Evidence map›Paper›PMID 31921549›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2020

TRIM14 Promotes Noncanonical NF-κB Activation by Modulating p100/p52 Stability via Selective Autophagy.

Meixin Chen, Zhiyao Zhao, Qingcai Meng, Puping Liang, Zexiong Su, Yaoxing Wu, Junjiu Huang, Jun Cui

Open access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

38 citing papers in PubMed, 58 citations in OpenAlex.

  1. Role of autophagy in antiviral innate immunity.Cellular & molecular biology letters · 2026
    Review
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  15. An Antiviral Role for TRIM14 in Ebola Virus Infection.The Journal of infectious diseases · 2023
    Article
  16. Review
  17. Article
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  20. Ameliorating Effects ofInternational journal of molecular sciences · 2022
    Article
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

8 authors at 1 institution in 1 country.

Meixin ChenState Key Laboratory of Oncology in South China MOE Key Laboratory of Gene Function and Regulation School of Life Sciences Sun Yat-Sen University Guangzhou Guangdong 510006 China.
Zhiyao ZhaoState Key Laboratory of Oncology in South China MOE Key Laboratory of Gene Function and Regulation School of Life Sciences Sun Yat-Sen University Guangzhou Guangdong 510006 China.
Qingcai MengState Key Laboratory of Oncology in South China MOE Key Laboratory of Gene Function and Regulation School of Life Sciences Sun Yat-Sen University Guangzhou Guangdong 510006 China.
Puping LiangState Key Laboratory of Oncology in South China MOE Key Laboratory of Gene Function and Regulation School of Life Sciences Sun Yat-Sen University Guangzhou Guangdong 510006 China.
Zexiong SuState Key Laboratory of Oncology in South China MOE Key Laboratory of Gene Function and Regulation School of Life Sciences Sun Yat-Sen University Guangzhou Guangdong 510006 China.
Yaoxing WuState Key Laboratory of Oncology in South China MOE Key Laboratory of Gene Function and Regulation School of Life Sciences Sun Yat-Sen University Guangzhou Guangdong 510006 China.
Junjiu HuangState Key Laboratory of Oncology in South China MOE Key Laboratory of Gene Function and Regulation School of Life Sciences Sun Yat-Sen University Guangzhou Guangdong 510006 China.
Jun CuiState Key Laboratory of Oncology in South China MOE Key Laboratory of Gene Function and Regulation School of Life Sciences Sun Yat-Sen University Guangzhou Guangdong 510006 China.ORCID https://orcid.org/0000-0002-8000-3708
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The noncanonical NF-κB signaling pathway plays a critical role in a variety of biological functions including chronic inflammation and tumorigenesis. Activation of noncanonical NF-κB signaling largely relies on the abundance as well as the processing of the NF-κB family member p100/p52. Here, TRIM14 is identified as a novel positive regulator of the noncanonical NF-κB signaling pathway. TRIM14 promotes noncanonical NF-κB activation by targeting p100/p52 in vitro and in vivo. Furthermore, a mechanistic study shows that TRIM14 recruits deubiquitinase USP14 to cleave the K63-linked ubiquitin chains of p100/p52 at multiple sites, thereby preventing p100/p52 from cargo receptor p62-mediated autophagic degradation. TRIM14 deficiency in mice significantly impairs noncanonical NF-κB-mediated inflammatory responses as well as acute colitis and colitis-associated colon cancer development. Taken together, these findings establish the TRIM14-USP14 axis as a crucial checkpoint that controls noncanonical NF-κB signaling and highlight the crosstalk between autophagy and innate immunity.

Indexed as

inflammationnoncanonical NF‐κB signalingp100/p52selective autophagyTRIM14

Identifiers

PMID31921549
PMCPMC6947505
OpenAlexW2986148998

What OpenQuestion holds

Textmetadata
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.