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. 2016 Jan 11;11(1):e0146433. doi: 10.1371/journal.pone.0146433

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© 2016 Koppaka et al

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Fig 1 — hTCEpi cell lines were transduced with viral particles to stably express wild-type ALDH3A1 (hTCEpi-TR-ALDH3A1wt), mutant (catalytically-inactive) ALDH3A1 (hTCEpi-TR-ALDH3A1mu) or no ALDH3A1 (hTCEpi-TR-Lenti) under the control of a tetracycline-sensitive repressor. Following tetracycline treatment (0–1.0 mg/L) for 72 hr, (A) induction of ALDH3A1 mRNA was measured by Q-PCR; mRNA abundance in copy numbers is presented as mean ± standard error (n = 3). (B) Induction of ALDH3A1 protein was determined by Western blotting. (C) ALDH3A1 catalytic activity was assayed by measuring NADPH production using benzaldehyde as a substrate; data are presented as mean ± standard error (n = 3).