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. 2017 Apr 6;8(4):e2729. doi: 10.1038/cddis.2017.153

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Copyright © 2017 The Author(s)

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International 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/4.0/

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Downregulation of GSK3β activity mediated by CST1 knockdown induces cellular glycogen accumulation. (a and b) Modulation of phospho-GS in CST1 knockdown cells. MDA-MB-231 cells were transduced with a control short hairpin (shRNA) or shCST1 (a) and, in some experiments, cells were replenished with rCys-SN (b). (c and d) Analysis of glycogen accumulation in the cytosol. MDA-MB-231 cells were transduced with a control shRNA or shCST1 in the presence or absence of rCys-SN (c) and, in some experiments, transduction was performed after transfection with pcDNA, pcDNA-GSK3β or pcDNA-GSK3β-S9A (d) Glycogen accumulation was quantified as the percentage of PAS staining-positive cells (magenta) and photographed. Scale bars, 50 μm. ***P<0.001 by Student's t-test