Evidence map›Paper›PMID 28825160›Full record

ArticleMolecular and cellular biochemistry2018

Functional validation of ATF4 and GADD34 in Neuro2a cells by CRISPR/Cas9-mediated genome editing.

Kentaro Oh-Hashi, Naoki Sugiura, Fumimasa Amaya, Ken-Ichi Isobe, Yoko Hirata

Abstract readValidation Study
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
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  3. Elucidation of OSW-1-Induced Stress Responses in Neuro2a Cells.International journal of molecular sciences · 2023
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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 2 institutions in 1 country.

Kentaro Oh-HashiUnited Graduate School of Drug Discovery and Medical Information Sciences, Gifu University, 1-1 Yanagido, Gifu, 501-1193, Japan. oohashi@gifu-u.ac.jp.
Naoki SugiuraDepartment of Chemistry and Biomolecular Science, Faculty of Engineering, Gifu University, 1-1 Yanagido, Gifu, 501-1193, Japan.
Fumimasa AmayaDepartment of Anesthesiology, Kyoto Prefectural University of Medicine, Kawaramachi-Hirokoji, Kamikyo-ku, Kyoto, 602-0841, Japan.
Ken-Ichi IsobeNagoya Wemen University, 3-40, Shioji, Mizuho-ku, Nagoya, 467-8610, Japan.
Yoko HirataUnited Graduate School of Drug Discovery and Medical Information Sciences, Gifu University, 1-1 Yanagido, Gifu, 501-1193, Japan.
Gifu University · JPKyoto Prefectural University of Medicine · JP

Funding

Grant-in-Aid for Challenging Exploratory Research 17K19901Grant-in-Aid for Scientific Research (B) 16H05280Grant-in-Aid for Scientific Research (B) 26670692
6 · The paper itself

Abstract

Activating transcription factor 4 (ATF4), which is ubiquitously expressed, plays a crucial role in regulating various stress-responsive genes under pathophysiological conditions. Further, growth arrest and DNA damage-inducible gene 34 (GADD34), a downstream target of ATF4, has been reported to negatively regulate ATF4 expression. To understand the relationship between intrinsic ATF4 and GADD34 under resting and ER stress conditions, we used a novel gene editing approach, CRISPR/Cas9, to integrate antibiotic-resistant genes into the target genes, ATF4 and GADD34. First, we manipulated the ATF4 gene in the mouse neuroblastoma cell line, Neuro2a, and compared the ER stress responses between parental and ATF4-edited Neuro2a cells. Next, we established Neuro2a cells with edited GADD34 and ATF4/GADD34 genes and found that ATF4 acts as a proapoptotic factor, but GADD34 depletion did not attenuate the expression of cleaved caspase-3 induced by tunicamycin treatment. These findings provide new insights into the ATF4 signaling cascades. Additionally, the rapid establishment of cells lacking multiple genes using this CRISPR/Cas9 system will be a powerful tool for exploring various cellular issues under pathophysiological conditions.

Indexed as

Activating Transcription Factor 4CRISPR-Cas SystemsGene EditingProtein Phosphatase 1AnimalsCell LineGene Expression RegulationHumansMiceSignal TransductionActivating Transcription Factor 4Atf4 protein, mousePpp1r15a protein, mouseProtein Phosphatase 1ATF4CRIPSR/Cas9ER stressGADD34

Identifiers

PMID28825160
OpenAlexW2750416164

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.