Evidence map›Paper›PMID 28561022›Full record

ArticleNature communications2017

IL-17 induced NOTCH1 activation in oligodendrocyte progenitor cells enhances proliferation and inflammatory gene expression.

Chenhui Wang, Cun-Jin Zhang, Bradley N Martin, Katarzyna Bulek, Zizhen Kang, Junjie Zhao, Guanglin Bian, Julie A Carman, Ji Gao, Ashok Dongre and 7 more

Open 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. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

72 citing papers in PubMed, 119 citations in OpenAlex.

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    Review
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12 more citing papers are in PubMed but not listed here.

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

17 authors at 8 institutions in 2 countries.

Chenhui WangKey Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan 430074, China.
Cun-Jin ZhangDepartment of Immunology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
Bradley N MartinDepartment of Immunology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
Katarzyna BulekDepartment of Immunology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
Zizhen KangDepartment of Immunology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
Junjie ZhaoDepartment of Immunology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
Guanglin BianDepartment of Immunology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
Julie A CarmanDiscovery Biology, Bristol-Myers Squibb, Princeton, New Jersey 08540, USA.
Ji GaoDiscovery Biology, Bristol-Myers Squibb, Princeton, New Jersey 08540, USA.
Ashok DongreDiscovery Biology, Bristol-Myers Squibb, Princeton, New Jersey 08540, USA.
Haibo XueThe Department of Endocrinology and Metabolism, Binzhou Medical University Hospital. Binzhou City, Shandong Province 256603, China.
Stephen D MillerDepartment of Microbiology-Immunology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA.
Youcun QianThe Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences/Shanghai Jiao Tong University School of Medicine, Shanghai 200031, China.
Dolores HambardzumyanDepartment of Pediatrics, Aflac Cancer and Blood Disorders Center, Emory University. 201 Dowman Drive. Atlanta, Georgia 30322 USA.
Tom HamiltonDepartment of Immunology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
Richard M RansohoffBiogen Idec, Cambridge, Massachusetts 02142, USA.
Xiaoxia LiDepartment of Immunology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
Cleveland Clinic · USBristol-Myers Squibb (United States) · USBinzhou University · CNBiogen (United States) · USChinese Academy of Sciences · CNEmory University · USNorthwestern University · USWuhan Institute of Bioengineering · CN

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
Targeting pathological hyaluronan matricesP01HL103453 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI REIZES, OFER · 2011 to 2020
$26.8M
Airway redox biochemistry as a deteriminant of asthma phenotype during adolescen*U10HL109250 · NHLBI · UNIVERSITY OF VIRGINIA · PI ERZURUM, SERPIL C., GASTON, BENJAMIN · 2011 to 2016
$4.2M
Molecular and Cellular Mechanisms of IL-17 SignalingR01NS071996 · NINDS · CLEVELAND CLINIC LERNER COM-CWRU · PI LI, XIAOXIA · 2011 to 2015
$1.9M
NCI NIH HHS P01 CA062220NHLBI NIH HHS P01 HL029582NHLBI NIH HHS P01 HL103453NHLBI NIH HHS U10 HL109250NINDS NIH HHS R01 NS071996
6 · The paper itself

Abstract

NOTCH1 signalling contributes to defective remyelination by impairing differentiation of oligodendrocyte progenitor cells (OPCs). Here we report that IL-17 stimulation induces NOTCH1 activation in OPCs, contributing to Th17-mediated demyelinating disease. Mechanistically, IL-17R interacts with NOTCH1 via the extracellular domain, which facilitates the cleavage of NOTHC1 intracellular domain (NICD1). IL-17-induced NOTCH1 activation results in the interaction of IL-17R adaptor Act1 with NICD1, followed by the translocation of the Act1-NICD1 complex into the nucleus. Act1-NICD1 are recruited to the promoters of several NOTCH1 target genes (including STEAP4, a metalloreductase important for inflammation and cell proliferation) that are specifically induced in the spinal cord by Th17 cells. A decoy peptide disrupting the IL-17RA-NOTCH1 interaction inhibits IL-17-induced NOTCH1 activation and attenuates Th17-mediated experimental autoimmune encephalitis (EAE). Taken together, these findings demonstrate critical crosstalk between the IL-17 and NOTCH1 pathway, regulating Th17-induced inflammatory and proliferative genes to promote demyelinating disease.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsAstrocytesCell DifferentiationCell ProliferationCoculture TechniquesEncephalomyelitis, Autoimmune, ExperimentalFemaleHEK293 CellsHeLa CellsHumansImmunoglobulin J Recombination Signal Sequence-Binding ProteinInterleukin-17MiceMice, Inbred C57BLMice, TransgenicAdaptor Proteins, Signal TransducingIL17RA protein, humanImmunoglobulin J Recombination Signal Sequence-Binding ProteinInterleukin-17NOTCH1 protein, humanRBPJ protein, humanReceptor, Notch1Receptors, Interleukin-17TRAF3IP2 protein, humanTumor Necrosis Factor Receptor-Associated Peptides and Proteins

Identifiers

PMID28561022
PMCPMC5460031
OpenAlexW2619660012

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.