Evidence map›Paper›PMID 38866307›Full record

ArticleBrain research2024

Hypersensitivity to type I interferon as a cause of hydrocephalus development.

Kei-Ichiro Arimoto, Yue Zhang, Shinobu Matsuura, Sayuri Miyauchi, Dong-Er Zhang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Brain research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

5 authors.

Kei-Ichiro ArimotoMoores UCSD Cancer Center, University of California, San Diego, 3855 Health Sciences Drive, La Jolla, CA 92093, USA; Department of Pathology, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Yue ZhangMoores UCSD Cancer Center, University of California, San Diego, 3855 Health Sciences Drive, La Jolla, CA 92093, USA.
Shinobu MatsuuraMoores UCSD Cancer Center, University of California, San Diego, 3855 Health Sciences Drive, La Jolla, CA 92093, USA.
Sayuri MiyauchiMoores UCSD Cancer Center, University of California, San Diego, 3855 Health Sciences Drive, La Jolla, CA 92093, USA.
Dong-Er ZhangMoores UCSD Cancer Center, University of California, San Diego, 3855 Health Sciences Drive, La Jolla, CA 92093, USA; Department of Pathology, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA; Department of Molecular Biology, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA. Electronic address: d7zhang@health.ucsd.edu.

Funding

ISG15 and Protein ISGylation in CancerR01CA177305 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ZHANG, DONG-ER · 2013 to 2023
$3.7M
USP18 in Cancer DevelopmentR01CA232147 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ZHANG, DONG-ER · 2019 to 2023
$1.9M
Novel molecular targets of RUNX in hematopoietic stem/progenitor cellsF32HL091641 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MATSUURA, SHINOBU · 2008 to 2010
$155k
NCI NIH HHS R01 CA177305NCI NIH HHS R01 CA232147NHLBI NIH HHS F32 HL091641
6 · The paper itself

Abstract

Ubiquitin specific protease 18 (USP18) serves as a potent inhibitor of Type I interferon (IFN) signaling. Previous studies have shown that Usp18 deficient (homozygous Usp18 gene knockout) mice exhibit hydrocephalus; however, the precise molecular mechanism underlying hydrocephalus development remains elusive. In this study, we demonstrate that mice lacking both type I IFN receptor subunit 1 (Ifnar1) and Usp18 (Ifnar1/Usp18 double knockout mice) are viable and do not display a hydrocephalus phenotype. Moreover, we observed that suppression of USP18 in ependymal cells treated with IFN significantly increased cell death, including pyroptosis, and decreased proliferation. These findings suggest that heightened sensitivity to type I IFN during brain development contributes to the onset of hydrocephalus. Furthermore, they imply that inhibition of IFN signaling may hold promise as a therapeutic strategy for hydrocephalus.

Indexed as

HydrocephalusInterferon Type IMice, KnockoutReceptor, Interferon alpha-betaUbiquitin ThiolesteraseAnimalsBrainCell ProliferationEpendymaMiceMice, Inbred C57BLPyroptosisSignal TransductionIfnar1 protein, mouseInterferon Type IReceptor, Interferon alpha-betaUbiquitin ThiolesteraseUsp18 protein, mouseEpendymal cellsHydrocephalusIFN responsePyroptosisUbiquitin specific protease 18 (USP18)

Identifiers

PMID38866307
PMCPMC12092069

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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.