Evidence map›Paper›PMID 33723808›Full record

ArticleVirologica Sinica2021

The CREB Regulated Transcription Coactivator 2 Suppresses HIV-1 Transcription by Preventing RNA Pol II from Binding to HIV-1 LTR.

Ling Ma, Shumin Chen, Zhen Wang, Saisai Guo, Jianyuan Zhao, Dongrong Yi, Quanjie Li, Zhenlong Liu, Fei Guo, Xiaoyu Li and 4 more

Open access · greenAbstract read
In one paragraph

Article in Virologica Sinica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.3field-weighted citation impact, top 24% 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

6 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
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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 4 institutions in 2 countries.

Ling Ma *Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical School, Beijing, 100050, China.
Shumin Chen *Department of Blood Transfusion, The Affiliated Hospital of Qingdao University, Qingdao 266000, China.
Zhen Wang *Lady Davis Institute, Jewish General Hospital, McGill University, Montreal, QC, H3T 1E2, Canada.
Saisai GuoInstitute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical School, Beijing, 100050, China.
Jianyuan ZhaoInstitute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical School, Beijing, 100050, China.
Dongrong YiInstitute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical School, Beijing, 100050, China.
Quanjie LiInstitute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical School, Beijing, 100050, China.
Zhenlong LiuLady Davis Institute, Jewish General Hospital, McGill University, Montreal, QC, H3T 1E2, Canada.
Fei GuoInstitute of Pathogen Biology, Chinese Academy of Medical Sciences and Peking Union Medical School, Beijing, 100176, China.
Xiaoyu LiInstitute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical School, Beijing, 100050, China.
Pingping JiaBeijing Shijitan Hospital, Capital Medical University, Beijing, 100038, China.
Jiwei DingInstitute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical School, Beijing, 100050, China. dingjiwei@imb.pumc.edu.cn.ORCID http://orcid.org/0000-0003-1942-4885
Chen LiangLady Davis Institute, Jewish General Hospital, McGill University, Montreal, QC, H3T 1E2, Canada.
Shan CenInstitute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical School, Beijing, 100050, China. shancen@imb.pumc.edu.cn.ORCID http://orcid.org/0000-0003-3358-0411
Chinese Academy of Medical Sciences & Peking Union Medical College · CNJewish General Hospital · CACapital Medical University · CNQingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The CREB-regulated transcriptional co-activators (CRTCs), including CRTC1, CRTC2 and CRTC3, enhance transcription of CREB-targeted genes. In addition to regulating host gene expression in response to cAMP, CRTCs also increase the infection of several viruses. While human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR) promoter harbors a cAMP response element and activation of the cAMP pathway promotes HIV-1 transcription, it remains unknown whether CRTCs have any effect on HIV-1 transcription and HIV-1 infection. Here, we reported that CRTC2 expression was induced by HIV-1 infection, but CRTC2 suppressed HIV-1 infection and diminished viral RNA expression. Mechanistic studies revealed that CRTC2 inhibited transcription from HIV-1 LTR and diminished RNA Pol II occupancy at the LTR independent of its association with CREB. Importantly, CRTC2 inhibits the activation of latent HIV-1. Together, these data suggest that in response to HIV-1 infection, cells increase the expression of CRTC2 which inhibits HIV-1 gene expression and may play a role in driving HIV-1 into latency.

Indexed as

HIV-1HIV InfectionsTranscription FactorsHIV Long Terminal RepeatHumansRNA Polymerase IIVirus LatencyCRTC1 protein, humanCRTC2 protein, humanCRTC3 protein, humanRNA Polymerase IITranscription FactorsCREB regulated transcription coactivator 2 (CRTC2)Human immunodeficiency virus (HIV)InfectionLatencyLong terminal repeat (LTR)RNA polymerase II (RNA Pol II)Viral transcriptionVirology

Identifiers

PMID33723808
PMCPMC8379306
OpenAlexW3139061917

What OpenQuestion holds

Textmetadata
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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.