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. 2020 Sep 7;79(12):1635–1643. doi: 10.1136/annrheumdis-2020-217904

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© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution 4.0 Unported (CC BY 4.0) license, which permits others to copy, redistribute, remix, transform and build upon this work for any purpose, provided the original work is properly cited, a link to the licence is given, and indication of whether changes were made. See: https://creativecommons.org/licenses/by/4.0/.

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RIP3 overexpression alters gene expression patterns via the negative regulator TRIM24. (A) Transcriptional regulators were analysed by Ingenuity Pathway Analysis (IPA) software (QIAGEN, https://www.qiagenbioinformatics.com/products/ingenuitypathway-analysis) to predict upstream regulators based on microarray data. Analysed data were filtered by activation Z-score >1 or <-1, and regulators were not required to be expressed in the samples analysed. (B) Mouse embryonic fibroblasts (MEFs) and (C) chondrocytes were infected with Ad-C or Ad-Trim24 shRNA at the indicated multiplicity of infection (MOI). Cell lysates were analysed by western blotting (left) (n=3) and quantitative PCR (qPCR) (right) (n=4). (D) Western blot analysis of RIP3, p-RIP3 and TRIM24 in chondrocytes infected with Ad-C or Ad-Rip3 (left) (n=3). qPCR analysis of Rip3 and Trim24 in chondrocytes infected with Ad-C or Ad-Rip3 (right) (n=4). Values are expressed as the mean±SEM. Statistical analyses were performed using two-tailed t-tests.