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Type: Journal article
Title: The Extracellular Molecular Chaperone Clusterin Inhibits Amyloid Fibril Formation and Suppresses Cytotoxicity Associated with Semen-Derived Enhancer of Virus Infection (SEVI)
Author: Elias, A.K.
Wilson, M.R.
Carver, J.A.
Musgrave, I.F.
Citation: Cells, 2022; 11(20):3259-1-3259-12
Publisher: MDPI AG
Issue Date: 2022
ISSN: 2073-4409
Statement of
Abigail K. Elias, Mark R. Wilson, John A. Carver and Ian F. Musgrave
Abstract: Clusterin is a glycoprotein present at high concentrations in many extracellular fluids, including semen. Its increased expression accompanies disorders associated with extracellular amyloid fibril accumulation such as Alzheimer’s disease. Clusterin is an extracellular molecular chaperone which prevents the misfolding and amorphous and amyloid fibrillar aggregation of a wide variety of unfolding proteins. In semen, amyloid fibrils formed from a 39-amino acid fragment of prostatic acid phosphatase, termed Semen-derived Enhancer of Virus Infection (SEVI), potentiate HIV infectivity. In this study, clusterin potently inhibited the in vitro formation of SEVI fibrils, along with dissociating them. Furthermore, clusterin reduced the toxicity of SEVI to pheochromocytoma-12 cells. In semen, clusterin may play an important role in preventing SEVI amyloid fibril formation, in dissociating SEVI fibrils and in mitigating their enhancement of HIV infection.
Keywords: protein aggregation; SEVI; clusterin; amyloid fibril; cytotoxicity; molecular chaperone
Description: Published: 17 October 2022
Rights: © 2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https:// 4.0/).
DOI: 10.3390/cells11203259
Grant ID:
Appears in Collections:Pharmacology publications

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