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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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ER stress-induced caspase-8 activation occurs independently of the death receptors TNFR1, FAS, or DR5. (a–h) Ripk1^+/+ MEFs were transfected with a control non-silencing siRNA (siNS) or or with siRNA targeting Tnfr1 (siTnfr1), Fas (siFas), Dr5 (siDr5), or Fadd (siFadd), and then exposed to 1 μg/ml Tu for 12 h (a, c, e, and g). As control to test the functionality of repression, the cells were stimulated with TNF in combination with TAK1 inhibitor (TAK1i) (b), or with anti-Fas antibody (d), or Trail (f and h) in combination with cycloheximide (CHX) (d, f, and h). The cells were then lysed and immunoblotted as indicated. (i) Ripk1^+/+ MEFs were transfected as before, stimulated with 1 μg/ml Tunicamycin, and then the percentage of cell death was measured in function of time using the Fluostar Omega fluorescence plate reader. Error bars represent S.E.M. of three independent experiments