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The Role of Primary Cilia in the Crosstalk between the Ubiquitin–Proteasome System and Autophagy
Protein degradation is a pivotal process for eukaryotic development and homeostasis. The majority of proteins are degraded by the ubiquitin–proteasome system and by autophagy. Recent studies describe a crosstalk between these two main eukaryotic degradation systems which allows for establishing a ki...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6468794/ https://www.ncbi.nlm.nih.gov/pubmed/30875746 http://dx.doi.org/10.3390/cells8030241 |
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author | Wiegering, Antonia Rüther, Ulrich Gerhardt, Christoph |
author_facet | Wiegering, Antonia Rüther, Ulrich Gerhardt, Christoph |
author_sort | Wiegering, Antonia |
collection | PubMed |
description | Protein degradation is a pivotal process for eukaryotic development and homeostasis. The majority of proteins are degraded by the ubiquitin–proteasome system and by autophagy. Recent studies describe a crosstalk between these two main eukaryotic degradation systems which allows for establishing a kind of safety mechanism. If one of these degradation systems is hampered, the other compensates for this defect. The mechanism behind this crosstalk is poorly understood. Novel studies suggest that primary cilia, little cellular protrusions, are involved in the regulation of the crosstalk between the two degradation systems. In this review article, we summarise the current knowledge about the association between cilia, the ubiquitin–proteasome system and autophagy. |
format | Online Article Text |
id | pubmed-6468794 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-64687942019-04-23 The Role of Primary Cilia in the Crosstalk between the Ubiquitin–Proteasome System and Autophagy Wiegering, Antonia Rüther, Ulrich Gerhardt, Christoph Cells Review Protein degradation is a pivotal process for eukaryotic development and homeostasis. The majority of proteins are degraded by the ubiquitin–proteasome system and by autophagy. Recent studies describe a crosstalk between these two main eukaryotic degradation systems which allows for establishing a kind of safety mechanism. If one of these degradation systems is hampered, the other compensates for this defect. The mechanism behind this crosstalk is poorly understood. Novel studies suggest that primary cilia, little cellular protrusions, are involved in the regulation of the crosstalk between the two degradation systems. In this review article, we summarise the current knowledge about the association between cilia, the ubiquitin–proteasome system and autophagy. MDPI 2019-03-14 /pmc/articles/PMC6468794/ /pubmed/30875746 http://dx.doi.org/10.3390/cells8030241 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Wiegering, Antonia Rüther, Ulrich Gerhardt, Christoph The Role of Primary Cilia in the Crosstalk between the Ubiquitin–Proteasome System and Autophagy |
title | The Role of Primary Cilia in the Crosstalk between the Ubiquitin–Proteasome System and Autophagy |
title_full | The Role of Primary Cilia in the Crosstalk between the Ubiquitin–Proteasome System and Autophagy |
title_fullStr | The Role of Primary Cilia in the Crosstalk between the Ubiquitin–Proteasome System and Autophagy |
title_full_unstemmed | The Role of Primary Cilia in the Crosstalk between the Ubiquitin–Proteasome System and Autophagy |
title_short | The Role of Primary Cilia in the Crosstalk between the Ubiquitin–Proteasome System and Autophagy |
title_sort | role of primary cilia in the crosstalk between the ubiquitin–proteasome system and autophagy |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6468794/ https://www.ncbi.nlm.nih.gov/pubmed/30875746 http://dx.doi.org/10.3390/cells8030241 |
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