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Enrichment of Detergent-insoluble Protein Aggregates from Human Postmortem Brain

Enrichment of Detergent-insoluble Protein Aggregates from Human Postmortem Brain

Published on: October 24, 2017

Neddylation dysfunction in Alzheimer's disease.

Yuzhi Chen¹, Rachael L Neve, Helena Liu

¹Department of Geriatrics and Department of Neurobiology & Developmental Sciences, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA. chenyuzhi@uams.edu

Journal of Cellular and Molecular Medicine

|July 19, 2012

Summary

Neddylation, a key regulator of ubiquitination, involves APP-BP1 and Uba3 in activating nedd8. This process modifies Cullin-RING ligases and APP, with neddylation dysfunction linked to Alzheimer's disease.

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Area of Science:

Biochemistry
Molecular Biology
Neuroscience

Background:

Ubiquitin-dependent proteolysis regulates protein degradation.
Neddylation is a crucial regulatory pathway for ubiquitination.
APP-binding protein (APP-BP1) and Uba3 are central to neddylation.

Purpose of the Study:

To review the functions of neddylation.
To summarize evidence linking neddylation dysfunction to Alzheimer's disease.

Main Methods:

Literature review of neddylation pathways.
Analysis of the role of APP-BP1, Uba3, and nedd8.
Examination of neddylation's impact on Cullin-RING ligases and APP.

Main Results:

Neddylation activates nedd8, analogous to ubiquitin-activating enzyme E1.
Activated nedd8 modifies and activates Cullin-RING ligases (CRLs).
Evidence suggests neddylation modifies Type-1 transmembrane receptors, including APP.

Conclusions:

Neddylation is a significant regulatory pathway for ubiquitination.
Dysfunction in neddylation pathways is implicated in Alzheimer's disease pathogenesis.