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. 2014 Dec 4;5(12):e1555. doi: 10.1038/cddis.2014.523

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Copyright © 2014 Macmillan Publishers Limited

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 3.0 Unported License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/3.0/

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Ripk1 acts upstream of caspase-8 during ER stress-mediated death. (a) Ripk1^+/+ and Ripk1^−/− MEFs were exposed to 1 μg/ml tunicamycin (Tu) for the indicated time, and then lysed and immunoblotted as indicated. (b and c) Ripk1^+/+ and Ripk1^−/− MEF transduced with a control shRNA (shCtrl) or with shRNA targeting caspase-8 (shC8) were treated with 1 μg/ml Tu, and then lysed and immunblotted as indicated. Arrows indicated cleaved fragments of proteins. (d) Ripk1^+/+ MEFs were stimulated with 1 μg/ml Tu for the indicated time, or incubated for 30 min with a TAK1 inhibitor (TAK1i) before stimulation with TNF for 2 h. Caspase-8 immunoprecipitates (IP) and cell lysates (Input 3%) were analyzed by immunoblot (IB) as indicated