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Excess soluble iron or loss of RAB7A restores RKO metabolic homeostasis under VPS34 inhibition.

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posted on 24.08.2020, 17:33 by Marek J. Kobylarz, Jonathan M. Goodwin, Zhao B. Kang, John W. Annand, Sarah Hevi, Ellen O’Mahony, Gregory McAllister, John Reece-Hoyes, Qiong Wang, John Alford, Carsten Russ, Alicia Lindeman, Martin Beibel, Guglielmo Roma, Walter Carbone, Judith Knehr, Joseph Loureiro, Christophe Antczak, Dmitri Wiederschain, Leon O. Murphy, Suchithra Menon, Beat Nyfeler

(A–D) Mitochondrial respiration defect due to PIK-III treatment. RKO CTRL cells were treated with the indicated concentrations of PIK-III along with vehicle for 24 hours and mitochondrial respiration rates for OCR, (A) and ECAR, (B) were assessed using the Seahorse XFe96 analyzer. Data in the form of technical replicates were averaged and presented as the mean ± SD (n = 11 or 12 wells). RKO CTRL cells were treated with the indicated concentrations of PIK-III along with 50 μM FAC for 24 hours and mitochondrial respiration was assessed by measuring the OCR, (C) and the ECAR, (D). Data in the form of technical replicates were averaged and presented as the mean ± SD (n = 11 or 12 wells). (E–H) Mitochondrial respiration defect due to VPS34 inhibition is RAB7A-dependent. RKO CTRL or RAB7A KO cells were treated with the indicated concentrations of PIK-III for 24 hours and mitochondrial respiration was assessed by measuring the OCR (E, G) or the ECAR (F, H). Data in the form of technical replicates were averaged and presented as the mean ± SD (n = 7 or 8 wells).

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