Evidence map›Paper›PMID 28418037›Full record

ArticleScientific reports2017

Mitochondrial C11orf83 is a potent Antiviral Protein Independent of interferon production.

Yun Yang, Shaoquan Xiong, Bei Cai, Hui Luo, E Dong, Qiqi Li, Gaili Ji, Chengjian Zhao, Yanjun Wen, Yuquan Wei and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 47% 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

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Innate Antiviral Immunity in the Skin.Trends in immunology · 2018
    Review
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

11 authors at 2 institutions in 1 country.

Yun YangState Key Laboratory of Biotherapy and Cancer center/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, 610041, Chengdu, China.
Shaoquan XiongState Key Laboratory of Biotherapy and Cancer center/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, 610041, Chengdu, China.
Bei CaiDepartment of Laboratory Medicine/Research Center of Clinical Laboratory Medicine, West China Hospital, Sichuan University, 610041, Chengdu, China.
Hui LuoState Key Laboratory of Biotherapy and Cancer center/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, 610041, Chengdu, China.
E DongState Key Laboratory of Biotherapy and Cancer center/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, 610041, Chengdu, China.
Qiqi LiState Key Laboratory of Biotherapy and Cancer center/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, 610041, Chengdu, China.
Gaili JiState Key Laboratory of Biotherapy and Cancer center/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, 610041, Chengdu, China.
Chengjian ZhaoState Key Laboratory of Biotherapy and Cancer center/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, 610041, Chengdu, China.
Yanjun WenState Key Laboratory of Biotherapy and Cancer center/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, 610041, Chengdu, China.
Yuquan WeiState Key Laboratory of Biotherapy and Cancer center/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, 610041, Chengdu, China.
Hanshuo YangState Key Laboratory of Biotherapy and Cancer center/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, 610041, Chengdu, China.
Sichuan University · CNState Key Laboratory of Biotherapy

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria have a central position in innate immune response via the adaptor protein MAVS in mitochondrial outer membrane to limit viral replication by inducing interferon production. Here, we reported that C11orf83, a component of complex III of electronic transfer chain in mitochondrial inner membrane, was a potent antiviral protein independent of interferon production. C11orf83 expression significantly increased in response to viral infection, and endows cells with stronger capability of inhibiting viral replication. Deletion of C11orf83 permits viral replication easier and cells were more vulnerable to viral killing. These effects mainly were mediated by triggering OAS3-RNase L system. C11orf83 overexpression induced higher transcription of OAS3, and knockdown either OAS3 or RNase L impaired the antiviral capability of C11orf83. Interestingly, the signaling from C11orf83 to OAS3-RNase L was independent of interferon production. Thus, our findings suggested a new antiviral mechanism by bridging cell metabolic machinery component with antiviral effectors.

Indexed as

Host-Pathogen Interactions2',5'-Oligoadenylate SynthetaseAnimalsCarrier ProteinsChlorocebus aethiopsCRISPR-Cas SystemsEndoribonucleasesGene DeletionGene Expression RegulationGenes, ReporterGreen Fluorescent ProteinsHEK293 CellsHep G2 CellsHumansHuman Umbilical Vein Endothelial CellsImmunity, Innate2-5A-dependent ribonuclease2',5'-Oligoadenylate SynthetaseCarrier ProteinsEndoribonucleasesenhanced green fluorescent proteinGreen Fluorescent ProteinsInterferon-gammaLuciferasesOAS3 protein, humanUQCC3 protein, human

Identifiers

PMID28418037
PMCPMC5394693
OpenAlexW2606292501

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.