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TRIM14 expression is regulated by IRF‐1 and IRF‐2

Tripartite motif‐containing 14 (TRIM14) is a mitochondrial adaptor that promotes innate immune signaling and plays important roles in antiviral defense. Expression of TRIM14 is induced by interferon (IFN)‐I. However, the mechanism by which IFN‐I induces TRIM14 production is not yet determined. In th...

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Autores principales: Cui, Jingang, Xu, Xiao, Li, Yutong, Hu, Xiaomei, Xie, Yingpeng, Tan, Juan, Qiao, Wentao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6668374/
https://www.ncbi.nlm.nih.gov/pubmed/31150153
http://dx.doi.org/10.1002/2211-5463.12682
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author Cui, Jingang
Xu, Xiao
Li, Yutong
Hu, Xiaomei
Xie, Yingpeng
Tan, Juan
Qiao, Wentao
author_facet Cui, Jingang
Xu, Xiao
Li, Yutong
Hu, Xiaomei
Xie, Yingpeng
Tan, Juan
Qiao, Wentao
author_sort Cui, Jingang
collection PubMed
description Tripartite motif‐containing 14 (TRIM14) is a mitochondrial adaptor that promotes innate immune signaling and plays important roles in antiviral defense. Expression of TRIM14 is induced by interferon (IFN)‐I. However, the mechanism by which IFN‐I induces TRIM14 production is not yet determined. In this study, we have examined the function of TRIM14 promoter and found that a GC box and an IFN‐stimulated response element (ISRE) are necessary for the basal level transcription of TRIM14. We further observed that IFN‐I activates the TRIM14 promoter through the ISRE. In particular, interferon regulatory factor (IRF)‐1 and IRF‐2 bind to the TRIM14 promoter and activate transcription of TRIM14. Moreover, knockdown of IRF‐1 reduces the stimulation of TRIM14 transcription by IFN‐α, suggesting that IRF‐1 is involved in the activation of TRIM14 by IFN‐I. IRF‐2 has little effect on IFN‐α‐induced TRIM14 transcription but is essential for the basal transcription of TRIM14.
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spelling pubmed-66683742019-08-06 TRIM14 expression is regulated by IRF‐1 and IRF‐2 Cui, Jingang Xu, Xiao Li, Yutong Hu, Xiaomei Xie, Yingpeng Tan, Juan Qiao, Wentao FEBS Open Bio Research Articles Tripartite motif‐containing 14 (TRIM14) is a mitochondrial adaptor that promotes innate immune signaling and plays important roles in antiviral defense. Expression of TRIM14 is induced by interferon (IFN)‐I. However, the mechanism by which IFN‐I induces TRIM14 production is not yet determined. In this study, we have examined the function of TRIM14 promoter and found that a GC box and an IFN‐stimulated response element (ISRE) are necessary for the basal level transcription of TRIM14. We further observed that IFN‐I activates the TRIM14 promoter through the ISRE. In particular, interferon regulatory factor (IRF)‐1 and IRF‐2 bind to the TRIM14 promoter and activate transcription of TRIM14. Moreover, knockdown of IRF‐1 reduces the stimulation of TRIM14 transcription by IFN‐α, suggesting that IRF‐1 is involved in the activation of TRIM14 by IFN‐I. IRF‐2 has little effect on IFN‐α‐induced TRIM14 transcription but is essential for the basal transcription of TRIM14. John Wiley and Sons Inc. 2019-07-01 /pmc/articles/PMC6668374/ /pubmed/31150153 http://dx.doi.org/10.1002/2211-5463.12682 Text en © 2019 The Authors. Published by FEBS Press and John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Articles
Cui, Jingang
Xu, Xiao
Li, Yutong
Hu, Xiaomei
Xie, Yingpeng
Tan, Juan
Qiao, Wentao
TRIM14 expression is regulated by IRF‐1 and IRF‐2
title TRIM14 expression is regulated by IRF‐1 and IRF‐2
title_full TRIM14 expression is regulated by IRF‐1 and IRF‐2
title_fullStr TRIM14 expression is regulated by IRF‐1 and IRF‐2
title_full_unstemmed TRIM14 expression is regulated by IRF‐1 and IRF‐2
title_short TRIM14 expression is regulated by IRF‐1 and IRF‐2
title_sort trim14 expression is regulated by irf‐1 and irf‐2
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6668374/
https://www.ncbi.nlm.nih.gov/pubmed/31150153
http://dx.doi.org/10.1002/2211-5463.12682
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