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. 2022 Feb 25;50(5):2700–2718. doi: 10.1093/nar/gkac104

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© The Author(s) 2022. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 3. — Microglial activation in the absence of ATM is mediated via RELB. (A) Representative immunoblot analysis of siRNA-mediated silencing of RELB or all NF-κB members (NF-κB^pan) in WT and ATM KO HMC3 cells. Loading control: GAPDH. Quantification of protein levels is relative to loading control. (B) Phagocytosis levels (5 μm beads) of WT and ATM KO HMC3 cells treated with control (Ctrl), RELB or NF-κB^pan siRNA. Phagocytosis is relative to WT HMC3 treated with Ctrl siRNA. Mean ± S.D. shown (n = 4). Two-way ANOVA with Tukey's multiple comparison's test used. (C) RT-qPCR analysis of the indicated cytokines as in (B). Expression is relative to WT HMC3 treated with control siRNA (Ctrl). Reference gene: RSP13. Mean ± S.D. shown (n = 3). Two-way ANOVA with Tukey's multiple comparison's test used.