Neddylation dysfunction in Alzheimer's disease

Ubiquitin-dependent proteolysis is a major mechanism that downregulates misfolded proteins or those that have finished a programmed task. In the last two decades, neddylation has emerged as a major regulatory pathway for ubiquitination. Central to the neddylation pathway is the amyloid precursor pro...

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Main Authors: Chen, Yuzhi, Neve, Rachael L., Liu, Helena
Other Authors: Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
Format: Article
Language:en_US
Published: John Wiley & Sons, Inc 2014
Online Access:http://hdl.handle.net/1721.1/89400
https://orcid.org/0000-0002-3854-5968
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author Chen, Yuzhi
Neve, Rachael L.
Liu, Helena
author2 Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
author_facet Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
Chen, Yuzhi
Neve, Rachael L.
Liu, Helena
author_sort Chen, Yuzhi
collection MIT
description Ubiquitin-dependent proteolysis is a major mechanism that downregulates misfolded proteins or those that have finished a programmed task. In the last two decades, neddylation has emerged as a major regulatory pathway for ubiquitination. Central to the neddylation pathway is the amyloid precursor protein (APP)-binding protein APP-BP1, which together with Uba3, plays an analogous role to the ubiquitin-activating enzyme E1 in nedd8 activation. Activated nedd8 covalently modifies and activates a major class of ubiquitin ligases called Cullin-RING ligases (CRLs). New evidence suggests that neddylation also modifies Type-1 transmembrane receptors such as APP. Here we review the functions of neddylation and summarize evidence suggesting that dysfunction of neddylation is involved in Alzheimer's disease.
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spelling mit-1721.1/894002022-10-02T05:23:28Z Neddylation dysfunction in Alzheimer's disease Chen, Yuzhi Neve, Rachael L. Liu, Helena Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences Massachusetts Institute of Technology. Department of Materials Science and Engineering Neve, Rachael L. Liu, Helena Ubiquitin-dependent proteolysis is a major mechanism that downregulates misfolded proteins or those that have finished a programmed task. In the last two decades, neddylation has emerged as a major regulatory pathway for ubiquitination. Central to the neddylation pathway is the amyloid precursor protein (APP)-binding protein APP-BP1, which together with Uba3, plays an analogous role to the ubiquitin-activating enzyme E1 in nedd8 activation. Activated nedd8 covalently modifies and activates a major class of ubiquitin ligases called Cullin-RING ligases (CRLs). New evidence suggests that neddylation also modifies Type-1 transmembrane receptors such as APP. Here we review the functions of neddylation and summarize evidence suggesting that dysfunction of neddylation is involved in Alzheimer's disease. National Institutes of Health (U.S.) (NIH/NIA RO1 AG034980) 2014-09-09T19:13:42Z 2014-09-09T19:13:42Z 2012-11 2012-02 Article http://purl.org/eprint/type/JournalArticle 15821838 http://hdl.handle.net/1721.1/89400 Chen, Yuzhi, Rachael L. Neve, and Helena Liu. “Neddylation Dysfunction in Alzheimer’s Disease.” J. Cell. Mol. Med. 16, no. 11 (October 29, 2012): 2583–2591. https://orcid.org/0000-0002-3854-5968 en_US http://dx.doi.org/10.1111/j.1582-4934.2012.01604.x Journal of Cellular and Molecular Medicine Creative Commons Attribution http://creativecommons.org/licenses/by/3.0/ application/pdf John Wiley & Sons, Inc Wiley Blackwell
spellingShingle Chen, Yuzhi
Neve, Rachael L.
Liu, Helena
Neddylation dysfunction in Alzheimer's disease
title Neddylation dysfunction in Alzheimer's disease
title_full Neddylation dysfunction in Alzheimer's disease
title_fullStr Neddylation dysfunction in Alzheimer's disease
title_full_unstemmed Neddylation dysfunction in Alzheimer's disease
title_short Neddylation dysfunction in Alzheimer's disease
title_sort neddylation dysfunction in alzheimer s disease
url http://hdl.handle.net/1721.1/89400
https://orcid.org/0000-0002-3854-5968
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