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. 2019 Dec 27;16:275. doi: 10.1186/s12974-019-1669-z

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 2 — IL-1β treatment of both NT2 cells and rat primary neurons decreased the steady-state levels of PINK1 and of Ser₆₅-phosphorylated ubiquitin (P-Ub); conversely, IL-1β increased the levels of Ser₆₅-phosphorylated parkin (P-parkin). a Representative western immunoblots depicting PINK1 levels in IL-1β treated vs untreated NT2 and rat primary neuronal cell cultures, representing 6 independent experiments. b Quantification of PINK1 levels in both NT2 cells (p = 0.01), and primary rat neurons (p = 0.05). c Representative western immunoblots of IL-1β treated vs untreated NT2 and rat primary neuronal cell cultures (n = 6 and 3 technical repeats, respectively). d Quantification of P-Ub levels in both NT2 (p = 0.03) and rat primary neurons (p = 0.005)