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Cells 2019, 8(1), 70; https://doi.org/10.3390/cells8010070

Possible Mechanisms by which Stefin B could Regulate Proteostasis and Oxidative Stress

Department of Biochemistry and Molecular and Structural Biology, Jožef Stefan Institute, Jamova 39, 1000 Ljubljana, Slovenia
Received: 8 November 2018 / Revised: 19 December 2018 / Accepted: 9 January 2019 / Published: 18 January 2019
(This article belongs to the Special Issue Proteostasis and Autophagy)
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Abstract

Human stefin B is a protease inhibitor from the family of cystatins. It was reported that it forms oligomers in cells. We have shown that it has a role in cell’s response to misfolded proteins. We also have shown that its oligomers bind amyloid-beta (Aβ). Here, we discuss ways, how stefin B could reduce build-up of protein aggregates by other proteins and consequently reduces ROS and, how this might be connected to autophagy. When overexpressed, stefin B forms protein aggregates itself and these protein aggregates induce autophagy. Similarly, cystatin C was shown to bind Aβ and to induce autophagy. It is also suggested how more knowledge about the role of stefin B in a cell’s response to misfolded proteins could be used to modulate progressive myoclonus epilepsy of type 1 EPM1 disease. View Full-Text
Keywords: cystatin B; amyloid; oligomers toxicity; protein aggregation; autophagy; oxidative stress cystatin B; amyloid; oligomers toxicity; protein aggregation; autophagy; oxidative stress
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Žerovnik, E. Possible Mechanisms by which Stefin B could Regulate Proteostasis and Oxidative Stress. Cells 2019, 8, 70.

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