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MiR-1303 Regulates Mycobacteria Induced Autophagy by Targeting Atg2B
MicroRNAs are emerging post-transcriptional regulators of gene expressions in both innate immunity and adaptive immunity. In mycobacteria infection, autophagy plays an important role in innate defense mechanism and is tightly regulated by the autophagy-related proteins. Here, we show that Atg2B is i...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4714759/ https://www.ncbi.nlm.nih.gov/pubmed/26771516 http://dx.doi.org/10.1371/journal.pone.0146770 |
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author | Au, Kin Yi Pong, John C. H. Ling, Wai Lim Li, James C. B. |
author_facet | Au, Kin Yi Pong, John C. H. Ling, Wai Lim Li, James C. B. |
author_sort | Au, Kin Yi |
collection | PubMed |
description | MicroRNAs are emerging post-transcriptional regulators of gene expressions in both innate immunity and adaptive immunity. In mycobacteria infection, autophagy plays an important role in innate defense mechanism and is tightly regulated by the autophagy-related proteins. Here, we show that Atg2B is involved in the regulation of mycobacteria-induced autophagy. MiR-1303, which function is not defined yet, is found to negatively regulate mycobacteria-induced Atg2B protein production, ultimately down-regulate mycobacteria-induced autophagy. MiR-1303 production is shown to be upregulated during BCG infection and its production is regulated by PI3K and NFκB. It is also demonstrated that miR-1303 targets putative target sites on Atg2B and possibly represses its translation. |
format | Online Article Text |
id | pubmed-4714759 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-47147592016-01-30 MiR-1303 Regulates Mycobacteria Induced Autophagy by Targeting Atg2B Au, Kin Yi Pong, John C. H. Ling, Wai Lim Li, James C. B. PLoS One Research Article MicroRNAs are emerging post-transcriptional regulators of gene expressions in both innate immunity and adaptive immunity. In mycobacteria infection, autophagy plays an important role in innate defense mechanism and is tightly regulated by the autophagy-related proteins. Here, we show that Atg2B is involved in the regulation of mycobacteria-induced autophagy. MiR-1303, which function is not defined yet, is found to negatively regulate mycobacteria-induced Atg2B protein production, ultimately down-regulate mycobacteria-induced autophagy. MiR-1303 production is shown to be upregulated during BCG infection and its production is regulated by PI3K and NFκB. It is also demonstrated that miR-1303 targets putative target sites on Atg2B and possibly represses its translation. Public Library of Science 2016-01-15 /pmc/articles/PMC4714759/ /pubmed/26771516 http://dx.doi.org/10.1371/journal.pone.0146770 Text en © 2016 Au et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Article Au, Kin Yi Pong, John C. H. Ling, Wai Lim Li, James C. B. MiR-1303 Regulates Mycobacteria Induced Autophagy by Targeting Atg2B |
title | MiR-1303 Regulates Mycobacteria Induced Autophagy by Targeting Atg2B |
title_full | MiR-1303 Regulates Mycobacteria Induced Autophagy by Targeting Atg2B |
title_fullStr | MiR-1303 Regulates Mycobacteria Induced Autophagy by Targeting Atg2B |
title_full_unstemmed | MiR-1303 Regulates Mycobacteria Induced Autophagy by Targeting Atg2B |
title_short | MiR-1303 Regulates Mycobacteria Induced Autophagy by Targeting Atg2B |
title_sort | mir-1303 regulates mycobacteria induced autophagy by targeting atg2b |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4714759/ https://www.ncbi.nlm.nih.gov/pubmed/26771516 http://dx.doi.org/10.1371/journal.pone.0146770 |
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