Search results for "S6K"

showing 4 items of 4 documents

The Intracellular Cleavage Product of the NG2 Proteoglycan Modulates Translation and Cell-Cycle Kinetics via Effects on mTORC1/FMRP Signaling

2018

The NG2 proteoglycan is expressed by oligodendrocyte precursor cells (OPCs) and is abundantly expressed by tumors such as melanoma and glioblastoma. Functions of NG2 include an influence on proliferation, migration and neuromodulation. Similar to other type-1 membrane proteins, NG2 undergoes proteolysis, generating a large ectodomain, a C-terminal fragment (CTF) and an intracellular domain (ICD) via sequential action of α- and γ-secretases which is enhanced by neuronal activity. Functional roles of NG2 have so far been shown for the full-length protein, the released ectodomain and CTF, but not for the ICD. In this study, we characterized the role of the NG2 ICD in OPC and Human Embryonic Ki…

0301 basic medicinePopulationP70-S6 Kinase 1mTORC1γ-secretaselcsh:RC321-57103 medical and health sciencesCellular and Molecular NeuroscienceNG2educationlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryPI3K/AKT/mTOR pathwayOriginal Researcheducation.field_of_studyChemistryICDHEK 293 cellsTranslation (biology)S6K1Cell biologystomatognathic diseases030104 developmental biologyEctodomainnervous systemeEF2mTORPhosphorylationFMRPOPCNeuroscienceFrontiers in Cellular Neuroscience
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Intronic L1 insertion and F268S, novel mutations in RPS6KA3 (RSK2) causing Coffin-Lowry syndrome

2003

Two novel mutations of the ribosomal S6 kinase 2 gene (also known as RSK2) have been identified in two unrelated patients with Coffin–Lowry syndrome. The first mutation consists of a de novo insertion of a 5′-truncated LINE-1 element at position −8 of intron 3, which leads to a skipping of exon 4, leading to a shift of the reading frame and a premature stop codon. The L1 fragment (2800 bp) showed a rearrangement with a small deletion, a partial inversion of the ORF 2, flanked by short direct repeats which duplicate the acceptor splice site. However, cDNA analysis of the patient shows that both sites are apparently not functional. The second family showed the nucleotide change 803T>C in exon…

GeneticsCoffin–Lowry syndromeMutationSplice site mutationIntronMonozygotic twinBiologymedicine.diseasemedicine.disease_causeExonRPS6KA3GeneticsmedicineDirect repeatGenetics (clinical)Clinical Genetics
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Growth hormone replacement therapy prevents sarcopenia by a dual mechanism: improvement of protein balance and of antioxidant defenses.

2013

The aim of our study was to elucidate the role of growth hormone (GH) replacement therapy in three of the main mechanisms involved in sarcopenia: alterations in mitochondrial biogenesis, increase in oxidative stress, and alterations in protein balance. We used young and old Wistar rats that received either placebo or low doses of GH to reach normal insulin-like growth factor-1 values observed in the young group. We found an increase in lean body mass and plasma and hepatic insulin-like growth factor-1 levels in the old animals treated with GH. We also found a lowering of age-associated oxidative damage and an induction of antioxidant enzymes in the skeletal muscle of the treated animals. GH…

Malemedicine.medical_specialtyAgingSarcopeniaIGF-1. Mitochondrial biogenesis Myostatin p70S6KHormone Replacement TherapyMyostatinProtein degradationmedicine.disease_causeAntioxidantsInternal medicineMedicineAnimalsRats WistarMuscle Skeletalbiologybusiness.industryProtein turnoverSkeletal muscleProteinsmedicine.diseaseMitochondria MuscleRatsSomatropinEndocrinologymedicine.anatomical_structureMitochondrial biogenesisSarcopeniaGrowth Hormonebiology.proteinBody CompositionGeriatrics and GerontologybusinessOxidative stressThe journals of gerontology. Series A, Biological sciences and medical sciences
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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 acetonitrile 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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