Evidence map›Paper›PMID 32047096›Full record

ArticleGenetics2020

Decoupling of Apoptosis from Activation of the ER Stress Response by the

Rebecca A S Palu, Hans M Dalton, Clement Y Chow

Open access · greenAbstract read
In one paragraph

Article in Genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 29% 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

8 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Natural Genetic Variation Screen inG3 (Bethesda, Md.) · 2019
    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

3 authors at 1 institution in 1 country.

Rebecca A S PaluDepartment of Human Genetics, University of Utah School of Medicine, 15 N 2030 E Salt Lake City, Utah 84112.ORCID 0000-0001-9444-8815
Hans M DaltonDepartment of Human Genetics, University of Utah School of Medicine, 15 N 2030 E Salt Lake City, Utah 84112.
Clement Y ChowDepartment of Human Genetics, University of Utah School of Medicine, 15 N 2030 E Salt Lake City, Utah 84112 cchow@genetics.utah.edu.ORCID 0000-0002-3104-7923
University of Utah · US

Funding

Investigating the impact of genetic variation on the ER stress response, protein folding, and diseaseR35GM124780 · NIGMS · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Clement Chow · 2017 to 2026
$4.0M
University of Utah Interdisciplinary Training Program in Computational Approaches to Diabetes and Metabolism ResearchT32DK110966 · NIDDK · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Karen Louise Eilbeck, Marcus Guy Pezzolesi · 2016 to 2026
$2.6M
NIDDK NIH HHS T32 DK110966NIGMS NIH HHS R35 GM124780
6 · The paper itself

Abstract

Endoplasmic reticulum (ER) stress-induced apoptosis is a primary cause and modifier of degeneration in a number of genetic disorders. Understanding how genetic variation influences the ER stress response and subsequent activation of apoptosis could improve individualized therapies and predictions of outcomes for patients. In this study, we find that the uncharacterized, membrane-bound metallopeptidase

Indexed as

ApoptosisEndoplasmic Reticulum StressAnimalsCyclin-Dependent Kinase 5Drosophila melanogasterDrosophila ProteinsEpistasis, GeneticN-AcetylgalactosaminyltransferasesUnfolded Protein Responsebeta4GalNAcTB protein, DrosophilaCdk5 protein, DrosophilaCyclin-Dependent Kinase 5Drosophila ProteinsN-AcetylgalactosaminyltransferasesapoptosisER stressmetallopeptidasemodifier genes

Identifiers

PMID32047096
PMCPMC7153941
OpenAlexW3006639319

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.