Evidence map›Paper›PMID 31068071›Full record

ArticleAutophagy2020

LRRC59 modulates type I interferon signaling by restraining the SQSTM1/p62-mediated autophagic degradation of pattern recognition receptor DDX58/RIG-I.

Huifang Xian, Shuai Yang, Shouheng Jin, Yuxia Zhang, Jun Cui

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

49 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
  2. Regulation of Innate Immune Signaling by Autophagy.International journal of molecular sciences · 2026
    Review
  3. Role of autophagy in antiviral innate immunity.Cellular & molecular biology letters · 2026
    Review
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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

5 authors at 1 institution in 1 country.

Huifang XianDepartment of Internal Medicine, Guangzhou Institute of Pediatrics, Guangzhou Women and Children's Medical Center, and MOE Key Laboratory of Gene Function and Regulation, School of Life Sciences, Sun Yat-sen University, Guangzhou, GD, China.
Shuai YangDepartment of Internal Medicine, Guangzhou Institute of Pediatrics, Guangzhou Women and Children's Medical Center, and MOE Key Laboratory of Gene Function and Regulation, School of Life Sciences, Sun Yat-sen University, Guangzhou, GD, China.
Shouheng JinDepartment of Internal Medicine, Guangzhou Institute of Pediatrics, Guangzhou Women and Children's Medical Center, and MOE Key Laboratory of Gene Function and Regulation, School of Life Sciences, Sun Yat-sen University, Guangzhou, GD, China.
Yuxia ZhangDepartment of Internal Medicine, Guangzhou Institute of Pediatrics, Guangzhou Women and Children's Medical Center, and MOE Key Laboratory of Gene Function and Regulation, School of Life Sciences, Sun Yat-sen University, Guangzhou, GD, China.
Jun CuiDepartment of Internal Medicine, Guangzhou Institute of Pediatrics, Guangzhou Women and Children's Medical Center, and MOE Key Laboratory of Gene Function and Regulation, School of Life Sciences, Sun Yat-sen University, Guangzhou, GD, China.ORCID 0000-0002-8000-3708
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DDX58/RIG-I, is a critical pattern recognition receptor for viral RNA, which plays an essential role in antiviral immunity. Its posttranslational modifications and stability are tightly regulated to mediate the moderate production of type I IFN to maintain the immune homeostasis. Recently, we reported that macroautophagy/autophagy balances type I IFN signaling through selective degradation of ISG15-associated DDX58 via LRRC25. However, the regulatory mechanism about the autophagic degradation of DDX58 remains largely undefined. Here, we identified LRRC59 as a vital positive regulator of DDX58-mediated type I IFN signaling. Upon virus infection, LRRC59 specifically interacted with ISG15-associated DDX58 and blocked its association with LRRC25, the secondary receptor to deliver DDX58 to autophagosomes for SQSTM1/p62-dependent degradation, leading to the stronger antiviral immune responses. Thus, our study reveals a novel regulatory role of selective autophagy in innate antiviral responses mediated by the cross-regulation of LRRC family members. These data further provide insights into the crosstalk between autophagy and innate immune responses.

Indexed as

AutophagyProteolysisSignal TransductionCell LineCytokinesDEAD Box Protein 58HumansInterferon Type IMembrane ProteinsModels, BiologicalProtein BindingProtein StabilityReceptors, ImmunologicSequestosome-1 ProteinUbiquitinsVirus DiseasesCytokinesDEAD Box Protein 58Interferon Type IISG15 protein, humanLRRC59 protein, humanMembrane ProteinsReceptors, ImmunologicRIGI protein, humanSequestosome-1 ProteinSQSTM1 protein, humanUbiquitinsAutophagic degradationcargo receptorDDX58/RIG-ILRRC59type I interferon

Identifiers

PMID31068071
PMCPMC6999607
OpenAlexW2943886226

What OpenQuestion holds

Textmetadata
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.