Evidence map›Paper›PMID 33523871›Full record

ArticleScience advances2021

Substrate-specific recognition of IKKs mediated by USP16 facilitates autoimmune inflammation.

Jian-Shuai Yu, Tao Huang, Yu Zhang, Xin-Tao Mao, Ling-Jie Huang, Yi-Ning Li, Ting-Ting Wu, Jiang-Yan Zhong, Qian Cao, Yi-Yuan Li and 1 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

26 citing papers in PubMed, 56 citations in OpenAlex.

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  15. Epithelial CRL4Digestive diseases and sciences · 2024
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  18. USP16 is an ISG15 cross-reactive deubiquitinase that targets pro-ISG15 and ISGylated proteins involved in metabolism.Proceedings of the National Academy of Sciences of the United States of America · 2023
    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

11 authors at 2 institutions in 1 country.

Jian-Shuai YuMOE Laboratory of Biosystem Homeostasis and Protection and Life Sciences Institute, Zhejiang University, Hangzhou 310058, China.ORCID 0000-0003-4033-9589
Tao HuangMOE Laboratory of Biosystem Homeostasis and Protection and Life Sciences Institute, Zhejiang University, Hangzhou 310058, China.ORCID 0000-0002-2723-3432
Yu ZhangSir Run Run Shaw Hospital, College of Medicine, Zhejiang University, Hangzhou 310016, China.ORCID 0000-0002-6736-5130
Xin-Tao MaoMOE Laboratory of Biosystem Homeostasis and Protection and Life Sciences Institute, Zhejiang University, Hangzhou 310058, China.
Ling-Jie HuangSir Run Run Shaw Hospital, College of Medicine, Zhejiang University, Hangzhou 310016, China.
Yi-Ning LiMOE Laboratory of Biosystem Homeostasis and Protection and Life Sciences Institute, Zhejiang University, Hangzhou 310058, China.
Ting-Ting WuSir Run Run Shaw Hospital, College of Medicine, Zhejiang University, Hangzhou 310016, China.
Jiang-Yan ZhongMOE Laboratory of Biosystem Homeostasis and Protection and Life Sciences Institute, Zhejiang University, Hangzhou 310058, China.
Qian CaoSir Run Run Shaw Hospital, College of Medicine, Zhejiang University, Hangzhou 310016, China.
Yi-Yuan LiKey Laboratory for Developmental Genes and Human Disease, Ministry of Education, Institute of Life Sciences, Jiangsu Province High-Tech Key Laboratory for Bio-Medical Research, Southeast University, Nanjing 210096, China. jjin4@zju.edu.cn 103200067@seu.edu.cn.ORCID 0000-0002-3859-0726
Jin JinMOE Laboratory of Biosystem Homeostasis and Protection and Life Sciences Institute, Zhejiang University, Hangzhou 310058, China. jjin4@zju.edu.cn 103200067@seu.edu.cn.ORCID 0000-0001-7887-5972
Zhejiang University · CNSir Run Run Shaw Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The classic NF-κB pathway plays crucial roles in various immune responses and inflammatory diseases. Its key kinase, IKKβ, participates in a variety of pathological and physiological processes by selectively recognizing its downstream substrates, including p105, p65, and IκBα, but the specific mechanisms of these substrates are unclear. Hyperactivation of one of the substrates, p105, is closely related to the onset of inflammatory bowel disease (IBD) in

Identifiers

PMID33523871
PMCPMC7806237
OpenAlexW3120859881

What OpenQuestion 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 OpenQuestion graph.