Evidence map›Paper›PMID 30024379›Full record

ArticleeLife2018

Inhibiting the integrated stress response pathway prevents aberrant chondrocyte differentiation thereby alleviating chondrodysplasia.

Cheng Wang, Zhijia Tan, Ben Niu, Kwok Yeung Tsang, Andrew Tai, Wilson C W Chan, Rebecca L K Lo, Keith K H Leung, Nelson W F Dung, Nobuyuki Itoh and 3 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

52 citing papers in PubMed, 94 citations in OpenAlex.

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  4. ElevatedInternational journal of molecular sciences · 2025
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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

13 authors at 3 institutions in 4 countries.

Cheng Wang *School of Biomedical Sciences, University of Hong Kong, Hong Kong, China.
Zhijia Tan *School of Biomedical Sciences, University of Hong Kong, Hong Kong, China.ORCID 0000-0003-2295-5169
Ben NiuSchool of Biomedical Sciences, University of Hong Kong, Hong Kong, China.
Kwok Yeung TsangSchool of Biomedical Sciences, University of Hong Kong, Hong Kong, China.
Andrew TaiSchool of Biomedical Sciences, University of Hong Kong, Hong Kong, China.
Wilson C W ChanSchool of Biomedical Sciences, University of Hong Kong, Hong Kong, China.ORCID 0000-0003-2381-2805
Rebecca L K LoSchool of Biomedical Sciences, University of Hong Kong, Hong Kong, China.
Keith K H LeungSchool of Biomedical Sciences, University of Hong Kong, Hong Kong, China.
Nelson W F DungSchool of Biomedical Sciences, University of Hong Kong, Hong Kong, China.
Nobuyuki ItohGraduate School of Pharmaceutical Sciences, University of Kyoto, Kyoto, Japan.
Michael Q ZhangDepartment of Biological Sciences, Center for Systems Biology, The University of Texas at Dallas, Richardson, United States.ORCID 0000-0002-7408-1830
Danny ChanSchool of Biomedical Sciences, University of Hong Kong, Hong Kong, China.ORCID 0000-0003-3824-5778
Kathryn Song Eng CheahSchool of Biomedical Sciences, University of Hong Kong, Hong Kong, China.ORCID 0000-0003-0802-8799
University of Hong Kong · HKKyoto Pharmaceutical University · JPThe University of Texas at Dallas · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The integrated stress response (ISR) is activated by diverse forms of cellular stress, including endoplasmic reticulum (ER) stress, and is associated with diseases. However, the molecular mechanism(s) whereby the ISR impacts on differentiation is incompletely understood. Here, we exploited a mouse model of Metaphyseal Chondrodysplasia type Schmid (MCDS) to provide insight into the impact of the ISR on cell fate. We show the protein kinase RNA-like ER kinase (PERK) pathway that mediates preferential synthesis of ATF4 and CHOP, dominates in causing dysplasia by reverting chondrocyte differentiation via ATF4-directed transactivation of

Indexed as

Cell DifferentiationStress, PhysiologicalAcetamidesActivating Transcription Factor 4AnimalsApoptosisBase SequenceCell SurvivalChondrocytesChondrogenesisCyclohexylamineseIF-2 KinaseEndoplasmic Reticulum StressEukaryotic Initiation Factor-2Fibroblast Growth FactorsGrowth Plate2-(4-chlorophenoxy)-N-(4-(2-(4-chlorophenoxy)acetamido)cyclohexyl)acetamideAcetamidesActivating Transcription Factor 4CyclohexylamineseIF-2 KinaseEukaryotic Initiation Factor-2fibroblast growth factor 21Fibroblast Growth FactorsSOX9 Transcription FactorTranscription Factor CHOPATF4chondrodysplasiadevelopmental biologyendoplasmic reticulum stressintegrated stress responseISRIBmouseprotein kinase RNA-like ER kinase pathway

Identifiers

PMID30024379
PMCPMC6053305
OpenAlexW2883916878

What OpenQuestion 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 OpenQuestion graph.