.
Nicholas J Lennemannc Department of Pediatrics , University of Pittsburgh , Pittsburgh , PA , USA.ORCID 0000-0002-6379-0965
Amélie Bernarda Life Sciences Institute, University of Michigan , Ann Arbor , MI , USA.
Aileen Ariosaa Life Sciences Institute, University of Michigan , Ann Arbor , MI , USA.
Carolyn B Coynec Department of Pediatrics , University of Pittsburgh , Pittsburgh , PA , USA.ORCID 0000-0002-1884-6309
Karla Kirkegaardb Department of Genetics , Stanford University School of Medicine , Stanford , CA , USA.
Daniel J Klionskya Life Sciences Institute, University of Michigan , Ann Arbor , MI , USA.ORCID 0000-0002-7828-8118
University of Michigan · USStanford University · USUniversity of Pittsburgh · US

Funding

ALTERNATIVE VACUOLAR TARGETING MECHANISMS IN YEASTR01GM053396 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KLIONSKY, DANIEL J. · 1995 to 2018
$12.1M
Viral use and mimicry of autophagy pathway and componentsR01AI134912 · NIAID · STANFORD UNIVERSITY · PI KIRKEGAARD, KARLA · 2018 to 2021
$1.6M
Characterizing the role of ER-shaping proteins during RNA virus infectionF32AI122456 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LENNEMANN, NICHOLAS J · 2016 to 2016
$56k
NIAID NIH HHS F32 AI122456NIAID NIH HHS R01 AI134912NIGMS NIH HHS R01 GM053396
6 · The paper itself

Abstract

Macroautophagy/autophagy is a conserved catabolic process that promotes survival during stress. Autophagic dysfunction is associated with pathologies such as cancer and neurodegenerative diseases. Thus, autophagy must be strictly modulated at multiple levels (transcriptional, post-transcriptional, translational and post-translational) to prevent deregulation. Relatively little is known about the post-transcriptional control of autophagy. Here we report that the exoribonuclease Xrn1/XRN1 functions as a negative autophagy factor in the yeast Saccharomyces cerevisiae and in mammalian cells. In yeast, chromosomal deletion of XRN1 enhances autophagy and the frequency of autophagosome formation. Loss of Xrn1 results in the upregulation of autophagy-related (ATG) transcripts under nutrient-replete conditions, and this effect is dependent on the ribonuclease activity of Xrn1. Xrn1 expression is regulated by the yeast transcription factor Ash1 in rich conditions. In mammalian cells, siRNA depletion of XRN1 enhances autophagy and the replication of 2 picornaviruses. This work provides insight into the role of the RNA decay factor Xrn1/XRN1 as a post-transcriptional regulator of autophagy.

Indexed as

AutophagyTranscription, GeneticAutophagosomesExoribonucleasesHeLa CellsHumansMicrotubule-Associated ProteinsRepressor ProteinsRNA, MessengerSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsASH1 protein, S cerevisiaeExoribonucleasesMicrotubule-Associated ProteinsRepressor ProteinsRNA, MessengerSaccharomyces cerevisiae ProteinsXRN1 protein, humanXRN1 protein, S cerevisiaeAsh1Atg8autophagosomeautophagy relatedBECN1coxsackievirus BCRISPRCVBDcp2LC3macroautophagymRNApicornaviruspoliovirusRNARNA decaystressvacuoleyeast

Identifiers

PMID29465287
PMCPMC6070002
OpenAlexW2791986625

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.