Evidence map›Paper›PMID 29280086›Full record

ArticleMolecular and cellular biochemistry2018

Negative regulation of MAVS-mediated innate immune response by ASC.

Yue Han, Xiang He, Congwen Wei, Ting Song, Ling Zou, Zihui Li, Jiazhou Ye, Lunan Qi, Lequn Li, Hui Zhong and 1 more

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. 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.

Yue HanDepartment of Interventional Therapy, National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100850, People's Republic of China.
Xiang HeState Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Biotechnology, Beijing, 100850, People's Republic of China.
Congwen WeiState Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Biotechnology, Beijing, 100850, People's Republic of China.
Ting SongState Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Biotechnology, Beijing, 100850, People's Republic of China.
Ling ZouDepartment of Hepatobiliary Surgery, Affiliated Tumor Hospital of Guangxi Medical University, He Di Road 71#, Nanning, 530021, People's Republic of China.
Zihui LiDepartment of Hepatobiliary Surgery, Affiliated Tumor Hospital of Guangxi Medical University, He Di Road 71#, Nanning, 530021, People's Republic of China.
Jiazhou YeDepartment of Hepatobiliary Surgery, Affiliated Tumor Hospital of Guangxi Medical University, He Di Road 71#, Nanning, 530021, People's Republic of China.
Lunan QiDepartment of Hepatobiliary Surgery, Affiliated Tumor Hospital of Guangxi Medical University, He Di Road 71#, Nanning, 530021, People's Republic of China.
Lequn LiDepartment of Hepatobiliary Surgery, Affiliated Tumor Hospital of Guangxi Medical University, He Di Road 71#, Nanning, 530021, People's Republic of China.
Hui ZhongState Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Biotechnology, Beijing, 100850, People's Republic of China.
Feixiang WuDepartment of Hepatobiliary Surgery, Affiliated Tumor Hospital of Guangxi Medical University, He Di Road 71#, Nanning, 530021, People's Republic of China. wufx2013@163.com.

Funding

Key Laboratory of Early Prevention and Treatment for Regional High Frequency Tumor, Ministry of Education GKZ201604Key project of Guangxi Health and Family Planning Commission S201513Key project of Guangxi science and technology department GuiKe AB 16380242
6 · The paper itself

Abstract

Stringent control of the type I interferon signaling pathways is critical to effective host immune responses, however, the molecular mechanisms that negatively regulate these pathways are still poorly understood. Here, we show that apoptosis speck-like protein (ASC), an adaptor protein of inflammasome complex, can inhibit IFN-β signaling response by interacting with mitochondrial antiviral signaling protein (MAVS). Importantly, ASC-specific siRNA knockdown enhanced virus-induced type I interferon production, with consequent reduction of virus replication. Taken together, these results suggest that ASC, as a negative regulator of the MAVS-mediated innate immunity, may play an important role in host protection upon virus infection.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCARD Signaling Adaptor ProteinsCells, CulturedGene Knockdown TechniquesHEK293 CellsHost-Pathogen InteractionsHumansImmunity, InnateInflammasomesInterferon-betaMCF-7 CellsMiceRNA, Small InterferingSignal TransductionVirus DiseasesAdaptor Proteins, Signal TransducingCARD Signaling Adaptor ProteinsInflammasomesInterferon-betaMAVS protein, humanPYCARD protein, humanRNA, Small InterferingASCInnate immunityMAVS

Identifiers

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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.