Evidence map›Paper›PMID 29184100›Full record

ArticleScientific reports2017

AKT-mTOR signaling modulates the dynamics of IRE1 RNAse activity by regulating ER-mitochondria contacts.

Miguel Sanchez-Alvarez, Miguel Angel Del Pozo, Chris Bakal

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.8field-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

26 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. mTOR pathway mediates endoplasmic reticulum stress-induced CD4Apoptosis : an international journal on programmed cell death · 2022
    Article
  11. Review
  12. Article
  13. Article
  14. Regulation of lipid metabolism by the unfolded protein response.Journal of cellular and molecular medicine · 2021
    Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 2 countries.

Miguel Sanchez-AlvarezDynamical Cell Systems Team, Division of Cancer Biology, The Institute of Cancer Research-Chester Beatty laboratories, 237 Fulham Rd, SW3 6JB, London, United Kingdom. msancheza@cnic.es.
Miguel Angel Del PozoMechanoadaptation and Caveolae Biology Lab, Area of Cell and Developmental Biology, National Centre for Cardiovascular Research (CNIC), c/Melchor Fernandez Almagro, 8, CP, 28029, Madrid, Spain.
Chris BakalDynamical Cell Systems Team, Division of Cancer Biology, The Institute of Cancer Research-Chester Beatty laboratories, 237 Fulham Rd, SW3 6JB, London, United Kingdom. cbakal@icr.ac.uk.
Institute of Cancer Research · GBSpanish National Centre for Cardiovascular Research · ES

Funding

Biotechnology and Biological Sciences Research Council BB/J017183/1Cancer Research UK C37275/1A20146Worldwide Cancer Research 15-0404
6 · The paper itself

Abstract

Inositol Requiring Enzyme-1 (IRE1) is the most conserved transducer of the Unfolded Protein Response (UPR), a surveillance mechanism that ensures homeostasis of the endoplasmic reticulum (ER) in eukaryotes. IRE1 activation orchestrates adaptive responses, including lipid anabolism, metabolic reprogramming, increases in protein folding competency, and ER expansion/remodeling. However, we still know surprisingly little regarding the principles by which this ER transducer is deactivated upon ER stress clearance. Here we show that Protein Kinase B-mechanistic Target of Rapamycin (PKB/AKT-mTOR) signaling controls the dynamics of IRE1 deactivation by regulating ER-mitochondria physical contacts and the autophosphorylation state of IRE1. AKT-mTOR-mediated attenuation of IRE1 activity is important for ER remodelling dynamics and cell survival in the face of recursive, transient ER stress. Our observations suggest that IRE1 attenuation is an integral component of anabolic programmes regulated by AKT-mTOR. We suggest that AKT-mTOR activity is part of a 'timing mechanism' to deactivate IRE1 immediately following engagement of the UPR, in order to limit prolonged IRE1 RNAse activity that could lead to damaging inflammation or apoptosis.

Identifiers

PMID29184100
PMCPMC5705697
OpenAlexW2770649429

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.