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Open AccessJournal ArticleDOI

mTORC1 Links Protein Quality and Quantity Control by Sensing Chaperone Availability

TLDR
It is demonstrated that cells distinguish moderate reductions in protein quality from severe protein misfolding using molecular chaperones to differentially regulate mTORC1 signaling, and the tight linkage between protein quality and quantity control provides a plausible mechanism coupling protein mis folding with metabolic dyshomeostasis.
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The ER Stress Inducer l-Azetidine-2-Carboxylic Acid Elevates the Levels of Phospho-eIF2α and of LC3-II in a Ca2+-Dependent Manner

TL;DR: The proline analogue l-azetidine-2-carboxylic acid was used to induce ER stress, and its effect on autophagy and Ca2+ homeostasis and it was deduced that activation of the PERK branch is required for the AZC-induced lipidation of LC3.
Journal ArticleDOI

Hepatic DNAJB9 Drives Anabolic Biasing to Reduce Steatosis and Obesity.

TL;DR: Restoration of hepatic DNAJB9 expression effectively improves insulin sensitivity, restores protein synthesis, and suppresses food intake, accompanied by reduced hepatic steatosis and adiposity in multiple mouse models of obesity.
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The EGFR-HSF1 axis accelerates the tumorigenesis of pancreatic cancer

TL;DR: In this article, the authors found that pharmacological inhibition of heat shock factor 1 (HSF1) slowed pancreatic cancer initiation and suppressed the pancreatitis-induced formation of pancreatic precancerous lesion.

A systems biology perspective on the consequences of aneuploidy in human cells

TL;DR: The analysis shows that despite the variability in chromosome content, aneuploidy triggers uniform transcriptional response in human cells, which might represent novel biomarkers to assess the malignant potential of a tumor.

Heat Shock Gene Dysregulation and Inactivation of Drug Therapy

Ian Martins
TL;DR: The success of the use of these chronic disease medications may require nutritional interventions that accelerate drug metabolism and improve insulin resistance and endocrine therapy associated with the delay in the pathogenesis of NAFLD.
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Journal ArticleDOI

TOR signaling in growth and metabolism.

TL;DR: The physiological consequences of mammalianTORC1 dysregulation suggest that inhibitors of mammalian TOR may be useful in the treatment of cancer, cardiovascular disease, autoimmunity, and metabolic disorders.
Journal ArticleDOI

mTOR Interacts with Raptor to Form a Nutrient-Sensitive Complex that Signals to the Cell Growth Machinery

TL;DR: It is reported that mTOR forms a stoichiometric complex with raptor, an evolutionarily conserved protein with at least two roles in the mTOR pathway that through its association with mTOR regulates cell size in response to nutrient levels.
Journal ArticleDOI

TSC2 is phosphorylated and inhibited by Akt and suppresses mTOR signalling

TL;DR: It is shown that TSC1–TSC2 inhibits the p70 ribosomal protein S6 kinase 1 and activates the eukaryotic initiation factor 4E binding protein 1 (4E-BP1, an inhibitor of translational initiation) and these functions are mediated by inhibition of the mammalian target of rapamycin (mTOR).
Journal ArticleDOI

Rictor, a novel binding partner of mTOR, defines a rapamycin-insensitive and raptor-independent pathway that regulates the cytoskeleton.

TL;DR: It is found that the rictor-mTOR complex modulates the phosphorylation of Protein Kinase C alpha (PKCalpha) and the actin cytoskeleton, suggesting that this aspect of TOR signaling is conserved between yeast and mammals.
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