Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2023 Apr 25;44(9):1906–1919. doi: 10.1038/s41401-023-01091-w

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Fig. 1 — a Western blotting revealed that treatment with DPT at 450 nmol/L induced a reduction in cytoplasmic TAX1BP1, but improved mitochondrial TAX1BP1 in a time-dependent manner. b Representative images of confocal microscopy combined with immunochemical staining showed that TAX1BP1 accumulated apparently in mitochondria of the U87 cells treated with 450 nmol/L DPT for 24 h, when compared with that in control cells. c Representative images of confocal microscopy combined with immunochemical staining showed that AIF decreased in mitochondria, but accumulated apparently in nucleus of the U87 cell treated with 450 nmol/L DPT for 24 h. d Western blotting revealed that the increased TAX1BP1 and the decreased AIF in mitochondrial fractions caused by 450 nmol/L DTP at 24 h were both obviously inhibited when TAX1BP1 was knocked down with siRNA. Concomitantly, the upregulated AIF in nuclear fractions was prevented as well. e Flow cytometry analysis with JC-1 staining showed that the depleted mitochondrial membrane potentials caused by 450 nmol/L DPT at 24 h was apparently inhibited when TAX1BP1 was knocked down with siRNA. f LDH release assay showed that knockdown of TAX1BP1 with siRNA significantly prevented the glioma cell death induced by 450 nmol/L DPT at 24 h. The values are expressed as mean ± SD (n = 5 per group).