Evidence map›Paper›PMID 27173017›Full record

ArticleNature communications2016

miR-216b regulation of c-Jun mediates GADD153/CHOP-dependent apoptosis.

Zhenhua Xu, Yiwen Bu, Nilesh Chitnis, Costas Koumenis, Serge Y Fuchs, J Alan Diehl

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

51 citing papers in PubMed, 87 citations in OpenAlex.

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  18. Frontiers in oncology · 2022
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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

6 authors at 2 institutions in 1 country.

Zhenhua XuDepartment of Biochemistry, Hollings Cancer Center, Medical University of South Carolina, 86 Jonathan Lucas Street, 3400, Charleston, South Carolina 29425, USA.
Yiwen BuDepartment of Biochemistry, Hollings Cancer Center, Medical University of South Carolina, 86 Jonathan Lucas Street, 3400, Charleston, South Carolina 29425, USA.
Nilesh ChitnisDepartment of Biochemistry, Hollings Cancer Center, Medical University of South Carolina, 86 Jonathan Lucas Street, 3400, Charleston, South Carolina 29425, USA.
Costas KoumenisDepartment of Radiation Oncology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
Serge Y FuchsDepartment of Animal Biology, School of Veterinary Medicine, 380 S. University Avenue, Philadelphia, Pennsylvania 19104, USA.
J Alan DiehlDepartment of Biochemistry, Hollings Cancer Center, Medical University of South Carolina, 86 Jonathan Lucas Street, 3400, Charleston, South Carolina 29425, USA.
Medical University of South Carolina · USUniversity of Pennsylvania · US

Funding

TRANSLATIONAL CONTROL IN ADAPTATION TO HYPOXIAP01CA104838 · NCI · UNIVERSITY OF PENNSYLVANIA · PI DIEHL, JOHN ALAN · 2004 to 2018
$17.6M
UPR, interferon signaling and tumorigenesisP01CA165997 · NCI · UNIVERSITY OF PENNSYLVANIA · PI KOUMENIS, CONSTANTINOS · 2013 to 2023
$10.9M
Role of HOS in Cell Transformation and ApoptosisR01CA092900 · NCI · UNIVERSITY OF PENNSYLVANIA · PI FUCHS, SERGE Y · 2001 to 2021
$5.3M
NCI NIH HHS P01 CA104838NCI NIH HHS P01 CA165997NCI NIH HHS R01 CA092900
6 · The paper itself

Abstract

The ability of the unfolded protein response, UPR, to regulate cell homeostasis through both gene expression and protein synthesis has been well documented. One primary pro-apoptotic protein that responds to both PERK and Ire1 signalling is the CHOP/GADD153 transcription factor. Although CHOP deficiency delays onset of cell death, questions remain regarding how CHOP regulates apoptosis. Here, we provide evidence demonstrating that CHOP/GADD153-dependent apoptosis reflects expression of micro-RNA, miR-216b. MiR-216b accumulation requires PERK-dependent induction of CHOP/GADD153, which then directly regulates miR-216b expression. As maximal expression of miR-216b is antagonized by Ire1, miR-216b accumulation reflects the convergence of PERK and Ire1 activities. Functionally, miR-216b directly targets c-Jun, thereby reducing AP-1-dependent transcription and sensitizing cells to ER stress-dependent apoptosis. These results provide direct insight into the molecular mechanisms of CHOP/GADD153-dependent cell death.

Indexed as

ApoptosisAnimalsCell LineCell Line, TumorCell SurvivaleIF-2 KinaseEndoplasmic Reticulum StressEndoribonucleasesHumansMiceMicroRNAsProtein Serine-Threonine KinasesProto-Oncogene Proteins c-junTranscription Factor CHOPUnfolded Protein ResponseDDIT3 protein, humanEIF2AK3 protein, humaneIF-2 KinaseEndoribonucleasesERN1 protein, humanMicroRNAsMIRN216 microRNA, humanProtein Serine-Threonine KinasesProto-Oncogene Proteins c-junTranscription Factor CHOP

Identifiers

PMID27173017
PMCPMC4869177
OpenAlexW2390815994

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.