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mTORC1 Links Protein Quality and Quantity Control by Sensing Chaperone Availability

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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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Seven sirtuins for seven deadly diseases ofaging

TL;DR: Since sirtuins are crucial to pathways that counter the decline in health that accompanies aging, pharmacological agents that boost sirtuin activity have clinical potential in treatment of diabetes, cardiovascular disease, dementia, osteoporosis, arthritis, and other conditions.
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Cellular stress response pathways and ageing: intricate molecular relationships

TL;DR: The molecular mechanisms that link ageing to main stress response pathways are surveyed, and how each pathway contributes to modulate the ageing process is discussed.
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Cotranslational Response to Proteotoxic Stress by Elongation Pausing of Ribosomes

TL;DR: It is reported that intracellular proteotoxic stress reduces global protein synthesis by halting ribosomes on transcripts during elongation, suggesting a dual role of molecular chaperones in facilitating polypeptide elongation and cotranslational folding.
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The Stress of Protein Misfolding: From Single Cells to Multicellular Organisms

TL;DR: This work will address how protein homeostasis (proteostasis) is achieved at the level of the cell and organism, and how the threshold of the stress response is set to detect and combat protein misfolding.
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Degradation of the Endoplasmic Reticulum by Autophagy during Endoplasmic Reticulum Stress in Arabidopsis

TL;DR: It is suggested that autophagy serves as a pathway for the turnover of ER membrane and its contents in response to ER stress in plants.
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CHIP deficiency decreases longevity, with accelerated aging phenotypes accompanied by altered protein quality control.

TL;DR: Investigation of the influence that protein quality control exerts on the aging process by using CHIP−/− mice reveals that impaired proteinquality control contributes to cellular senescence and implicates CHIP-dependent quality control mechanisms in the regulation of mammalian longevity in vivo.
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Evidence for a mechanism of repression of heat shock factor 1 transcriptional activity by a multichaperone complex.

TL;DR: Evidence is presented herein that trimeric hHSF1 has the propensity to dynamically associate with an Hsp90-immunophilin-p23 complex through its regulatory domain, and this repression mechanism may be required for a proportional transcriptional response to stress.
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mTOR-mediated regulation of translation factors by amino acids

TL;DR: The mammalian-target-of-rapamycin (mTOR) is a multidomain protein that is important in regulating several components of the translational machinery and the existence of novel mTOR-regulated kinases that control eEF2 kinase is suggested.
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Misfolded Proteins Are Competent to Mediate a Subset of the Responses to Heat Shock in Saccharomyces cerevisiae

TL;DR: It is concluded that misfolded proteins are competent to specifically trigger activation of heat shock factor in response to heat shock.
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Hydrogen Peroxide Activates p70S6k Signaling Pathway

TL;DR: The results suggest that ROS act as a messenger in growth factor-induced p70S6k signaling pathway and down-regulation of 12-O-tetradecanoylphorbol-13-acetate (TPA)-responsive protein kinase C (PKC) by chronic pretreatment with TPA or a specific PKC inhibitor Ro-31-8220 did not block the activation of p70s6kby ROS.
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