Search results for " S6 kinase"

showing 3 items of 13 documents

In human endothelial cells rapamycin causes mTORC2 inhibition and impairs cell viability and function.

2008

Aim Drug-eluting stents are widely used to prevent restenosis but are associated with late endothelial damage. To understand the basis for this effect, we have studied the consequences of a prolonged incubation with rapamycin on the viability and functions of endothelial cells. Methods and results Human umbilical vein or aorta endothelial cells were exposed to rapamycin in the absence or in the presence of tumour necrosis factor α (TNFα). After a 24 h-incubation, rapamycin (100 nM) caused a significant cell loss associated with the increase of both apoptosis and necrosis, as quantified by propidium iodide staining, caspase 3 activity, and lactate dehydrogenase release. Rapamycin also impair…

Time FactorsPhysiologyApoptosismTORC1Polymerase Chain Reactionchemistry.chemical_compoundCell MovementStress FibersMicroscopy ConfocalCaspase 3TOR Serine-Threonine KinasesNitric Oxide Synthase Type IIIRibosomal Protein S6 Kinases 70-kDaUp-RegulationEndothelial stem cellmedicine.anatomical_structureBiochemistryCardiology and Cardiovascular MedicineE-SelectinEndotheliumNitric Oxide Synthase Type IIICell SurvivalBlotting WesternEnzyme-Linked Immunosorbent AssayBiologyMechanistic Target of Rapamycin Complex 1Nitric OxideTacrolimusNecrosisTheophyllinePhysiology (medical)medicineHumansImmunoprecipitationViability assayPropidium iodideProtein kinase BAdaptor Proteins Signal TransducingSirolimusDose-Response Relationship DrugL-Lactate DehydrogenaseTumor Necrosis Factor-alphaEndothelial CellsProteinsCardiovascular AgentsRegulatory-Associated Protein of mTORMolecular biologyRapamycin-Insensitive Companion of mTOR ProteinchemistryMultiprotein ComplexesTOR Serine-Threonine KinasesCarrier ProteinsProtein KinasesTranscription FactorsCardiovascular research
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The deubiquitinase USP11 is a versatile and conserved regulator of autophagy

2021

Autophagy is a major cellular quality control system responsible for the degradation of proteins and organelles in response to stress and damage to maintain homeostasis. Ubiquitination of autophagy-related proteins or regulatory components is important for the precise control of autophagy pathways. Here, we show that the deubiquitinase ubiquitin-specific protease 11 (USP11) restricts autophagy and that KO of USP11 in mammalian cells results in elevated autophagic flux. We also demonstrate that depletion of the USP11 homolog H34C03.2 in Caenorhabditis elegans triggers hyperactivation of autophagy and protects the animals against human amyloid-β peptide 42 aggregation-induced paralysis. USP11…

autophagyhAβ42 human amyloid-β protein 1 to 42Lipid kinase activityPI(3)P phosphatidylinositol-3-phosphatemTORC1BiochemistryCell LineGene Knockout Techniqueschemistry.chemical_compoundubiquitinAnimalsHumansULK1 unc-51-like autophagy activating kinase 1WIPI WD-repeat domain phosphoinositide-interacting proteinPI3KC3-C1Caenorhabditis elegansCaenorhabditis elegans ProteinsmTORC1Molecular BiologyMechanistic target of rapamycinUSP11 ubiquitin-specific protease 11proteostasisAmyloid beta-PeptidesS6K S6 kinasebiologyPhosphatidylinositol 3-phosphateAutophagyDUB deubiquitinaseLFQ label-free quantificationIP immunoprecipitationNHT nonhuman targetingPI3KC3-C1 class III phosphatidylinositol 3-kinase complex ICell BiologyACN acetonitrileAβ amyloid-βNRBF2 nuclear receptor-binding factor 2Peptide FragmentsCell biologydeubiquitinase (DUB)ProteostasischemistryProteotoxicitymTORC1 mechanistic target of rapamycin complex 1biology.proteinAutophagy-Related Protein-1 HomologBSA bovine serum albuminThiolester HydrolasesResearch ArticleJournal of Biological Chemistry
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Translation of HTT mRNA with expanded CAG repeats is regulated by the MID1-PP2A protein complex.

2012

Expansion of CAG repeats is a common feature of various neurodegenerative disorders, including Huntington's disease. Here we show that expanded CAG repeats bind to a translation regulatory protein complex containing MID1, protein phosphatase 2A and 40S ribosomal S6 kinase. Binding of the MID1-protein phosphatase 2A protein complex increases with CAG repeat size and stimulates translation of the CAG repeat expansion containing messenger RNA in a MID1-, protein phosphatase 2A- and mammalian target of rapamycin-dependent manner. Our data indicate that pathological CAG repeat expansions upregulate protein translation leading to an overproduction of aberrant protein and suggest that the MID1-com…

metabolism [Microtubule Proteins]General Physics and AstronomyHTT protein humanRibosomal s6 kinaseMice0302 clinical medicinemetabolism [Transcription Factors]Protein Phosphatase 2Luciferasesgenetics [Nerve Tissue Proteins]genetics [Protein Biosynthesis]0303 health sciencesHuntingtin ProteinMultidisciplinarybiologyTOR Serine-Threonine KinasesNuclear ProteinsTranslation (biology)3. Good healthmetabolism [Luciferases]Microtubule Proteinsddc:500metabolism [Nuclear Proteins]genetics [Trinucleotide Repeat Expansion]Protein Bindingcongenital hereditary and neonatal diseases and abnormalitiesMTOR protein humanUbiquitin-Protein LigasesBlotting WesternNerve Tissue Proteinsmetabolism [TOR Serine-Threonine Kinases]metabolism [RNA Messenger]General Biochemistry Genetics and Molecular Biology03 medical and health sciencesgenetics [RNA Messenger]mental disordersHuntingtin ProteinAnimalsHumansEukaryotic Small Ribosomal SubunitRNA MessengerNucleotide Motifs030304 developmental biologyMessenger RNAmetabolism [Nerve Tissue Proteins]RNAmetabolism [Protein Phosphatase 2]General ChemistryProtein phosphatase 2Molecular biologynervous system diseasesProtein Biosynthesisbiology.proteinTrinucleotide repeat expansionTrinucleotide Repeat Expansion030217 neurology & neurosurgeryMid1 protein humanHeLa CellsTranscription FactorsNature communications
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