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Articles by Benoit Viollet
AMPKα regulates glycolytic reprogramming to sustain NK cell proliferation and effector function
Abstract Natural killer (NK) cells are critical innate lymphocytes that mediate early anti-viral immunity through cytotoxicity and cytokine production. Activation of NK cells require metabolic reprogramming to sustain proliferation and effector functions; however, the molecular regulators coordinating this process remain incompletely defined.
Phenformin, But Not Metformin, Delays Development of T Cell Acute Lymphoblastic Leukemia/Lymphoma via Cell-Autonomous AMPK Activation
Main text (Cell Reports , 690–698.e1–e4; April 16, 2019) A reader pointed out a problem with Figure 4E in this paper. The anti-phospho-4EBP1 western blots for F04 and F15 cells were flagged as potential duplicates. When the original data was requested by the editor, the authors realized that one of the image files was accidentally mislabelled.
Fueling metabolic adaptation: lysosomal AMPK ignites glutaminolysis - Cell Research
The capacity to effectively adapt metabolism to environmental demands is crucial for cell viability, proliferation, and function. Recent discoveries in Cell Research have highlighted the role of the lysosomal pool of AMPK in promoting glutaminolysis during glucose shortage through the activation of a PDZD8-GLS1 axis.
The AMPK-related kinase NUAK1 controls cortical axons branching by locally modulating mitochondrial metabolic functions - Nature Communications
Abstract The cellular mechanisms underlying axonal morphogenesis are essential to the formation of functional neuronal networks. We previously identified the autism-linked kinase NUAK1 as a central regulator of axon branching through the control of mitochondria trafficking. However, (1) the relationship between mitochondrial position, function and axon branching and (2) the downstream effectors whereby NUAK1 regulates axon branching remain unknown.
The AMPK-Sirtuin 1-YAP axis is regulated by fluid flow intensity and controls autophagy flux in kidney epithelial cells - Nature Communications
Abstract Shear stress generated by urinary fluid flow is an important regulator of renal function. Its dysregulation is observed in various chronic and acute kidney diseases. Previously, we demonstrated that primary cilium-dependent autophagy allows kidney epithelial cells to adapt their metabolism in response to fluid flow. Here, we show that nuclear YAP/TAZ negatively regulates autophagy flux in kidney epithelial cells subjected to fluid flow.
Metformin: update on mechanisms of action and repurposing potential - Nature Reviews Endocrinology
Abstract Currently, metformin is the first-line medication to treat type 2 diabetes mellitus (T2DM) in most guidelines and is used daily by >200 million patients. Surprisingly, the mechanisms underlying its therapeutic action are complex and are still not fully understood. Early evidence highlighted the liver as the major organ involved in the effect of metformin on reducing blood levels of glucose.
AMPK deficiency in smooth muscles causes persistent pulmonary hypertension of the new-born and premature death - Nature Communications
Abstract AMPK has been reported to facilitate hypoxic pulmonary vasoconstriction but, paradoxically, its deficiency precipitates pulmonary hypertension. Here we show that AMPK-α1/α2 deficiency in smooth muscles promotes persistent pulmonary hypertension of the new-born.
Aβ42 oligomers trigger synaptic loss through CAMKK2-AMPK-dependent effectors coordinating mitochondrial fission and mitophagy - Nature Communications
Abstract During the early stages of Alzheimer’s disease (AD) in both mouse models and human patients, soluble forms of Amyloid-β 1–42 oligomers (Aβ42o) trigger loss of excitatory synapses (synaptotoxicity) in cortical and hippocampal pyramidal neurons (PNs) prior to the formation of insoluble amyloid plaques.
Glucose availability but not changes in pancreatic hormones sensitizes hepatic AMPK activity during nutritional transition in rodents
Camille Huet1, Nadia Boudaba1, Bruno Guigas2, Benoit Viollet3 and Marc Foretz4* 1Institut Cochin - Inserm U1016 - CNRS UMR8104 - Université de Paris, France 2Leiden University, Netherlands 3INSERM, France 4Institut Cochin - Inserm U1016 - CNRS UMR8104 - Université de Paris, France ↵* Corresponding author; email: marc.foretz{at}inserm.fr Author contributions: C.H., N.B., B.G., and M.F. investigation; N.B. and M.F. formal analysis; N.B., B.V., and M.F. funding acquisition; N.B. and M.F....
Understanding the glucoregulatory mechanisms of metformin in type 2 diabetes mellitus
1. Davies, M. J. et al. Management of hyperglycemia in type 2 diabetes, 2018. A consensus report by the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD). Diabetes Care 41, 2669–2701 (2018). PubMed Google Scholar 2. Davies, M. J. et al. Management of hyperglycaemia in type 2 diabetes, 2018. A consensus report by the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD). Diabetologia 61, 2461–2498 (2018).
Correction: AMPKα1 deletion shortens erythrocyte life span in mice: Role of oxidative stress.
See original article: Wang et al. 285 (26): 19976. VOLUME 285 (2010) PAGES 19976–19985 Supplemental Fig. 4 was mislabeled. This error has now been corrected and does not affect the results or conclusions of this work. The authors apologize for the error. © 2019 by The American Society for Biochemistry and Molecular Biology, Inc. Published in the U.S.A. The American Society for Biochemistry and Molecular Biology, Inc. Published in the U.S.A. Submit your work to JBC. You'll be in good company.
AMP-activated protein kinase upregulates MAP kinase interacting serine/threonine kinase 1a-dependent phosphorylation of eukaryotic translation initiation factor 4E
AMP-activated protein kinase (AMPK) is a molecular energy sensor that acts to sustain cellular energy balance. Although AMPK is implicated in the regulation of a multitude of ATP-dependent cellular processes, exactly how these processes are controlled by AMPK and the identity of AMPK targets and pathways continues to evolve. We here identify MAP kinase interacting serine/threonine-protein kinase 1a (MNK1a) as a novel AMPK target.
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