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. 2020 Feb 24;21(4):1533. doi: 10.3390/ijms21041533

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© 2020 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 (http://creativecommons.org/licenses/by/4.0/).

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Dysregulated phosphoinositide-3-kinase (PI3K), the serine-threonine protein kinase (AKT) and autophagy pathways in the liver of beclin1^+/− zebrafish. Expressions of mRNA in 16-month-old zebrafish evaluated by qRT-PCR for PI3K subunits and anti-apoptotic genes (A) and autophagy-related genes (B). (C) Representative immunoblots showing the relative protein expression of Akt, P-Akt, P62, LC3-I-II, Atg5-Atg12 conjugate. β-actin was used as vehicle control. (D) The ratio of P-Akt/Akt, P62/β-actin, LC3-II/LC3-I, and Atg5-atg12/β-actin quantified by NIH software Image J. (E) (a–c) Immunofluorescence of P62 showing protein increasing around the necrosis tissue of beclin1^+/−.(d–f) Immunofluorescence of liver tissues probed against LC3-II revealed a severe reduction in beclin1^+/−. CV: central vein; NC: Necrosis. Data expressed as mean ± SD. * p < 0.05, ** p < 0.01, and *** p < 0.001.