Evidence map›Paper›PMID 28990926›Full record

ArticleeLife2017

IRAK2 directs stimulus-dependent nuclear export of inflammatory mRNAs.

Hao Zhou, Katarzyna Bulek, Xiao Li, Tomasz Herjan, Minjia Yu, Wen Qian, Han Wang, Gao Zhou, Xing Chen, Hui Yang and 16 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 24% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
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  14. Exploring the multifunctionality of SR proteins.Biochemical Society transactions · 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

26 authors at 8 institutions in 4 countries.

Hao Zhou *Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.ORCID http://orcid.org/0000-0001-9109-2489
Katarzyna Bulek *Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.
Xiao Li *Department of Genetics, Stanford University School of Medicine, Stanford, United States.
Tomasz Herjan *Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.
Minjia YuDepartment of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.
Wen QianDepartment of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.
Han WangDepartment of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.
Gao ZhouDepartment of Genetics, Stanford University School of Medicine, Stanford, United States.
Xing ChenDepartment of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.
Hui YangDepartment of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.
Lingzi HongDepartment of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.
Junjie ZhaoDepartment of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.
Luke QinDepartment of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.
Koichi FukudaDepartment of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.
Annette FlothoZentrum für Molekulare Biologie der Universität Heidelberg, DKFZ-ZMBH Alliance, Heidelberg, Germany.
Ji GaoDiscovery Biology, Bristol-Myers Squibb, Princeton, United States.
Ashok DongreDiscovery Biology, Bristol-Myers Squibb, Princeton, United States.
Julie A CarmanDiscovery Biology, Bristol-Myers Squibb, Princeton, United States.
Zizhen KangDepartment of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.
Bing SuShanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Timothy S KernSchool of Medicine, Case Western Reserve University, Cleveland, United States.
Jonathan D SmithDepartment of Cellular and Molecular Medicine, Lerner Research Institute Cleveland Clinic, Cleveland, United States.
Thomas A HamiltonDepartment of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.
Frauke MelchiorZentrum für Molekulare Biologie der Universität Heidelberg, DKFZ-ZMBH Alliance, Heidelberg, Germany.ORCID http://orcid.org/0000-0001-9546-8797
Paul L FoxDepartment of Cellular and Molecular Medicine, Lerner Research Institute Cleveland Clinic, Cleveland, United States.
Xiaoxia LiDepartment of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, United States.ORCID http://orcid.org/0000-0002-4872-9525
Cleveland Clinic Lerner College of Medicine · USBristol-Myers Squibb (United States) · USHeidelberg University · DEShanghai Jiao Tong University · CNJagiellonian University · PLLouis Stokes Cleveland VA Medical Center · USMount Auburn Hospital · USStanford University · US

Funding

TELOMERASE INACTIVATION BY RNASE L SIGNALS CELL DEATHP01CA062220 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI LI, XIAOXIA, STARK, GEORGE ROBERT · 1994 to 2020
$35.6M
Vascular Cell function and AtherosclerosisP01HL029582 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI FOX, PAUL L · 1985 to 2019
$32.0M
NCI NIH HHS P01 CA062220NHLBI NIH HHS P01 HL029582
6 · The paper itself

Abstract

Expression of inflammatory genes is determined in part by post-transcriptional regulation of mRNA metabolism but how stimulus- and transcript-dependent nuclear export influence is poorly understood. Here, we report a novel pathway in which LPS/TLR4 engagement promotes nuclear localization of IRAK2 to facilitate nuclear export of a specific subset of inflammation-related mRNAs for translation in murine macrophages. IRAK2 kinase activity is required for LPS-induced RanBP2-mediated IRAK2 sumoylation and subsequent nuclear translocation. Array analysis showed that an SRSF1-binding motif is enriched in mRNAs dependent on IRAK2 for nuclear export. Nuclear IRAK2 phosphorylates SRSF1 to reduce its binding to target mRNAs, which promotes the RNA binding of the nuclear export adaptor ALYREF and nuclear export receptor Nxf1 loading for the export of the mRNAs. In summary, LPS activates a nuclear function of IRAK2 that facilitates the assembly of nuclear export machinery to export selected inflammatory mRNAs to the cytoplasm for translation.

Indexed as

Active Transport, Cell NucleusAnimalsInterleukin-1 Receptor-Associated KinasesLipopolysaccharidesMacrophagesMiceNucleocytoplasmic Transport ProteinsPhosphorylationRNA-Binding ProteinsRNA, MessengerSerine-Arginine Splicing FactorsSumoylationInterleukin-1 Receptor-Associated KinasesLipopolysaccharidesNucleocytoplasmic Transport ProteinsNXF1 protein, mouseRNA-Binding ProteinsRNA, MessengerSerine-Arginine Splicing FactorsSrsf1 protein, mousecell biologyimmunologyinflammationmousenuclear translocationRNA exportsumoylationtoll-like receptor

Identifiers

PMID28990926
PMCPMC5675595
OpenAlexW2763193663

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.