Evidence map›Paper›PMID 32283527›Full record

ArticleiScience2020

Inhibition of cGAS-Mediated Interferon Response Facilitates Transgene Expression.

Yajuan Fu, Yijun Fang, Zhang Lin, Lei Yang, Liqun Zheng, Hao Hu, Tingting Yu, Baoting Huang, Suxing Chen, Hanze Wang and 4 more

Open access · goldAbstract read
In one paragraph

Article in iScience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

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  13. Transcriptomic analysis of the innate immune response toMolecular therapy. Nucleic acids · 2023
    Article
  14. Review
  15. Tools to Investigate the Peroxisome-Dependent Antiviral Response.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  16. Review
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  19. Article
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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

14 authors at 1 institution in 1 country.

Yajuan FuFujian Key Laboratory of Innate Immune Biology, Biomedical Research Center of South China, College of Life Science, Fujian Normal University Qishan Campus, College Town, Fuzhou, Fujian Province 350117, China.
Yijun FangFujian Key Laboratory of Innate Immune Biology, Biomedical Research Center of South China, College of Life Science, Fujian Normal University Qishan Campus, College Town, Fuzhou, Fujian Province 350117, China.
Zhang LinFujian Key Laboratory of Innate Immune Biology, Biomedical Research Center of South China, College of Life Science, Fujian Normal University Qishan Campus, College Town, Fuzhou, Fujian Province 350117, China.
Lei YangFujian Key Laboratory of Innate Immune Biology, Biomedical Research Center of South China, College of Life Science, Fujian Normal University Qishan Campus, College Town, Fuzhou, Fujian Province 350117, China.
Liqun ZhengFujian Key Laboratory of Innate Immune Biology, Biomedical Research Center of South China, College of Life Science, Fujian Normal University Qishan Campus, College Town, Fuzhou, Fujian Province 350117, China.
Hao HuFujian Key Laboratory of Innate Immune Biology, Biomedical Research Center of South China, College of Life Science, Fujian Normal University Qishan Campus, College Town, Fuzhou, Fujian Province 350117, China.
Tingting YuFujian Key Laboratory of Innate Immune Biology, Biomedical Research Center of South China, College of Life Science, Fujian Normal University Qishan Campus, College Town, Fuzhou, Fujian Province 350117, China.
Baoting HuangFujian Key Laboratory of Innate Immune Biology, Biomedical Research Center of South China, College of Life Science, Fujian Normal University Qishan Campus, College Town, Fuzhou, Fujian Province 350117, China.
Suxing ChenFujian Key Laboratory of Innate Immune Biology, Biomedical Research Center of South China, College of Life Science, Fujian Normal University Qishan Campus, College Town, Fuzhou, Fujian Province 350117, China.
Hanze WangFujian Key Laboratory of Innate Immune Biology, Biomedical Research Center of South China, College of Life Science, Fujian Normal University Qishan Campus, College Town, Fuzhou, Fujian Province 350117, China.
Shan XuFujian Key Laboratory of Innate Immune Biology, Biomedical Research Center of South China, College of Life Science, Fujian Normal University Qishan Campus, College Town, Fuzhou, Fujian Province 350117, China.
Wei BaoFujian Normal University Hospital, Fujian Normal University Qishan Campus, College Town, Fuzhou, Fujian Province 350117, China.
Qi ChenFujian Key Laboratory of Innate Immune Biology, Biomedical Research Center of South China, College of Life Science, Fujian Normal University Qishan Campus, College Town, Fuzhou, Fujian Province 350117, China. Electronic address: nfsw@fjnu.edu.cn.
Lijun SunFujian Key Laboratory of Innate Immune Biology, Biomedical Research Center of South China, College of Life Science, Fujian Normal University Qishan Campus, College Town, Fuzhou, Fujian Province 350117, China. Electronic address: sunlijun@fjnu.edu.cn.
Fujian Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA transfection is often the bottleneck of research and gene therapy practices. To explore the mechanism regulating transgene expression, we investigated the role of the cGAS-STING signaling pathway, which induces type-I interferons in response to DNA. We confirmed that deletion of cGAS enhances transgene expression at the protein level by ~2- to 3-fold. This enhancement is inversely correlated with the expression of interferons and interferon stimulated genes (ISGs), which suppress expression of transfected genes at the mRNA level. Mechanistically, DNA transfection activates the cGAS-STING pathway and induces the expression of the OAS family proteins, leading to the activation of RNaseL and degradation of mRNA derived from transgenes. Administration of chemical inhibitors that block cGAS-mediated signaling cascades improves the expression of transgenes by ~1.5- to 3-fold in multiple cell lines and primary cells, including T cells. These data suggest that targeting the cGAS-STING pathway can improve transgene expression, and this strategy may be applied to gene therapy.

Indexed as

Biological SciencesMolecular BiologyMolecular Mechanism of Gene Regulation

Identifiers

PMID32283527
PMCPMC7155207
OpenAlexW3013655213

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.