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. 2001 May 28;153(5):1011–1022. doi: 10.1083/jcb.153.5.1011

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© 2001 The Rockefeller University Press

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).

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The A1 GSE interferes with a step common to the activation of BiP and ATF4 in the UPR. (A) Immunoblot of ATF4 in tunicamycin-treated parental and A1-transduced CHO cells (upper panel). Anti-eIF2α immunoblot of the same membrane serves as a control of protein loading (lower panel). (B) Northern blot of RNA from tunicamycin-treated parental and A1-transduced CHO cells. The blot was hybridized sequentially with BiP, the insert of the A1 retrovirus, and GAPDH radiolabeled probes.