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. 2017 Nov 6;3:17076. doi: 10.1038/cddiscovery.2017.76

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Copyright © 2017 The Author(s)

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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Ablating GRP75 preserves mitochondrial morphology and attenuates mitochondrial ROS formation in response to glutamate treatment. (a) Representative images of mitochondrial morphology in HT22 CTR and cells transfected with scrambled siRNA (Scr) or siRNA against GRP75 (si01, si02) in the presence or absence of glutamate (16 h). Mitochondria are stained with MitoTracker Green. Scale bar: 10 μm, 63× magnification, n=3. (b, c) Representative measurement of mitochondrial ROS following glutamate exposure (16 h) in (b) HT22 CTR and cells transfected with scrambled siRNA (Scr) or siRNA against GRP75 (si01, si02), and (c) HT22 and GRP75 KO cells. Data are presented as mean + S.D., n=3, ***P<0.0001 compared with control, ^###P<0.0001 compared with glutamate. CTR, control cells.