Evidence map›Paper›PMID 28168305›Full record

ArticleNucleic acids research2017

CNBP acts as a key transcriptional regulator of sustained expression of interleukin-6.

Eunhye Lee, Taeyun A Lee, Ji Hyun Kim, Areum Park, Eun A Ra, Sujin Kang, Hyun Jin Choi, Junhee L Choi, Hyunbin D Huh, Ji Eun Lee and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

30 citing papers in PubMed, 48 citations in OpenAlex.

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  11. Cellular nucleic acid-binding protein restricts SARS-CoV-2 by regulating interferon and disrupting RNA-protein condensates.Proceedings of the National Academy of Sciences of the United States of America · 2023
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  17. The role of Insulin-like growth factor 2 mRNA-binding proteins (IGF2BPs) as mInternational journal of biological sciences · 2022
    Review
  18. 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

12 authors at 3 institutions in 1 country.

Eunhye LeeDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul 03722, South Korea.
Taeyun A LeeDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul 03722, South Korea.
Ji Hyun KimDepartment of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University, Seoul 06351, South Korea.
Areum ParkDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul 03722, South Korea.
Eun A RaDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul 03722, South Korea.
Sujin KangDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul 03722, South Korea.
Hyun Jin ChoiDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul 03722, South Korea.
Junhee L ChoiDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul 03722, South Korea.
Hyunbin D HuhDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul 03722, South Korea.
Ji Eun LeeDepartment of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University, Seoul 06351, South Korea.
Sungwook LeeCancer Immunology Branch, Research Institute, National Cancer Center, 323 Ilsan-ro, Ilsandong-gu, Goyang-si, Gyeonggi-do 10408, South Korea.
Boyoun ParkDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul 03722, South Korea.
Yonsei University · KRSungkyunkwan University · KRNational Cancer Center · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcription of inflammatory genes is an essential step in host defense activation. Here, we show that cellular nucleic acid-binding protein (CNBP) acts as a transcription regulator that is required for activating the innate immune response. We identified specific CNBP-binding motifs present in the promoter region of sustained inflammatory cytokines, thus, directly inducing the expression of target genes. In particular, lipopolysaccharide (LPS) induced cnbp expression through an NF-κB-dependent manner and a positive autoregulatory mechanism, which enables prolonged il-6 gene expression. This event depends strictly on LPS-induced CNBP nuclear translocation through phosphorylation-mediated dimerization. Consequently, cnbp-depleted zebrafish are highly susceptible to Shigella flexneri infection in vivo. Collectively, these observations identify CNBP as a key transcriptional regulator required for activating and maintaining the immune response.

Indexed as

Transcriptional ActivationAnimalsBase SequenceCell NucleusCells, CulturedConsensus SequenceCytokinesDysentery, BacillaryHumansInterleukin-12 Subunit p40Interleukin-6MiceNF-kappa BPromoter Regions, GeneticProtein DomainsProtein MultimerizationCnbp protein, mouseCytokinesInterleukin-12 Subunit p40Interleukin-6interleukin-6, mouseNF-kappa BRNA-Binding ProteinsTranscription Factors

Identifiers

PMID28168305
PMCPMC5389554
OpenAlexW2586312591

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.