Evidence map›Paper›PMID 39420190›Full record

ArticleCell death discovery2024

N4BP3 facilitates NOD2-MAPK/NF-κB pathway in inflammatory bowel disease through mediating K63-linked RIPK2 ubiquitination.

Wang Jiang, Yan Zhao, Min Han, Jiafan Xu, Kun Chen, Yi Liang, Jie Yin, Jinyue Hu, Yueming Shen

Erratum issuedAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Wang Jiang *Department of Digestive Diseases, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, 161 Shaoshan Road, Changsha, 410000, China.ORCID http://orcid.org/0009-0000-6229-1702
Yan Zhao *Department of Pathology, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, 161 Shaoshan Road, Changsha, 410000, China.
Min HanDepartment of Cardiovascular Diseases, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, 161 Shaoshan Road, Changsha, 410000, China.
Jiafan XuDepartment of Digestive Diseases, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, 161 Shaoshan Road, Changsha, 410000, China.
Kun ChenDepartment of Orthopaedics, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, Hunan, China.
Yi LiangDepartment of Gastrointestinal Surgery, The Second Affiliated Hospital, Hengyang Medical School, University of South China, 35 Jiefang Road, Hengyang, 421000, China.
Jie YinDepartment of Digestive Diseases, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, 161 Shaoshan Road, Changsha, 410000, China.
Jinyue HuMedical Research Center, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, 410004, China.
Yueming ShenDepartment of Digestive Diseases, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, 161 Shaoshan Road, Changsha, 410000, China. 2018050504@usc.edu.cn.ORCID http://orcid.org/0000-0002-7234-5492

Funding

Natural Science Foundation of Hunan Province (Hunan Provincial Natural Science Foundation) 2023JJ30067
6 · The paper itself

Abstract

The NOD2 signaling pathway, which plays an important role in the mechanisms of inflammatory bowel disease (IBD) development, has been closely associated with ubiquitination. It was revealed in this study that NOD2 receptor activation could obviously affect the expression of 19 ubiquitination-related genes, with N4BP3 being the most prominently expressed and upregulated. In addition, N4BP3 knockdown was found to reduce the mRNA levels of MDP-induced inflammatory factors, while N4BP3 overexpression elevated their mRNA levels as well as the levels of phospho-ERK1/2, phospho-JNK, phospho-P38 and phospho-NF-κB P65 proteins. Immunoprecipitation tests showed that N4BP3 could pull down RIPK2 and promote its K63-linked ubiquitination. In human tissue specimen assays and mouse experiments, we found that the expression of N4BP3 was significantly elevated in Crohn's disease (CD) patients and IBD mice, and N4BP3 knockdown reduced the dextran sulfate sodium-induced pathological score and the expression of inflammatory factors in the mouse colon tissue. In conclusion, N4BP3 is able to interact with RIPK2 and promote its K63-linked ubiquitination, to further promote the NOD2-MAPK/NF-κB pathway, thereby increasing promoting the release of inflammation factors and the degree of IBD inflammation.

Identifiers

PMID39420190
PMCPMC11487068

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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.