AMPK-Dependent Degradation of TXNIP upon Energy Stress Leads to Enhanced Glucose Uptake via GLUT1
Ning Wu,Bin Zheng,Adam J. Shaywitz,Yossi Dagon,Christine Tower,Gary Bellinger,Che Hung Shen,Jennifer Wen,John M. Asara,Timothy E. McGraw,Barbara B. Kahn,Lewis C. Cantley,Lewis C. Cantley +12 more
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TLDR
The glucose influx through GLUT1 restores ATP-to-ADP ratios in the short run and ultimately induces TXNIP protein production to suppress glucose uptake once energy homeostasis is reestablished.About:
This article is published in Molecular Cell.The article was published on 2013-03-28 and is currently open access. It has received 500 citations till now. The article focuses on the topics: TXNIP & Thioredoxin-Interacting Protein.read more
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AMPK: guardian of metabolism and mitochondrial homeostasis.
Sébastien Herzig,Reuben J. Shaw +1 more
TL;DR: How AMPK functions as a central mediator of the cellular response to energetic stress and mitochondrial insults and coordinates multiple features of autophagy and mitochondrial biology is discussed.
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AMPK: Mechanisms of Cellular Energy Sensing and Restoration of Metabolic Balance
Daniel Garcia,Reuben J. Shaw +1 more
TL;DR: The recently solved crystal structure of AMPK has shed light both into how nucleotides activate AMPK and, importantly, also into the sites bound by small molecule activators, thus providing a path for improved drugs.
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The PI3K–AKT network at the interface of oncogenic signalling and cancer metabolism
Gerta Hoxhaj,Brendan D. Manning +1 more
TL;DR: The PI3K–AKT signalling network is discussed and its control of cancer cell metabolism through both direct and indirect regulation of nutrient transport and metabolic enzymes, thereby connecting oncogenic signalling and metabolic reprogramming to support cancer cell survival and proliferation.
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Regulation and function of AMPK in physiology and diseases
TL;DR: The current understanding of the molecular and physiological regulation of AMPK and its metabolic and physiological functions are discussed and the mechanisms underlying the versatile roles of AM PK in diabetes and cancer are discussed.
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NLRP3 inflammasome: From a danger signal sensor to a regulatory node of oxidative stress and inflammatory diseases
Amna Abderrazak,Tatiana Syrovets,Dominique Couchie,Khadija El Hadri,Bertrand Friguet,Thomas Simmet,Mustapha Rouis,Mustapha Rouis,Mustapha Rouis +8 more
TL;DR: This review has updated knowledge on NLRP3 inflammasome assembly and activation and on the pyrin domain inNLRP3 that could represent a drug target to treat sterile inflammatory diseases, and reported mutations in NL RP3 that were found to be associated with certain diseases.
References
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Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation
TL;DR: It is proposed that the metabolism of cancer cells, and indeed all proliferating cells, is adapted to facilitate the uptake and incorporation of nutrients into the biomass needed to produce a new cell.
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AMPK: a nutrient and energy sensor that maintains energy homeostasis
TL;DR: AMP-activated protein kinase conserves ATP levels through the regulation of processes other than metabolism, such as the cell cycle and neuronal membrane excitability.
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AMPK phosphorylation of raptor mediates a metabolic checkpoint.
Dana M. Gwinn,David B. Shackelford,Daniel F. Egan,Maria M. Mihaylova,Annabelle Mery,Debbie S. Vasquez,Benjamin E. Turk,Reuben J. Shaw +7 more
TL;DR: AMPK directly phosphorylates the mTOR binding partner raptor on two well-conserved serine residues, and this phosphorylation induces 14-3-3 binding to raptor, uncovering a conserved effector of AMPK that mediates its role as a metabolic checkpoint coordinating cell growth with energy status.
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The AMPK signalling pathway coordinates cell growth, autophagy and metabolism
TL;DR: A number of recent breakthroughs in the mechanistic understanding of AMPK function are reviewed, focusing on a number of newly identified downstream effectors of AM PK.
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Thioredoxin-interacting protein links oxidative stress to inflammasome activation
TL;DR: The participation of TXNIP in the NLRP3 inflammasome activation may provide a mechanistic link to the observed involvement of IL-1β in the pathogenesis of type 2 diabetes.