Editorial Note to: Glucose Addiction of TSC Null Cells Is Caused by Failed mTORC1-Dependent Balancing of Metabolic Demand with Supply

(Molecular Cell 38, 487–499; May 28, 2010) We, the editors of Molecular Cell, were contacted by a concerned reader who informed us about duplicated image that appears in Figure 2A and S1E above paper. These images are pictures untreated control TSC2-/- p53-/- mouse embryonic fibroblasts. The authors no longer have access to original data published 11 years ago, but they believe these likely came from same experiment. Dr. Blenis apologized for inadvertent duplication not clearly labeling Without data, correction is possible. Given age paper does compromise conclusions paper, based on information available at this time, we further action warranted. Glucose Addiction TSC Null Cells Is Caused Failed mTORC1-Dependent Balancing Metabolic Demand with SupplyChoo et al.Molecular CellMay 2010In BriefThe mTORC1-signaling pathway integrates environmental conditions into distinct signals cell growth balancing anabolic catabolic processes. Accordingly, energetic stress inhibits mTORC1 signaling predominantly through AMPK-dependent activation TSC1/2. Thus, TSC1/2−/− cells hypersensitive glucose deprivation, has been linked increased p53 translation apoptosis. Herein, show inhibition during deprivation prevented only execution death, also induction stress. Full-Text PDF Open Archive