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Selective autophagic degradation of the IKK complex in Drosophila is mediated by Kenny/IKKγ to control inflammation
Implication of autophagy in the downregulation of immune signaling pathways through the degradation of their components constitutes an emerging field of investigation. Our work showed that the selective interaction of Drosophila protein Kenny/IKKγ (CG16910) with the autophagic machinery is required...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Taylor & Francis
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6961681/ https://www.ncbi.nlm.nih.gov/pubmed/31993495 http://dx.doi.org/10.1080/23723556.2019.1682309 |
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author | Jacomin, Anne-Claire Nezis, Ioannis P. |
author_facet | Jacomin, Anne-Claire Nezis, Ioannis P. |
author_sort | Jacomin, Anne-Claire |
collection | PubMed |
description | Implication of autophagy in the downregulation of immune signaling pathways through the degradation of their components constitutes an emerging field of investigation. Our work showed that the selective interaction of Drosophila protein Kenny/IKKγ (CG16910) with the autophagic machinery is required for the degradation of the I-kappa B kinase complex. This regulatory mechanism is essential for the downregulation of the immune deficiency (IMD) pathway in response to commensal microbiota to prevent inflammation. |
format | Online Article Text |
id | pubmed-6961681 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Taylor & Francis |
record_format | MEDLINE/PubMed |
spelling | pubmed-69616812020-09-28 Selective autophagic degradation of the IKK complex in Drosophila is mediated by Kenny/IKKγ to control inflammation Jacomin, Anne-Claire Nezis, Ioannis P. Mol Cell Oncol Commentary Implication of autophagy in the downregulation of immune signaling pathways through the degradation of their components constitutes an emerging field of investigation. Our work showed that the selective interaction of Drosophila protein Kenny/IKKγ (CG16910) with the autophagic machinery is required for the degradation of the I-kappa B kinase complex. This regulatory mechanism is essential for the downregulation of the immune deficiency (IMD) pathway in response to commensal microbiota to prevent inflammation. Taylor & Francis 2019-11-06 /pmc/articles/PMC6961681/ /pubmed/31993495 http://dx.doi.org/10.1080/23723556.2019.1682309 Text en © 2019 The Author(s). Published with license by Taylor & Francis Group, LLC. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) ), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way. |
spellingShingle | Commentary Jacomin, Anne-Claire Nezis, Ioannis P. Selective autophagic degradation of the IKK complex in Drosophila is mediated by Kenny/IKKγ to control inflammation |
title | Selective autophagic degradation of the IKK complex in Drosophila is mediated by Kenny/IKKγ to control inflammation |
title_full | Selective autophagic degradation of the IKK complex in Drosophila is mediated by Kenny/IKKγ to control inflammation |
title_fullStr | Selective autophagic degradation of the IKK complex in Drosophila is mediated by Kenny/IKKγ to control inflammation |
title_full_unstemmed | Selective autophagic degradation of the IKK complex in Drosophila is mediated by Kenny/IKKγ to control inflammation |
title_short | Selective autophagic degradation of the IKK complex in Drosophila is mediated by Kenny/IKKγ to control inflammation |
title_sort | selective autophagic degradation of the ikk complex in drosophila is mediated by kenny/ikkγ to control inflammation |
topic | Commentary |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6961681/ https://www.ncbi.nlm.nih.gov/pubmed/31993495 http://dx.doi.org/10.1080/23723556.2019.1682309 |
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