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. 2020 Jan 23;12(2):280. doi: 10.3390/cancers12020280

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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SDHB deficiency activated NRF2-driven glutathione synthetic pathway. (A) antioxidative response element (ARE)-luciferase reporter assay showed increased NRF2 activity in SDHB^KD MPC and hpheo1 cells. *** p < 0.001. (B) Quantitative real-time PCR showed increased gene transcription of NRF2-associated genes Gclm and Slc7a11 in SDHB^KD MPC cells. *** p < 0.001. (C) Immunoblotting showed increased expression of NRF2 and its downstream targets in SDHB^KD MPC and hpheo1 cells. β-actin was used as internal control. (D) Cycloheximide (CHX) pulse chase assay showed elevated NRF2 protein stability in SDHB^KD hpheo1 cells. β-actin was used as internal control. (E) Quantification of NRF2 half-life from Figure 2D. (F) Chromatin immunoprecipitation (ChIP) PCR assay showed increased promoter affinity of NRF2 in SDHB^KD hpheo1 cells. * p < 0.05; ** p < 0.01; *** p < 0.001.