Evidence map›Paper›PMID 31213543›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

Genome-wide CRISPR screen identifies suppressors of endoplasmic reticulum stress-induced apoptosis.

Ronald A Panganiban, Hae-Ryung Park, Maoyun Sun, Maya Shumyatcher, Blanca E Himes, Quan Lu

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
3.7field-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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

  1. Pooled it
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  7. Article
  8. Review
  9. PANoptosis: a new insight for oral diseases.Molecular biology reports · 2024
    Review
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  12. Article
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  18. Massively Parallel CRISPR-Based Genetic Perturbation Screening at Single-Cell Resolution.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Review
  19. Review
  20. 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

6 authors at 2 institutions in 1 country.

Ronald A PanganibanProgram in Molecular and Integrative Physiological Sciences, Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA 02115.
Hae-Ryung ParkProgram in Molecular and Integrative Physiological Sciences, Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA 02115.
Maoyun SunProgram in Molecular and Integrative Physiological Sciences, Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA 02115.
Maya ShumyatcherDepartment of Biostatistics, Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104.
Blanca E HimesDepartment of Biostatistics, Epidemiology, and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104.
Quan LuProgram in Molecular and Integrative Physiological Sciences, Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA 02115; qlu@hsph.harvard.edu.
University of Pennsylvania · USHarvard University · US

Funding

Translational Research Support CoreP30ES000002 · NIEHS · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI JAIME ELIZABETH HART · 1985 to 2026
$44.6M
CEBPD-Mediated Mechanisms of Glucocorticoid Insensitivity in Severe AsthmaR01HL133433 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI HIMES, BLANCA E · 2017 to 2021
$3.2M
SPP1, Oxidative Stress, and Lead ToxicityR01ES029097 · NIEHS · HARVARD SCHOOL OF PUBLIC HEALTH · PI LU, QUAN · 2018 to 2022
$2.8M
MicroRNAs, ER stress and arsenic neurotoxicityK99ES029548 · NIEHS · HARVARD SCHOOL OF PUBLIC HEALTH · PI PARK, HAE-RYUNG · 2019 to 2020
$203k
NHLBI NIH HHS R01 HL133433NIEHS NIH HHS K99 ES029548NIEHS NIH HHS P30 ES000002NIEHS NIH HHS R01 ES029097
6 · The paper itself

Abstract

Sensing misfolded proteins in the endoplasmic reticulum (ER), cells initiate the ER stress response and, when overwhelmed, undergo apoptosis. However, little is known about how cells prevent excessive ER stress response and cell death to restore homeostasis. Here, we report the identification and characterization of cellular suppressors of ER stress-induced apoptosis. Using a genome-wide CRISPR library, we screen for genes whose inactivation further increases ER stress-induced up-regulation of C/EBP homologous protein 10 (CHOP)-the transcription factor central to ER stress-associated apoptosis. Among the top validated hits are two interacting components of the polycomb repressive complex (

Indexed as

ApoptosisCRISPR-Cas SystemsEndoplasmic Reticulum StressAnimalsEndoplasmic ReticulumFibroblastsGene Knockout TechniquesGenes, SuppressorGenome-Wide Association StudyHEK293 CellsHumansMiceSignal TransductionTranscription Factor CHOPUnfolded Protein ResponseDDIT3 protein, humanTranscription Factor CHOPenvironmental toxicantgenetic screenproteotoxicityUPR (unfolded protein response)

Identifiers

PMID31213543
PMCPMC6613086
OpenAlexW2949569579

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.