Evidence map›Paper›PMID 29255244›Full record

ArticleNature communications2017

ANGPTL8 negatively regulates NF-κB activation by facilitating selective autophagic degradation of IKKγ.

Yu Zhang, Xian Guo, Wanyao Yan, Yan Chen, Mengxiang Ke, Cheng Cheng, Xiuqin Zhu, Weili Xue, Qiaoqiao Zhou, Ling Zheng and 6 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 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
8.0field-weighted citation impact, top 2% 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

62 citing papers in PubMed, 106 citations in OpenAlex.

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2 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 4 institutions in 1 country.

Yu ZhangTongji School of Pharmacy, Huazhong University of Science & Technology, Wuhan, 430030, China.
Xian GuoTongji School of Pharmacy, Huazhong University of Science & Technology, Wuhan, 430030, China.
Wanyao YanTongji School of Pharmacy, Huazhong University of Science & Technology, Wuhan, 430030, China.
Yan ChenTongji School of Pharmacy, Huazhong University of Science & Technology, Wuhan, 430030, China.
Mengxiang KeTongji School of Pharmacy, Huazhong University of Science & Technology, Wuhan, 430030, China.
Cheng ChengTongji School of Pharmacy, Huazhong University of Science & Technology, Wuhan, 430030, China.
Xiuqin ZhuHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, 430072, China.
Weili XueHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, 430072, China.
Qiaoqiao ZhouTongji School of Pharmacy, Huazhong University of Science & Technology, Wuhan, 430030, China.
Ling ZhengHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, 430072, China.
Shun WangDepartment of Blood Transfusion, Wuhan Hospital of Traditional and Western Medicine, Wuhan, 430022, China.
Bin WuDepartment of Blood Transfusion, Wuhan Hospital of Traditional and Western Medicine, Wuhan, 430022, China.
Xinran LiuTongji School of Pharmacy, Huazhong University of Science & Technology, Wuhan, 430030, China.
Liang MaTongji School of Pharmacy, Huazhong University of Science & Technology, Wuhan, 430030, China.
Lianqi HuangTongji School of Pharmacy, Huazhong University of Science & Technology, Wuhan, 430030, China.
Kun HuangTongji School of Pharmacy, Huazhong University of Science & Technology, Wuhan, 430030, China. kunhuang2008@hotmail.com.
Huazhong University of Science and Technology · CNWuhan University · CNWuhan No.1 Hospital · CNWuhan Institute of Bioengineering · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive nuclear factor-κB (NF-κB) activation mediated by tumor necrosis factor α (TNFα) plays a critical role in inflammation. Here we demonstrate that angiopoietin-like 8 (ANGPTL8) functions as a negative feedback regulator in TNFα-triggered NF-κB activation intracellularly. Inflammatory stimuli induce ANGPTL8 expression, and knockdown or knockout of ANGPTL8 potentiates TNFα-induced NF-κB activation in vitro. Mechanistically, upon TNFα stimulation, ANGPTL8 facilitates the interaction of IKKγ with p62 via forming a complex, thus promoting the selective autophagic degradation of IKKγ. Furthermore, the N-terminal domain mediated self-oligomerization of ANGPTL8 is essential for IKKγ degradation and NF-κB activation. In vivo, circulating ANGPTL8 level is high in patients diagnosed with infectious diseases, and the ANGPTL8/p62-IKKγ axis is responsive to inflammatory stimuli in the liver of LPS-injected mice. Altogether, our study suggests the ANGPTL8/p62-IKKγ axis as a negative feedback loop that regulates NF-κB activation, and extends the role of selective autophagy in fine-tuned inflammatory responses.

Indexed as

AutophagyA549 CellsAngiopoietin-Like Protein 8Angiopoietin-like ProteinsAnimalsGene Expression RegulationHEK293 CellsHep G2 CellsHumansI-kappa B KinaseInflammationInterleukin-1betaMaleMice, Inbred C57BLNF-kappa BPeptide HormonesAngiopoietin-Like Protein 8Angiopoietin-like ProteinsANGPTL8 protein, humanI-kappa B KinaseInterleukin-1betaNF-kappa BPeptide HormonesSequestosome-1 ProteinSQSTM1 protein, human

Identifiers

PMID29255244
PMCPMC5735157
OpenAlexW2773542217

What OpenQuestion holds

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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.