Non-Proteasomal UbL-UbA Family of Proteins in Neurodegeneration

Ubiquitin-like/ubiquitin-associated proteins (UbL-UbA) are a well-studied family of non-proteasomal ubiquitin receptors that are evolutionarily conserved across species. Members of this non-homogenous family facilitate and support proteasomal activity by promoting different effects on proteostasis b...

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Main Authors: Salinee Jantrapirom, Luca Lo Piccolo, Masamitsu Yamaguchi
Format: Article
Language:English
Published: MDPI AG 2019-04-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/20/8/1893
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spelling doaj-1a2910a97b85401eafe067aa21c763fc2020-11-24T22:11:29ZengMDPI AGInternational Journal of Molecular Sciences1422-00672019-04-01208189310.3390/ijms20081893ijms20081893Non-Proteasomal UbL-UbA Family of Proteins in NeurodegenerationSalinee Jantrapirom0Luca Lo Piccolo1Masamitsu Yamaguchi2Department of Pharmacology, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, ThailandDepartment of Neurotherapeutics, Osaka University Graduate School of Medicine, Osaka 565-0871, JapanDepartment of Applied Biology, Kyoto Institute of Technology, Kyoto 606-8585, JapanUbiquitin-like/ubiquitin-associated proteins (UbL-UbA) are a well-studied family of non-proteasomal ubiquitin receptors that are evolutionarily conserved across species. Members of this non-homogenous family facilitate and support proteasomal activity by promoting different effects on proteostasis but exhibit diverse extra-proteasomal activities. Dysfunctional UbL-UbA proteins render cells, particularly neurons, more susceptible to stressors or aging and may cause earlier neurodegeneration. In this review, we summarized the properties and functions of UbL-UbA family members identified to date, with an emphasis on new findings obtained using <i>Drosophila</i> models showing a direct or indirect role in some neurodegenerative diseases.https://www.mdpi.com/1422-0067/20/8/1893UbL-UbAnon-proteasomal ubiquitin receptorproteostasisubiquitin-likeneurodegenerative diseases<i>Drosophila</i>
collection DOAJ
language English
format Article
sources DOAJ
author Salinee Jantrapirom
Luca Lo Piccolo
Masamitsu Yamaguchi
spellingShingle Salinee Jantrapirom
Luca Lo Piccolo
Masamitsu Yamaguchi
Non-Proteasomal UbL-UbA Family of Proteins in Neurodegeneration
International Journal of Molecular Sciences
UbL-UbA
non-proteasomal ubiquitin receptor
proteostasis
ubiquitin-like
neurodegenerative diseases
<i>Drosophila</i>
author_facet Salinee Jantrapirom
Luca Lo Piccolo
Masamitsu Yamaguchi
author_sort Salinee Jantrapirom
title Non-Proteasomal UbL-UbA Family of Proteins in Neurodegeneration
title_short Non-Proteasomal UbL-UbA Family of Proteins in Neurodegeneration
title_full Non-Proteasomal UbL-UbA Family of Proteins in Neurodegeneration
title_fullStr Non-Proteasomal UbL-UbA Family of Proteins in Neurodegeneration
title_full_unstemmed Non-Proteasomal UbL-UbA Family of Proteins in Neurodegeneration
title_sort non-proteasomal ubl-uba family of proteins in neurodegeneration
publisher MDPI AG
series International Journal of Molecular Sciences
issn 1422-0067
publishDate 2019-04-01
description Ubiquitin-like/ubiquitin-associated proteins (UbL-UbA) are a well-studied family of non-proteasomal ubiquitin receptors that are evolutionarily conserved across species. Members of this non-homogenous family facilitate and support proteasomal activity by promoting different effects on proteostasis but exhibit diverse extra-proteasomal activities. Dysfunctional UbL-UbA proteins render cells, particularly neurons, more susceptible to stressors or aging and may cause earlier neurodegeneration. In this review, we summarized the properties and functions of UbL-UbA family members identified to date, with an emphasis on new findings obtained using <i>Drosophila</i> models showing a direct or indirect role in some neurodegenerative diseases.
topic UbL-UbA
non-proteasomal ubiquitin receptor
proteostasis
ubiquitin-like
neurodegenerative diseases
<i>Drosophila</i>
url https://www.mdpi.com/1422-0067/20/8/1893
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