Evidence map›Paper›PMID 32046286›Full record

ReviewInternational journal of molecular sciences2020

Sledgehammer to Scalpel: Broad Challenges to the Heart and Other Tissues Yield Specific Cellular Responses via Transcriptional Regulation of the ER-Stress Master Regulator ATF6α.

Winston T Stauffer, Adrian Arrieta, Erik A Blackwood, Christopher C Glembotski

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. 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
–field-weighted citation impact
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.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Deciphering the Link Between ERFrontiers in aging neuroscience · 2022
    Review
  9. 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

4 authors.

Winston T StaufferDepartment of Biology, San Diego State University Heart Institute, San Diego State University, San Diego, CA 92182, USA.
Adrian ArrietaDepartment of Biology, San Diego State University Heart Institute, San Diego State University, San Diego, CA 92182, USA.
Erik A BlackwoodDepartment of Biology, San Diego State University Heart Institute, San Diego State University, San Diego, CA 92182, USA.
Christopher C GlembotskiDepartment of Biology, San Diego State University Heart Institute, San Diego State University, San Diego, CA 92182, USA.

Funding

The ER Stress-Induced Selenoprotein, SelenoS, Regulates Proteostasis and Cardiac HypertrophyR01HL149931 · NHLBI · UNIVERSITY OF ARIZONA · PI GLEMBOTSKI, CHRIS · 2020 to 2023
$1.7M
Harnessing the Adaptive ER Stress Response in Myocardial IschemiaR01HL135893 · NHLBI · UNIVERSITY OF ARIZONA · PI GLEMBOTSKI, CHRIS · 2017 to 2020
$1.5M
ATF6 is Required for ANP Secretion from the HeartR01HL141463 · NHLBI · UNIVERSITY OF ARIZONA · PI GLEMBOTSKI, CHRIS · 2019 to 2022
$1.5M
NHLBI NIH HHS R01 HL135893NHLBI NIH HHS R01 HL141463NHLBI NIH HHS R01 HL149931NIH HHS R01HL135893, R01 HL75573, R01 HL104535
6 · The paper itself

Abstract

There are more than 2000 transcription factors in eukaryotes, many of which are subject to complex mechanisms fine-tuning their activity and their transcriptional programs to meet the vast array of conditions under which cells must adapt to thrive and survive. For example, conditions that impair protein folding in the endoplasmic reticulum (ER), sometimes called ER stress, elicit the relocation of the ER-transmembrane protein, activating transcription factor 6α (ATF6α), to the Golgi, where it is proteolytically cleaved. This generates a fragment of ATF6α that translocates to the nucleus, where it regulates numerous genes that restore ER protein-folding capacity but is degraded soon after. Thus, upon ER stress, ATF6α is converted from a stable, transmembrane protein, to a rapidly degraded, nuclear protein that is a potent transcription factor. This review focuses on the molecular mechanisms governing ATF6α location, activity, and stability, as well as the transcriptional programs ATF6α regulates, whether canonical genes that restore ER protein-folding or unexpected, non-canonical genes affecting cellular functions beyond the ER. Moreover, we will review fascinating roles for an ATF6α isoform, ATF6β, which has a similar mode of activation but, unlike ATF6α, is a long-lived, weak transcription factor that may moderate the genetic effects of ATF6α.

Indexed as

Endoplasmic Reticulum StressTranscription, GeneticActivating Transcription Factor 6AnimalsGene Expression RegulationHumansMyocardiumProtein IsoformsTranscription FactorsActivating Transcription Factor 6ATF6 protein, humanProtein IsoformsTranscription FactorsATF6αATF6βbasic leucine-zippercardiacendoplasmic reticulumER stressOASISproteostasistranscriptional regulationUPR

Identifiers

PMID32046286
PMCPMC7037772

What Socratic 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 Socratic graph.