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. 2018 Aug 15;8:12236. doi: 10.1038/s41598-018-30362-4

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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CRELD2 deficiency in Neuro2a cells caused the cells vulnerable to tunicamycin. (A) The parental wild-type (WT), hygromycin selected (KD) and a cloned (KO) Neuro2a cells in 96-well plate were treated with Tm (1 μg/ml) or vehicle (Control, Con) for 24 h. Cell viability was measured as described in the Materials and methods section. Each value represented the mean ± SEM from 5 independent cultures. (B) The parental (WT), hygromycin selected (KD) and a cloned (KO) Neuro2a cells were treated with Tm for 24 h. The expression levels of the indicated protein were determined as described in the Materials and methods section. The values obtained from the parental Neuro2a cells after 24 h of treatment with Tm were considered as 100%. Relative amount of cleaved caspase-3 was calculated as described in the Materials and methods section. Each value represents the mean ± SEM from 5 independent cultures.