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. 2015 Mar 25;9:17. doi: 10.1186/s12918-015-0158-y

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© Dexter et al.; licensee BioMed Central. 2015

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Growth defects following Sln1 overexpression are not completely due to HOG pathway activation. A We assayed growth in wild-type and ssk1 Δ strains overexpressing Sln1 in response to β-estradiol or carrying an empty P _GAL1 vector control. Deletion of Ssk1, which prevented HOG pathway activation by Sln1, partially alleviated the growth defect due to Sln1 overexpression. B Growth of cells on plates containing 10 μM β-estradiol indicated that ssk1 Δ reduced the toxicity of Sln1 overexpression.