Evidence map›Paper›PMID 33564769›Full record

ArticlebioRxiv : the preprint server for biology2021

Targeting CTP Synthetase 1 to Restore Interferon Induction and Impede Nucleotide Synthesis in SARS-CoV-2 Infection.

Youliang Rao, Ting-Yu Wang, Chao Qin, Bianca Espinosa, Qizhi Liu, Arunika Ekanayake, Jun Zhao, Ali Can Savas, Shu Zhang, Mehrnaz Zarinfar and 6 more

Open access · greenAbstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed, 20 citations in OpenAlex.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 3 institutions in 2 countries.

Youliang RaoSection of Infection and Immunity, Herman Ostrow School of Dentistry, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90089, USA.
Ting-Yu WangSection of Infection and Immunity, Herman Ostrow School of Dentistry, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90089, USA.
Chao QinSection of Infection and Immunity, Herman Ostrow School of Dentistry, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90089, USA.
Bianca EspinosaDepartment of Chemistry, Dornsife College of Arts, Letters and Sciences, University of Southern California, Los Angeles, CA 90089, USA.
Qizhi LiuSection of Infection and Immunity, Herman Ostrow School of Dentistry, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90089, USA.
Arunika EkanayakeDepartment of Chemistry, Dornsife College of Arts, Letters and Sciences, University of Southern California, Los Angeles, CA 90089, USA.
Jun ZhaoSection of Infection and Immunity, Herman Ostrow School of Dentistry, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90089, USA.
Ali Can SavasSection of Infection and Immunity, Herman Ostrow School of Dentistry, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90089, USA.
Shu ZhangSection of Infection and Immunity, Herman Ostrow School of Dentistry, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90089, USA.
Mehrnaz ZarinfarSection of Infection and Immunity, Herman Ostrow School of Dentistry, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90089, USA.
Yongzhen LiuSection of Infection and Immunity, Herman Ostrow School of Dentistry, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90089, USA.
Wenjie ZhuCenter for Systems Medicine, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005; Suzhou Institute of Systems Medicine, Suzhou, Jiangsu 215123; Bioland Laboratory (Guangzhou Regenerative Medicine and Health Guangdong Laboratory), 510005 Guangzhou, China.
Nicholas GrahamMork Family Department of Chemical Engineering and Materials Science, Norris Comprehensive Cancer Center, Los Angeles, CA 90089, USA.
Taijiao JiangCenter for Systems Medicine, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005; Suzhou Institute of Systems Medicine, Suzhou, Jiangsu 215123; Bioland Laboratory (Guangzhou Regenerative Medicine and Health Guangdong Laboratory), 510005 Guangzhou, China.
Chao ZhangDepartment of Chemistry, Dornsife College of Arts, Letters and Sciences, University of Southern California, Los Angeles, CA 90089, USA.
Pinghui FengSection of Infection and Immunity, Herman Ostrow School of Dentistry, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90089, USA.
University of Southern California · USChinese Academy of Medical Sciences & Peking Union Medical College · CNUSC Norris Comprehensive Cancer Center · US

Funding

Exploring roles of protein deamidation in oral inflammationR35DE027556 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CHEN, CASEY · 2017 to 2020
$4.1M
Targeting an immune kinase to purge KSHV latent infectionR01DE026003 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CHEN, CASEY, ZHANG, CHAO · 2016 to 2020
$3.4M
NFAT activation in kGPCR tumorigenesisR01CA221521 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI FENG, PINGHUI · 2017 to 2021
$1.9M
NCI NIH HHS R01 CA221521NIDCR NIH HHS R01 DE026003NIDCR NIH HHS R35 DE027556
6 · The paper itself

Abstract

The newly emerged SARS-CoV-2 caused a global pandemic with astonishing mortality and morbidity. The mechanisms underpinning its highly infectious nature remain poorly understood. We report here that SARS-CoV-2 exploits cellular CTP synthetase 1 (CTPS1) to promote CTP synthesis and suppress interferon (IFN) induction. Screening a SARS-CoV-2 expression library identified ORF7b and ORF8 that suppressed IFN induction via inducing the deamidation of interferon regulatory factor 3 (IRF3). Deamidated IRF3 fails to bind the promoters of classic IRF3-responsible genes, thus muting IFN induction. Conversely, a shRNA-mediated screen focused on cellular glutamine amidotransferases corroborated that CTPS1 deamidates IRF3 to inhibit IFN induction. Functionally, ORF7b and ORF8 activate CTPS1 to promote

Identifiers

PMID33564769
PMCPMC7872357
OpenAlexW3126273453

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.