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. 2014 May 2;21(9):1388–1398. doi: 10.1038/cdd.2014.54

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Copyright © 2014 Macmillan Publishers Limited

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 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-nc-nd/3.0/

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SAG regulates apoptosis of J774 macrophages by modulating the balance between anti- and proapoptotic factors in a timely manner. LPS (10 ng/ml) and polyinosinic-polycytidylic acid (poly I:C) (10 μg/ml) stimulation resulted in bimodal peaks (at 3 and 24 h) of proapoptotic Bax and SARM, and a single peak (over 6–12 h) each of antiapoptotic SAG and Bcl-2 (a (i and iii) and b, blue box). SAG-knockdown cells maintained expression of Bcl-2 but sustained the expression of the proapoptotic Bax and SARM at high levels (over 3–36 h; a (ii and iv) and red box in b). The PAMP-challenged cells were examined by both (a) intracellular staining (see FACS analysis data; Supplementary Figure S5) and (b) immunoblotting analysis. Data are presented as fluorescence intensity ±S.D. (n=3)