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. 2016 Apr 7;7(4):e2183. doi: 10.1038/cddis.2016.89

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Copyright © 2016 Macmillan Publishers Limited

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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β-Arrestin-1 and β-arrestin-2 negatively regulated ATG12–ATG5 conjugation system in podocytes with HG treatment. (a) Representative western blotting gel documents and summarized data showing the effect of Arrb1 knockdown on the levels of ATG12–ATG5 and LC3-II/LC3-I. (b) Representative western blotting gel documents and summarized data showing the effect of Arrb2 knockdown on the levels of ATG12–ATG5 and LC3-II/LC3-I. (c) Immunoprecipitation assay showing that β-arrestin-1/2 interacted with ATG7 and the interactions between ATG7 and β-arrestin-1/2 were significantly enhanced in podocytes with HG treatment. (means±S.E.M.; n=6; *P<0.05 versus control, †P<0.05 versus scramble of HG treatment). (d) Representative western blotting gel documents and summarized data showing the levels of ATG12–ATG5 and LC3-II/LC3-I in the kidney from Arrb1^−/− diabetic mice. (e) Representative western blotting gel documents and summarized data showing the levels of ATG12–ATG5 and LC3-II/LC3-I in the kidney from Arrb2^−/− diabetic mice. Values are means±S.E.M.; *P<0.05 versus control, †P<0.05 versus WT STZ mice (n=8)