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. 2019 Jul 1;10:2901. doi: 10.1038/s41467-019-10681-4

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — AMPKα silencing partially reverses metabolic phenotypes of c-Src-deficient cells. a NIC/c-Src^+/+ cells and two independent NIC/c-Src^L/L cell lines were transduced with a retrovirus bearing shRNAs against Prkaa1 and Prkaa2 (AMPKα1 and AMPKα2). Immunoblots show expression of PRC2 components, mTORC1 activation and AMPK α1/α2 expression and activity. b Basal, maximal (FCCP), ATP-synthesis-coupled (Oligomycin A), and non-mitochondrial (rotenone/antimycin A) oxygen consumption rates (OCRs) of NIC cell lines expressing control or AMPK α1/α2 shRNAs. Representative of 2 cell lines per genotype. c, d Quantification of basal OCR and ECAR of cells as in b. e Glucose consumption and lactate levels in conditioned media from cells as in b. All bar charts show mean ± SEM, with * = p < 0.05 and ** = p < 0.01 (unpaired, two-tailed Student’s t-test)