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. 2018 Nov 22;8:17255. doi: 10.1038/s41598-018-35610-1

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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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Overexpression of HSF1 and HSF1-AB in CGNs. (A) CGNs were infected with Ad-HSF1, Ad-HSF1-AB, or Ad-GFP and treated with HK or LK for 8 hours. Immunostaining using FLAG or GFP antibody showed that HSF1 was mainly localized in the nucleus, while HSF1-AB and GFP were distributed in both the cytoplasm and the nucleus. (B) HSF1 and HSF1-AB were robustly expressed in the CGNs as shown by Western blot (WB) and RT-PCR analyses. Expression level of Hsp70, a known target gene of trimeric HSF1, was upregulated by wild-type HSF1 but not by HSF1-AB, which lacks the trimerizaiton domain. Level of an apoptotic marker, c-Jun, was dramatically increased by LK treatment. The darker intensity of signal for HSF1-AB relative to HSF1 is because of its higher stability (Qu and D’Mello, manuscript in preparation).