Evidence map›Paper›PMID 28511927›Full record

ArticleBiochimica et biophysica acta. Gene regulatory mechanisms2017

Coordinated regulation of IFITM1, 2 and 3 genes by an IFN-responsive enhancer through long-range chromatin interactions.

Ping Li, Ming-Lei Shi, Wen-Long Shen, Zhang Zhang, De-Jian Xie, Xiang-Yuan Zhang, Chao He, Yan Zhang, Zhi-Hu Zhao

Open access · greenAbstract read
In one paragraph

Article in Biochimica et biophysica acta. Gene regulatory mechanisms, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

17 citing papers in PubMed, 20 citations in OpenAlex.

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  5. The Culprit Behind HBV-Infected Hepatocytes: NTCP.Drug design, development and therapy · 2024
    Review
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  15. Article
  16. CRISPR-based strategies for studying regulatory elements and chromatin structure in mammalian gene control.Mammalian genome : official journal of the International Mammalian Genome Society · 2018
    Review
  17. Review
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

9 authors at 1 institution in 1 country.

Ping LiBeijing Institute of Biotechnology, No. 20, Dongdajie Street, Fengtai District, Beijing 100071, China.
Ming-Lei ShiBeijing Institute of Biotechnology, No. 20, Dongdajie Street, Fengtai District, Beijing 100071, China.
Wen-Long ShenBeijing Institute of Biotechnology, No. 20, Dongdajie Street, Fengtai District, Beijing 100071, China.
Zhang ZhangBeijing Institute of Biotechnology, No. 20, Dongdajie Street, Fengtai District, Beijing 100071, China.
De-Jian XieBeijing Institute of Biotechnology, No. 20, Dongdajie Street, Fengtai District, Beijing 100071, China.
Xiang-Yuan ZhangBeijing Institute of Biotechnology, No. 20, Dongdajie Street, Fengtai District, Beijing 100071, China.
Chao HeBeijing Institute of Biotechnology, No. 20, Dongdajie Street, Fengtai District, Beijing 100071, China.
Yan ZhangBeijing Institute of Biotechnology, No. 20, Dongdajie Street, Fengtai District, Beijing 100071, China. Electronic address: zany1983@163.com.
Zhi-Hu ZhaoBeijing Institute of Biotechnology, No. 20, Dongdajie Street, Fengtai District, Beijing 100071, China. Electronic address: zhaozh@bmi.ac.cn.
Beijing Fengtai Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interferon-induced transmembrane protein (IFITM) 1, 2 and 3 genes encode a family of interferon (IFN)-induced transmembrane proteins that block entry of a broad spectrum of pathogens. However, the transcriptional regulation of these genes, especially whether there exist any enhancers and their roles during the IFN induction process remain elusive. Here, through public data mining, episomal luciferase reporter assay and in vivo CRISPR-Cas9 genome editing, we identified an IFN-responsive enhancer located 35kb upstream of IFITM3 gene promoter upregulating the IFN-induced expression of IFITM1, 2 and 3 genes. Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer. Finally, we showed that in vivo truncation of the enhancer impaired IFN-induced resistance to influenza A virus (IAV) infection. These findings expand our understanding of the mechanisms underlying the transcriptional regulation of IFITM1, 2 and 3 expression and its ability to mediate IFN signaling.

Indexed as

A549 CellsAntigens, DifferentiationCell LineCell Line, TumorChromatinClustered Regularly Interspaced Short Palindromic RepeatsEnhancer Elements, GeneticGene EditingGene Expression RegulationHEK293 CellsHumansInfluenza A virusInfluenza, HumanInterferonsMembrane ProteinsPromoter Regions, GeneticAntigens, DifferentiationChromatinIFITM2 protein, humanIFITM3 protein, humanInterferonsleu-13 antigenMembrane ProteinsRNA-Binding ProteinsSTAT1 Transcription FactorEnhancerIFITMIFNInfluenza A virusLong-range interactions

Identifiers

PMID28511927
PMCPMC7102783
OpenAlexW2612829549

What OpenQuestion holds

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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.