Evidence map›Paper›PMID 28272405›Full record

ArticleNature communications2017

PARP1 promotes gene expression at the post-transcriptiona level by modulating the RNA-binding protein HuR.

Yueshuang Ke, Yanlong Han, Xiaolan Guo, Jitao Wen, Ke Wang, Xue Jiang, Xue Tian, Xueqing Ba, Istvan Boldogh, Xianlu Zeng

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
4.0field-weighted citation impact, top 5% 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, 77 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 2 countries.

Yueshuang KeThe Key Laboratory of Molecular Epigenetics of the Ministry of Education, Northeast Normal University, Changchun, Jilin 130024, China.
Yanlong HanInstitute of Genetics and Cytology, Northeast Normal University, Changchun, Jilin 130024, China.
Xiaolan GuoInstitute of Genetics and Cytology, Northeast Normal University, Changchun, Jilin 130024, China.
Jitao WenInstitute of Genetics and Cytology, Northeast Normal University, Changchun, Jilin 130024, China.
Ke WangInstitute of Genetics and Cytology, Northeast Normal University, Changchun, Jilin 130024, China.
Xue JiangInstitute of Genetics and Cytology, Northeast Normal University, Changchun, Jilin 130024, China.
Xue TianInstitute of Genetics and Cytology, Northeast Normal University, Changchun, Jilin 130024, China.
Xueqing BaThe Key Laboratory of Molecular Epigenetics of the Ministry of Education, Northeast Normal University, Changchun, Jilin 130024, China.
Istvan BoldoghDepartment of Microbiology and Immunology, Sealy Center for Molecular Medicine, University of Texas Medical Branch at Galveston, Galveston, Texas 77555, USA.
Xianlu ZengThe Key Laboratory of Molecular Epigenetics of the Ministry of Education, Northeast Normal University, Changchun, Jilin 130024, China.
Northeast Normal University · CNThe University of Texas Medical Branch at Galveston · US

Funding

Virus, Tissue Culture and ImmunoassayP01AI062885 · NIAID · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI CASOLA, ANTONELLA · 2005 to 2022
$23.9M
Linkage of Lung Inflammation to 8-oxoguanine and OGG1R01ES018948 · NIEHS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI BOLDOGH, ISTVAN STEVEN · 2010 to 2014
$1.5M
NIAID NIH HHS P01 AI062885NIEHS NIH HHS R01 ES018948
6 · The paper itself

Abstract

Poly(ADP-ribosyl)ation (PARylation) is mainly catalysed by poly-ADP-ribose polymerase 1 (PARP1), whose role in gene transcription modulation has been well established. Here we show that, in response to LPS exposure, PARP1 interacts with the adenylateuridylate-rich element-binding protein embryonic lethal abnormal vision-like 1 (Elavl1)/human antigen R (HuR), resulting in its PARylation, primarily at site D226. PARP inhibition and the D226 mutation impair HuR's PARylation, nucleocytoplasmic shuttling and mRNA binding. Increases in mRNA level or stability of pro-inflammatory cytokines/chemokines are abolished by PARP1 ablation or inhibition, or blocked in D226A HuR-expressing cells. The present study demonstrates a mechanism to regulate gene expression at the post-transcriptional level, and suggests that blocking the interaction of PARP1 with HuR could be a strategy to treat inflammation-related diseases that involve increased mRNA stability.

Indexed as

Gene Expression RegulationAnimalsChemokinesCytokinesELAV-Like Protein 1HEK293 CellsHumansInflammationLipopolysaccharidesMacrophages, PeritonealMiceMutationPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) Polymerase InhibitorsPoly ADP RibosylationProtein Processing, Post-TranslationalChemokinesCytokinesElavl1 protein, mouseELAV-Like Protein 1LipopolysaccharidesParp1 protein, mousePoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) Polymerase InhibitorsRNA, Messenger

Identifiers

PMID28272405
PMCPMC5344980
OpenAlexW2593505005

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.