Evidence map›Paper›PMID 30287689›Full record

ArticleThe Journal of biological chemistry2018

ER stress signaling has an activating transcription factor 6α (ATF6)-dependent "off-switch".

Franziska Walter, Aisling O'Brien, Caoimhín G Concannon, Heiko Düssmann, Jochen H M Prehn

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

84 citing papers in PubMed, 116 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Cellular Biology: Virus-Host Interactions and RNA Structure and Function.Current topics in microbiology and immunology · 2026
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. ATF6 Alleviates Endothelial Inflammation Following Extended Hepatectomy Through Inhibition of TRIM10/NF-κB Signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  18. Review
  19. Article
  20. Article

24 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Franziska WalterFrom the Centre for Systems Medicine, Department of Physiology and Medical Physics, Royal College of Surgeons in Ireland, 123 St. Stephens Green, Dublin 6, Ireland.
Aisling O'BrienFrom the Centre for Systems Medicine, Department of Physiology and Medical Physics, Royal College of Surgeons in Ireland, 123 St. Stephens Green, Dublin 6, Ireland.
Caoimhín G ConcannonFrom the Centre for Systems Medicine, Department of Physiology and Medical Physics, Royal College of Surgeons in Ireland, 123 St. Stephens Green, Dublin 6, Ireland.
Heiko DüssmannFrom the Centre for Systems Medicine, Department of Physiology and Medical Physics, Royal College of Surgeons in Ireland, 123 St. Stephens Green, Dublin 6, Ireland.
Jochen H M PrehnFrom the Centre for Systems Medicine, Department of Physiology and Medical Physics, Royal College of Surgeons in Ireland, 123 St. Stephens Green, Dublin 6, Ireland. Electronic address: jprehn@rcsi.ie.
Royal College of Surgeons in Ireland · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In response to an accumulation of unfolded proteins in the endoplasmic reticulum (ER) lumen, three ER transmembrane signaling proteins, inositol-requiring enzyme 1 (IRE1), PRKR-like ER kinase (PERK), and activating transcription factor 6α (ATF6α), are activated. These proteins initiate a signaling and transcriptional network termed the unfolded protein response (UPR), which re-establishes cellular proteostasis. When this restoration fails, however, cells undergo apoptosis. To investigate cross-talk between these different UPR enzymes, here we developed a high-content live cell screening platform to image fluorescent UPR-reporter cell lines derived from human SH-SY5Y neuroblastoma cells in which different ER stress signaling proteins were silenced through lentivirus-delivered shRNA constructs. We observed that loss of ATF6 expression results in uncontrolled IRE1-reporter activity and increases

Indexed as

Endoplasmic Reticulum StressActivating Transcription Factor 6Endoplasmic Reticulum Chaperone BiPEndoribonucleasesGene Expression RegulationHumansProtein DomainsProtein Serine-Threonine KinasesSignal TransductionX-Box Binding Protein 1Activating Transcription Factor 6ATF6 protein, humanEndoplasmic Reticulum Chaperone BiPEndoribonucleasesERN1 protein, humanHSPA5 protein, humanProtein Serine-Threonine KinasesX-Box Binding Protein 1XBP1 protein, humanAPY29ATF6cell deathc-Jun N-terminal kinase (JNK)endoplasmic reticulum stress (ER stress)fluorescent reporterGRP78high content imagingimagingIRE1lentivirusprotein misfoldingstress responseunfolded protein response (UPR)UPR reportersX-box binding protein 1 (XBP1)

Identifiers

PMID30287689
PMCPMC6254332
OpenAlexW2894695144

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.