Evidence map›Paper›PMID 39736320›Full record

ArticleVirologica Sinica2025

CRTC3 restricts SARS-CoV-2 replication and is antagonized by CREB.

Li Yang, Xiao-Tao Zeng, Rong-Hua Luo, Ying Tang, Si-Xue Ren, Xin-Yan Long, Xiang-Hui Fu, Wan-Jiang Zhang, Hai-Yan Ren, Yong-Tang Zheng and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Virologica Sinica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
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.

Li YangDepartment of Pulmonary and Critical Care Medicine, Respiratory Infection and Intervention Laboratory of Frontiers Science Center for Disease-related Molecular Network, and State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu 610041, China.
Xiao-Tao ZengDepartment of Pulmonary and Critical Care Medicine, Respiratory Infection and Intervention Laboratory of Frontiers Science Center for Disease-related Molecular Network, and State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu 610041, China; Research and Innovation Center, Pengzhou People's Hospital, Pengzhou 610000, China.
Rong-Hua LuoState Key Laboratory of Genetic Evolution & Animal Models, Key Laboratory of Bioactive Peptides of Yunnan Province, KIZ-CUHK Joint Laboratory of Bioresources and Molecular Research in Common Diseases, Center for Biosafety Mega-Science, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming 650201, China.
Ying TangDepartment of Pulmonary and Critical Care Medicine, Respiratory Infection and Intervention Laboratory of Frontiers Science Center for Disease-related Molecular Network, and State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu 610041, China.
Si-Xue RenDepartment of Pulmonary and Critical Care Medicine, Respiratory Infection and Intervention Laboratory of Frontiers Science Center for Disease-related Molecular Network, and State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu 610041, China.
Xin-Yan LongState Key Laboratory of Genetic Evolution & Animal Models, Key Laboratory of Bioactive Peptides of Yunnan Province, KIZ-CUHK Joint Laboratory of Bioresources and Molecular Research in Common Diseases, Center for Biosafety Mega-Science, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming 650201, China.
Xiang-Hui FuDepartment of Biotherapy, Center for Diabetes and Metabolism Research, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Chengdu 610041, China.
Wan-Jiang ZhangDepartment of Pathophysiology, Shihezi University School of Medicine, The Key Laboratory of Xinjiang Endemic and Ethnic Diseases, Shihezi 832003, China.
Hai-Yan RenDepartment of Pulmonary and Critical Care Medicine, Respiratory Infection and Intervention Laboratory of Frontiers Science Center for Disease-related Molecular Network, and State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu 610041, China. Electronic address: hyren@scu.edu.cn.
Yong-Tang ZhengState Key Laboratory of Genetic Evolution & Animal Models, Key Laboratory of Bioactive Peptides of Yunnan Province, KIZ-CUHK Joint Laboratory of Bioresources and Molecular Research in Common Diseases, Center for Biosafety Mega-Science, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming 650201, China. Electronic address: zhengyt@mail.kiz.ac.cn.
Wei ChengDepartment of Pulmonary and Critical Care Medicine, Respiratory Infection and Intervention Laboratory of Frontiers Science Center for Disease-related Molecular Network, and State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu 610041, China. Electronic address: chengweilab@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Virus-encoding RNA-dependent RNA polymerase (RdRp) is essential for genome replication and gene transcription of human coronaviruses (HCoVs), including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). We previously identified the interaction between the catalytic subunit NSP12 of SARS-CoV-2 RdRp and the host protein CREB-regulated transcription coactivator 3 (CRTC3), a member of the CRTC family that regulates cyclic AMP response element-binding protein (CREB)-mediated transcriptional activation. Currently, the implication of CRTC3 in the pathogenesis of HCoVs is poorly understood. Herein, we demonstrated that CRTC3 attenuates RdRp activity and SARS-CoV-2 genome replication, therefore reducing the production of progeny viruses. The interaction of CRTC3 with NSP12 contributes to its inhibitory effect on RdRp activity. Furthermore, we expanded the suppressive effects of two other CRTC family members (CRTC1 and CRTC2) on the RdRp activities of lethal HCoVs, including SARS-CoV-2 and Middle East respiratory syndrome coronavirus (MERS-CoV), along with the CREB antagonization. Overall, our research suggests that CRTCs restrict the replication of HCoVs and are antagonized by CREB, which not only provides new insights into the replication regulation of HCoVs, but also offers important information for the development of anti-HCoV interventions.

Indexed as

Cyclic AMP Response Element-Binding ProteinSARS-CoV-2Transcription FactorsVirus ReplicationAnimalsChlorocebus aethiopsCoronavirus RNA-Dependent RNA PolymeraseCOVID-19HEK293 CellsHumansMiddle East Respiratory Syndrome CoronavirusVero CellsViral Nonstructural ProteinsCoronavirus RNA-Dependent RNA PolymeraseCREB1 protein, humanCyclic AMP Response Element-Binding ProteinNSP12 protein, SARS-CoV-2Transcription FactorsViral Nonstructural ProteinsCREB-regulated transcription coactivator 3 (CRTC3)Cyclic AMP response element-binding protein (CREB)Human coronaviruses (HCoVs)RNA-Dependent RNA polymerase (RdRp)Virus-host interactionVirus replication

Identifiers

PMID39736320
PMCPMC11963146

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Registered trials

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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.