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. 2019 Oct 17;17(2):227–239. doi: 10.1080/15476286.2019.1674595

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© 2019 CNRS - Centre national de la recherche scientifique. Published by Informa UK Limited, trading as Taylor & Francis Group.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.

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Figure 1. — Monitoring of eRF3A and UPF1 knockdown in HCT 116 cells. (A) Western blot analysis of eRF3A and UPF1 in the two biological replicates (Rep1 and Rep2) of eRF3A-depleted cells (sh-eRF3A), UPF1-depleted cells (sh-UPF1) and control cells (sh-Ctrl); α-Tubulin (α-Tub) served as a loading control. (B) eRF3A and UPF1 mRNA levels in eRF3A-depleted (sh-eRF3A) and UPF1-depleted (sh-UPF1) and control (sh-Ctrl) cells for the two biological replicates of RNAseq experiments; normalized counts are expressed in RPKM (reads per kilobase million).