Evidence map›Paper›PMID 26590945›Full record

ArticleImmunologic research2016

Characterization of promoter of the tuberculosis-resistant gene intracellular pathogen resistance 1.

Yongyan Wu, Fayang Liu, Yan Zhang, Yongsheng Wang, Zekun Guo, Yong Zhang

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Article in Immunologic research, 2016. 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

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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

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Molecular and cellular biology · 2020
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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Yongyan WuCollege of Veterinary Medicine, Northwest A&F University, Yangling, 712100, Shaanxi, China.
Fayang LiuCollege of Veterinary Medicine, Northwest A&F University, Yangling, 712100, Shaanxi, China.
Yan ZhangCollege of Veterinary Medicine, Northwest A&F University, Yangling, 712100, Shaanxi, China.
Yongsheng WangCollege of Veterinary Medicine, Northwest A&F University, Yangling, 712100, Shaanxi, China.
Zekun GuoCollege of Veterinary Medicine, Northwest A&F University, Yangling, 712100, Shaanxi, China.
Yong ZhangCollege of Veterinary Medicine, Northwest A&F University, Yangling, 712100, Shaanxi, China. zhylab@hotmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tuberculosis is an infectious disease caused by Mycobacterium tuberculosis, which most commonly affects the lungs and causes over 1.3 million people die annually. Variation in host genes is known to influence susceptibility to tuberculosis. Expression of the intracellular pathogen resistance 1 (Ipr1) gene could enhance the host resistance to mycobacterium. Here, we analyzed the coding region sequence and promoter of Ipr1 gene of mouse strains C57BL/6 and BALB/c. We found that the coding sequences of Ipr1 gene both in C57BL/6 and in BALB/c mice encode the same protein, while the Ipr1 promoter of BALB/c exists a short deletion and showed a slight of decreased transcriptional activity when compared with C57BL/6. Moreover, the optimal and minimal Ipr1 promoter was identified by luciferase assays using truncated reporter constructs, and the region from -293 to +95 bp showed the highest transcriptional activity and responsible for IFN-γ stimulation. Furthermore, the results showed that IFN-γ activates JAK/STAT and NF-κB signaling pathways to induce Ipr1 expression, and the signal transducer and activator of transcription 1 (Stat1) are critical for IFN-γ-induced Ipr1 expression, because overexpression of Stat1 promotes Ipr1 transcription, but knockdown of Stat1 reduced Ipr1 expression. Collectively, for the first time, our study characterizes Ipr1 promoter and investigates the positive and negative regulation of Ipr1 expression, providing basic data for application of Ipr1 in animal breeding.

Indexed as

Gene Expression RegulationAnimalsCells, CulturedGenetic Predisposition to DiseaseHumansImmunity, InnateInterferon-gammaMacrophagesMiceMice, Inbred BALB CMice, Inbred C57BLMycobacterium tuberculosisPolymorphism, GeneticPromoter Regions, GeneticSTAT1 Transcription FactorTrans-ActivatorsIfi75 protein, mouseInterferon-gammaSTAT1 Transcription FactorTrans-ActivatorsGene promoterIFN-γIpr1MycobacteriumStat1

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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.