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One of the major features of NDs, such as Alzheimer's disease (AD), Parkinson's disease (PD) and Huntington's disease (HD), is the aggregation of specific misfolded proteins, which induces cellular dysfunction, neuronal death, loss of synaptic connections and eventually brain damage. By far, a great amount of evidence has suggested that TRIM family proteins play crucial roles in the turnover of normal regulatory and misfolded proteins. To maintain cellular protein quality control, cells rely on two major classes of proteostasis: molecular chaperones and the degradative systems, the latter includes the ubiquitin-proteasome system (UPS) and autophagy; and their dysfunction has been established to result in various physiological disorders including NDs. Emerging evidence has shown that TRIM proteins are key players in facilitating the clearance of misfolded protein aggregates associated with neurodegenerative disorders. Understanding the different pathways these TRIM proteins employ during episodes of neurodegenerative disorder represents a promising therapeutic target. In this review, we elucidated and summarized the diverse roles with underlying mechanisms of members of the TRIM family proteins in NDs.<\/jats:p>","DOI":"10.1098\/rsob.220098","type":"journal-article","created":{"date-parts":[[2022,8,10]],"date-time":"2022-08-10T03:36:55Z","timestamp":1660102615000},"update-policy":"https:\/\/doi.org\/10.1098\/crossmark-policy","source":"Crossref","is-referenced-by-count":48,"title":["TRIM family proteins: roles in proteostasis and neurodegenerative diseases"],"prefix":"10.1098","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5730-6479","authenticated-orcid":true,"given":"Yan","family":"Zhu","sequence":"first","affiliation":[{"name":"Shenzhen Laboratory of Tumor Cell Biology, Institute of Biomedicine and Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, People's Republic of China"},{"name":"University of Chinese Academy of Sciences, Beijing 100864, People's Republic of China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7659-128X","authenticated-orcid":false,"given":"Lukman O.","family":"Afolabi","sequence":"additional","affiliation":[{"name":"Shenzhen Laboratory of Tumor Cell Biology, Institute of Biomedicine and Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, People's Republic of China"},{"name":"University of Chinese Academy of Sciences, Beijing 100864, People's Republic of China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4793-5121","authenticated-orcid":false,"given":"Xiaochun","family":"Wan","sequence":"additional","affiliation":[{"name":"Shenzhen Laboratory of Tumor Cell Biology, Institute of Biomedicine and Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, People's Republic of China"},{"name":"University of Chinese Academy of Sciences, Beijing 100864, People's Republic of China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0167-7307","authenticated-orcid":false,"given":"Joong Sup","family":"Shim","sequence":"additional","affiliation":[{"name":"Cancer Centre, Faculty of Health Sciences, University of Macau, Avenida da Universidade, Taipa, Macau, People's Republic of China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4875-5811","authenticated-orcid":false,"given":"Liang","family":"Chen","sequence":"additional","affiliation":[{"name":"Shenzhen Laboratory of Tumor Cell Biology, Institute of Biomedicine and Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, People's Republic of China"},{"name":"University of Chinese Academy of Sciences, Beijing 100864, People's Republic of China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"175","published-online":{"date-parts":[[2022,8,10]]},"reference":[{"key":"e_1_3_5_2_2","doi-asserted-by":"publisher","DOI":"10.1101\/cshperspect.a028035"},{"key":"e_1_3_5_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2012.02.022"},{"key":"e_1_3_5_4_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrm3810"},{"key":"e_1_3_5_5_2","doi-asserted-by":"publisher","DOI":"10.1038\/s41593-018-0235-9"},{"key":"e_1_3_5_6_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrn.2016.178"},{"key":"e_1_3_5_7_2","first-page":"1","article-title":"Parkinson disease","volume":"3","author":"Poewe W","year":"2017","unstructured":"Poewe W, Seppi K, Tanner CM, Halliday GM, Brundin P, Volkmann J, Schrag A.-E., Lang AE. 2017 Parkinson disease. 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