Involvement of T-complex protein 1-ring complex/chaperonin containing T-complex protein 1 (TRiC/CCT) in retrograde axonal transport through tau phosphorylation
Either overexpression of a single or all eight subunits (CCT1-8) or treatment of the substrate-binding apical domain of yeast CCT1 (ApiCCT1) prevented mutant Huntingtin aggregation and improved cellular and neuronal functions (Zhao et al., 2016). [...]the average retrograde velocity (the relative ve...
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Published in | Neural regeneration research Vol. 14; no. 4; pp. 588 - 590 |
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Main Author | |
Format | Journal Article |
Language | English |
Published |
India
Wolters Kluwer India Pvt. Ltd
01.04.2019
Medknow Publications and Media Pvt. Ltd Medknow Publications & Media Pvt. Ltd Department of Neurosciences, University of California San Diego, La Jolla, CA, USA Medknow Publications & Media Pvt Ltd Wolters Kluwer Medknow Publications |
Subjects | |
Online Access | Get full text |
ISSN | 1673-5374 1876-7958 |
DOI | 10.4103/1673-5374.247460 |
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Summary: | Either overexpression of a single or all eight subunits (CCT1-8) or treatment of the substrate-binding apical domain of yeast CCT1 (ApiCCT1) prevented mutant Huntingtin aggregation and improved cellular and neuronal functions (Zhao et al., 2016). [...]the average retrograde velocity (the relative velocity calculated from moving time with pause time included) in CCT5-expressing neurons was significantly faster than observed in control neurons. [...]an overload of tau in axons may induce an adverse effect on axonal transport (Wang and Mandelkow, 2016). Furthermore, almost all the transfected CCT5 subunits formed a complex in which tau was absent (Chen et al., 2018b). [...]it is possible that the effect of CCT5 on tau phosphorylation requires an oligomeric complex that is either self-assembled by transfected CCT5 or assembled by CCT5 with other endogenous CCT subunits. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
ISSN: | 1673-5374 1876-7958 |
DOI: | 10.4103/1673-5374.247460 |