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Retromer dependent changes in cellular homeostasis and Parkinson's disease
To date, mechanistic treatments targeting the initial cause of Parkinson's disease (PD) are limited due to the underlying biological cause(s) been unclear. Endosomes and their associated cellular homeostasis processes have emerged to have a significant role in the pathophysiology associated wit...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Portland Press Ltd.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8709886/ https://www.ncbi.nlm.nih.gov/pubmed/34528672 http://dx.doi.org/10.1042/EBC20210023 |
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author | Yang, Zhe Li, Zebin Teasdale, Rohan D. |
author_facet | Yang, Zhe Li, Zebin Teasdale, Rohan D. |
author_sort | Yang, Zhe |
collection | PubMed |
description | To date, mechanistic treatments targeting the initial cause of Parkinson's disease (PD) are limited due to the underlying biological cause(s) been unclear. Endosomes and their associated cellular homeostasis processes have emerged to have a significant role in the pathophysiology associated with PD. Several variants within retromer complex have been identified and characterised within familial PD patients. The retromer complex represents a key sorting platform within the endosomal system that regulates cargo sorting that maintains cellular homeostasis. In this review, we summarise the current understandings of how PD-associated retromer variants disrupt cellular trafficking and how the retromer complex can interact with other PD-associated genes to contribute to the disease progression. |
format | Online Article Text |
id | pubmed-8709886 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Portland Press Ltd. |
record_format | MEDLINE/PubMed |
spelling | pubmed-87098862022-01-05 Retromer dependent changes in cellular homeostasis and Parkinson's disease Yang, Zhe Li, Zebin Teasdale, Rohan D. Essays Biochem Molecular Bases of Health & Disease To date, mechanistic treatments targeting the initial cause of Parkinson's disease (PD) are limited due to the underlying biological cause(s) been unclear. Endosomes and their associated cellular homeostasis processes have emerged to have a significant role in the pathophysiology associated with PD. Several variants within retromer complex have been identified and characterised within familial PD patients. The retromer complex represents a key sorting platform within the endosomal system that regulates cargo sorting that maintains cellular homeostasis. In this review, we summarise the current understandings of how PD-associated retromer variants disrupt cellular trafficking and how the retromer complex can interact with other PD-associated genes to contribute to the disease progression. Portland Press Ltd. 2021-12 2021-12-22 /pmc/articles/PMC8709886/ /pubmed/34528672 http://dx.doi.org/10.1042/EBC20210023 Text en © 2021 The Author(s). https://creativecommons.org/licenses/by/4.0/This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY) (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Molecular Bases of Health & Disease Yang, Zhe Li, Zebin Teasdale, Rohan D. Retromer dependent changes in cellular homeostasis and Parkinson's disease |
title | Retromer dependent changes in cellular homeostasis and Parkinson's disease |
title_full | Retromer dependent changes in cellular homeostasis and Parkinson's disease |
title_fullStr | Retromer dependent changes in cellular homeostasis and Parkinson's disease |
title_full_unstemmed | Retromer dependent changes in cellular homeostasis and Parkinson's disease |
title_short | Retromer dependent changes in cellular homeostasis and Parkinson's disease |
title_sort | retromer dependent changes in cellular homeostasis and parkinson's disease |
topic | Molecular Bases of Health & Disease |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8709886/ https://www.ncbi.nlm.nih.gov/pubmed/34528672 http://dx.doi.org/10.1042/EBC20210023 |
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