Evidence map›Paper›PMID 31225468›Full record

ArticleCell stress2018

A new way to regulate inflammation: selective autophagic degradation of IKKγ mediated by ANGPTL8.

Yu Zhang, Ling Zheng, Kun Huang

Open access · goldAbstract readComment
In one paragraph

Article in Cell stress, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Yu ZhangTongji School of Pharmacy, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, P.R.China, 430030.
Ling ZhengHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, P.R.China, 430072.
Kun HuangTongji School of Pharmacy, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, P.R.China, 430030.
Huazhong University of Science and Technology · CNWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transcription factor nuclear factor-κB (NF-κB) plays pivotal roles in the regulation of inflammation and immunity. However, the precise mechanism of NF-κB activation is not fully elucidated. We recently found that Angiopoietin like protein 8 (ANGPTL8, also known as Lipasin, RIFL, TD26 or C19orf80), which is a previously identified secreted metabolic regulator, also can work intracellularly as a negative feedback inhibitor of NF-κB activation. Mechanistically, ANGPTL8 is induced by TNFα stimulation, a classic inducer for NF-κB activation; then, the intracellular ANGPTL8 self-associates via its N-terminal region and interacts with Sequestosome-1 (p62/SQSTM1). The resulting ANGPTL8-p62 aggregates work as a platform in the recruitment and autophagic degradation of IκB kinase gamma (IKKγ/NEMO). Consistently, in patients diagnosed with infectious diseases, enhanced circulating ANGPTL8 levels were detected. These findings suggest a new role for selective autophagy in the regulation of signal transduction and inflammation.

Indexed as

ANGPTL8NF-κBoligomerizationselective autophagysignal transduction

Identifiers

PMID31225468
PMCPMC6558929
OpenAlexW2788448166

What OpenQuestion holds

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LicenceCC BY
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.