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Thomas Briston1†‡Jenna M. Stephen2‡
Luke W. Thomas2
Cinzia Esposito2
Yuen-Li Chung3Saiful E. Syafruddin4
Mark Turmaine5Lucas A. Maddalena2Basma Greef2
Gyorgy Szabadkai5,6,7
Patrick H. Maxwell8Sakari Vanharanta4
Margaret Ashcroft2*- 1Division of Medicine, Centre for Cell Signalling and Molecular Genetics, University College London, London, United Kingdom
- 2Department of Medicine, University of Cambridge, Cambridge, United Kingdom
- 3Cancer Research UK Cancer Imaging Centre, Institute of Cancer Research London, London, United Kingdom
- 4Medical Research Council Cancer Unit, Hutchison/MRC Research Centre, University of Cambridge, Cambridge, United Kingdom
- 5Division of Biosciences, Department of Cell and Developmental Biology, University College London, London, United Kingdom
- 6The Francis Crick Institute, London, United Kingdom
- 7Department of Biomedical Sciences, University of Padua, Padua, Italy
- 8Cambridge Institute for Medical Research, University of Cambridge, Cambridge, United Kingdom
A Corrigendum on
VHL-Mediated Regulation of CHCHD4 and Mitochondrial Function
By Briston T, Stephen JM, Thomas LW, Esposito C, Chung Y-L, Syafruddin SE, Turmaine M, Maddalena LA, Greef B, Szabadkai G, Maxwell PH, Vanharanta S and Ashcroft M (2018). Front. Oncol. 8:388. doi: 10.3389/fonc.2018.00388
In the original article, there was a mistake in Figure 4A as published. The figure text was mislabeled, and a lane-line was missing. The corrected Figure 4 appears below.
FIGURE 4
Figure 4 pVHL mutants differentially regulate mitochondrial protein expression, mtDNA copy number and ATP levels. (A) Western blots show HIF-1α, HIF-2α, GLUT-1, and BNIP3 protein levels in RCC10 cells expressing empty vector (pCMV), wild type pVHL (VHL), or pVHL mutants (R200W or N78S). α-tubulin and β-actin were used as load controls. (B) Relative expression of PHD3 mRNA in RCC10 cells described in (A), measured using RT-qPCR. Data were analyzed using the comparative Ct method. Data are presented as mean ± S.E.M. n = 3 (n.s. p > 0.05, *p < 0.05, and ***p < 0.001). (C) Western blots show expression of mitochondrial proteins CHCHD4 and VDAC1, and respiratory chain subunits NDUFB10 (CI), SDHA (CII), UQCRC2 (CIII), COX IV (CIV) in RCC10 cells described in (A). pVHL expression was assessed as a control for re-expression, and β-actin and α-tubulin were used as load controls. (D) Graph shows total cellular ATP content in RCC10 cells expressing wild type pVHL (VHL) or pVHL mutants (R200W or N78S), normalized to cell number (n = 4). (E) Graph shows mtDNA copy number in RCC10 cells expressing pVHL variants, calculated using the ratio of expression of mitochondrial ND1 gene to the single copy nuclear gene, β2M to by RT-qPCR. Data in (D, E) are presented as mean ± S.D. n = 6 (n.s. p > 0.05, *p < 0.05, **p < 0.01, and ***p < 0.001).
The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.
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Keywords: Hippel-Lindau protein (pVHL), hypoxia inducible factor, mitochondria, bioenergetics, metabolism, CHCHD4, respiratory chain
Citation: Briston T, Stephen JM, Thomas LW, Esposito C, Chung Y-L, Syafruddin SE, Turmaine M, Maddalena LA, Greef B, Szabadkai G, Maxwell PH, Vanharanta S and Ashcroft M (2021) Corrigendum: VHL-Mediated Regulation of CHCHD4 and Mitochondrial Function. Front. Oncol. 11:740273. doi: 10.3389/fonc.2021.740273
Received: 12 July 2021; Accepted: 26 August 2021;
Published: 23 September 2021.
Edited and reviewed by:
Keith R. Laderoute, Consultant, Redwood City, CA, United StatesCopyright © 2021 Briston, Stephen, Thomas, Esposito, Chung, Syafruddin, Turmaine, Maddalena, Greef, Szabadkai, Maxwell, Vanharanta and Ashcroft. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Margaret Ashcroft, bS5hc2hjcm9mdEBtZWRzY2hsLmNhbS5hYy51aw==
†Present Address: Thomas Briston, Hatfield Research Laboratories, Neurology Innovation Centre, Eisai Ltd., Hatfield, United Kingdom
‡These authors have contributed equally to this work