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. 2022 Mar 31;12:857968. doi: 10.3389/fonc.2022.857968

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Copyright © 2022 Liang, Zhu, Suo, Wei, Yu, Gu, Chen, Yuan, Shen, Li, Sun and Gao

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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SND1 promotes mitophagy through PGAM5. (A, B) Hep3B cells stably expressing shSND1 (A) or shPGAM5 (B) were treated with 10 μM FCCP for 6 h. Samples were collected for immunoblotting to analyze the expression of SND1, PGAM5, MFN1, TIM23, COX4, p-DRP1^S637, and DRP1. Actin served as loading control. LC3 protein levels were detected in Hep3B-shSND1 cells treated with FCCP. (C, D) Hep3B cells stably expressing shSND1 (C) or shPGAM5 (D) were treated with glucose-free medium for 24 h. Samples were collected for immunoblotting to analyze the expression of SND1, PGAM5, MFN1, TIM23, COX4, and p-DRP1^S637. Actin served as loading control. LC3 protein levels were detected in Hep3B-shSND1 cells treated with glucose-free medium. (E, F) Hep3B cells stably overexpressing SND1 with further PGAM5 knockdown by shRNAs were treated with FCCP for 6 h (E) or cultured with glucose-free medium for 24 h (F), followed by immunoblotting analysis with antibodies against SND1, PGAM5, MFN1, TIM23, COX4, and p-DRP1^S637. Actin served as loading control. (G, H) Hep3B cells stably overexpressing MTS-GFP with further SND1 knockdown (G) or PGAM5 knockdown (H) were cultured with FCCP for 6 h, followed by immunoblotting analysis with antibodies against SND1, PGAM5, MFN1, TIM23, COX4, GFP, and p-DRP1^S637. Actin served as loading control. (I) Hep3B cells with endogenous SND1 knockdown were further infected with viruses expressing Flag-EV, Flag-SND1, or Flag-SND1^Δ1-63. These cells were treated with FCCP for 6 h followed by immunoblotting analysis with antibodies against SND1, MFN1, TIM23, COX4, and p-DRP1^S637. Actin served as loading control. (J, K) Hep3B cells were infected virus expressing HA-DRP1 together with Flag-PGAM5 plasmids, and the binding activity of PGAM5 and DRP1 under FCCP treatment (J) or glucose deprivation conditions (K) was determined when we further knocked down SND1. Cell lysates were immunoprecipitated with anti-Flag antibody or IgG, followed by immunoblotting analysis with antibodies against HA, Flag, and SND1. Actin served as loading control.