Evidence map›Paper›PMID 30867837›Full record

ArticleTheranostics2019

Absence of GdX/UBL4A Protects against Inflammatory Diseases by Regulating NF-кB Signaling in Macrophages and Dendritic Cells.

Chunxiao Liu, Yifan Zhou, Mengdi Li, Ying Wang, Liu Yang, Shigao Yang, Yarui Feng, Yinyin Wang, Yangmeng Wang, Fangli Ren and 6 more

Open access · goldAbstract read
In one paragraph

Article in Theranostics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

22 citing papers in PubMed, 29 citations in OpenAlex.

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  14. The Dispensable Roles of X-LinkedFrontiers in genetics · 2021
    Article
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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

16 authors at 1 institution in 1 country.

Chunxiao LiuState Key Laboratory of Membrane Biology, School of Medicine, Tsinghua University, Beijing (100084), China.
Yifan ZhouInstitute for Immunology, School of Medicine, Tsinghua University, Beijing (100084), China.
Mengdi LiState Key Laboratory of Membrane Biology, School of Medicine, Tsinghua University, Beijing (100084), China.
Ying WangState Key Laboratory of Membrane Biology, School of Medicine, Tsinghua University, Beijing (100084), China.
Liu YangState Key Laboratory of Membrane Biology, School of Medicine, Tsinghua University, Beijing (100084), China.
Shigao YangState Key Laboratory of Membrane Biology, School of Medicine, Tsinghua University, Beijing (100084), China.
Yarui FengState Key Laboratory of Membrane Biology, School of Medicine, Tsinghua University, Beijing (100084), China.
Yinyin WangState Key Laboratory of Membrane Biology, School of Medicine, Tsinghua University, Beijing (100084), China.
Yangmeng WangState Key Laboratory of Membrane Biology, School of Medicine, Tsinghua University, Beijing (100084), China.
Fangli RenState Key Laboratory of Membrane Biology, School of Medicine, Tsinghua University, Beijing (100084), China.
Jun LiInstitute of Immunology, PLA, The Third Military Medical University, Chongqing, (400038), China.
Zhongjun DongInstitute for Immunology, School of Medicine, Tsinghua University, Beijing (100084), China.
Y Eugene ChinInstitute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai Jiaotong University School of Medicine, Shanghai (200025), China.
Xinyuan FuDepartment of Biochemistry, South University of Science and Technology of China, Shenzhen (518055), China.
Li WuInstitute for Immunology, School of Medicine, Tsinghua University, Beijing (100084), China.
Zhijie ChangState Key Laboratory of Membrane Biology, School of Medicine, Tsinghua University, Beijing (100084), China.
Tsinghua University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nuclear factor-kappa B (NF-κB) activation is critical for innate immune responses. However, cellular-intrinsic regulation of NF-κB activity during inflammatory diseases remains incompletely understood. Ubiquitin-like protein 4A (UBL4A, GdX) is a small adaptor protein involved in protein folding, biogenesis and transcription. Yet, whether GdX has a role during innate immune response is largely unknown.

Indexed as

Immunity, InnateSignal TransductionAnimalsColitisDendritic CellsDextran SulfateDisease Models, AnimalLipopolysaccharidesMacrophagesMiceMice, KnockoutNF-kappa BUbiquitinsDextran SulfateLipopolysaccharidesNF-kappa BUbiquitinsUbl4a protein, mousedendritic cellsGdX/UBL4AinflammationmacrophagesNF-κBp65/RelA

Identifiers

PMID30867837
PMCPMC6401509
OpenAlexW2917189190

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.