Search results for "Ubiquitin"

showing 10 items of 191 documents

Ubiquitin conjugating enzyme E2-N and sequestosome-1 (p62) are components of the ubiquitination process mediated by the malin-laforin E3-ubiquitin li…

2015

11 páginas, 9 figuras.

Ubiquitin-Protein LigasesUbiquitin-conjugating enzymeBiochemistryLafora diseaseSequestosome 1UbiquitinE2-conjugaseLaforinPhagosomesSequestosome-1 ProteinmedicineAutophagyLC3HumanseducationE3-ubiquitin ligaseAdaptor Proteins Signal Transducingchemistry.chemical_classificationDNA ligaseeducation.field_of_studybiologyUbiquitinationAutophagosomesCell Biologymedicine.diseaseProtein Tyrosine Phosphatases Non-ReceptorMalinUbiquitin ligaseCell biologyp62 (SQSTM1)UBE2NHEK293 CellschemistryBiochemistryGene Knockdown TechniquesUbiquitin-Conjugating Enzymesbiology.proteinCarrier ProteinsLaforinUbiquitin-Conjugating Enzyme E2 NProtein Binding
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dsRNA induces apoptosis through an atypical death complex associating TLR3 to caspase-8

2012

Toll-like receptor 3 (TLR3) is a pattern-recognition receptor known to initiate an innate immune response when stimulated by double-stranded RNA (dsRNA). Components of TLR3 signaling, including TIR domain-containing adapter inducing IFN-α (TRIF), have been demonstrated to contribute to dsRNA-induced cell death through caspase-8 and receptor interacting protein (RIP)1 in various human cancer cells. We provide here a detailed analysis of the caspase-8 activating machinery triggered in response to Poly(I:C) dsRNA. Engagement of TLR3 by dsRNA in both type I and type II lung cancer cells induces the formation of an atypical caspase-8-containing complex that is devoid of classical death receptors…

Ubiquitin-Protein LigasesvirusesApoptosischemical and pharmacologic phenomenaInhibitor of Apoptosis ProteinsCell Line TumorHumansFADDMolecular BiologyRNA Double-StrandedDeath domainCaspase 8Original PaperbiologyUbiquitinationRNA-Binding Proteinshemic and immune systemsMDA5Cell BiologyTNF Receptor-Associated Factor 2Fas receptorTRADDBaculoviral IAP Repeat-Containing 3 ProteinTNF Receptor-Associated Death Domain ProteinToll-Like Receptor 3Cell biologyNuclear Pore Complex ProteinsUbiquitin ligase complexDeath-inducing signaling complexTLR3biology.proteinSignal TransductionCell Death & Differentiation
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Depletion ofL-arginine induces autophagy as a cytoprotective response to endoplasmic reticulum stress in human T lymphocytes

2012

PMCID: PMC3494587

X-Box Binding Protein 1Proteasome Endopeptidase ComplexProgrammed cell deathXBP1CD3 ComplexMAP Kinase Signaling SystemRNA SplicingT-LymphocytesT cellDown-RegulationApoptosisRegulatory Factor X Transcription FactorsUbiquitin-Activating EnzymesProtein Serine-Threonine KinasesBiologyArginineLymphocyte ActivationAutophagy-Related Protein 7Jurkat cellsJurkat CellsEndoribonucleasesAutophagymedicineHumansMolecular BiologyCell ProliferationTOR Serine-Threonine KinasesAutophagyMembrane ProteinsCell BiologyBECN1Endoplasmic Reticulum StressG1 Phase Cell Cycle CheckpointsBasic Research Paper3. Good healthCell biologyDNA-Binding Proteinsmedicine.anatomical_structureCytoprotectionApoptosisUnfolded protein responseBeclin-1MitogensApoptosis Regulatory ProteinsLysosomesProto-Oncogene Proteins c-aktTranscription FactorsAutophagy
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Analysis of E2F1 by clAP1

2017

The cellular inhibitor of Apoptosis 1 (cIAP1) behaves as an E3 ubiquitin ligase and has oncogenic properties. Previously, our team has shown that cIAP1 can regulate the E2F1 transcription factor activity. My research project has been focused on deepening our current knowledge on this interaction. Firstly, we characterized the E2F1-cIAP1 interaction, then we analyzed the regulation of E2F1 by cIAP1 and finally assessed the importance of the cIAP1-E2F1 interaction for the oncogenic properties of cIAP1. I have demonstrated a interaction of E2F1 with the hydrophobic pocket of the BIR3 domain of cIAP1. Moreover, I highlighted that the alpha 1 helix of the BIR3 domain is mandatory for the stabili…

[SDV.SA] Life Sciences [q-bio]/Agricultural sciences[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyCIAP1E2F1UbiquitinylationIAP-Binding-MotifIBM
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Rôle des protéines de choc thermique dans la régulation du facteur de transcription HIF

2011

Both HIF1α and HIF2α proteins are highly involved in the development of pathologies, such as cancers, which are prime public health issues. These proteins are primarily controlled at the protein level by ubiquitin-dependant degradation, and regulate numerous cellular processes which are likely to favor the development of these diseases. A recent issue in therapeutic research is to identify partners that might regulate the expression and the activity of the HIFα proteins, with the aim to elaborate targeted therapies. Heat shock proteins (HSPs) form a family of proteins whose main function is to regulate protein homeostasis in cells, which they achieve through interaction with the ubiquitin-p…

[SDV.SA]Life Sciences [q-bio]/Agricultural sciences[SDV.SA] Life Sciences [q-bio]/Agricultural sciences[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyUbiquitinProtéine clienteDégradation protéasomaleHSP27UbiquitineClient proteinProteasomal degradation[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyHSP90Inhibiteurs d’HSP90HIF2α[ SDV.SA ] Life Sciences [q-bio]/Agricultural sciences[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyHSP90 inhibitors
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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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Excitotoxicity in AD is partially caused by the inactivation of APC/C-Cdh1 E3 Ubiquitin Ligase

2013

biologyChemistryPhysiology (medical)biology.proteinExcitotoxicitymedicinemedicine.disease_causeBiochemistryCell biologyCDH1Ubiquitin ligaseFree Radical Biology and Medicine
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Oxidative Stress And Ubiquitin Ligases: Their Involvement In Alzheimer’s Disease Pathophysiology

2015

Oxidative stress is a major hallmark in Alzheimer’s Disease. We showed that amyloid beta (Aβ 1-42 ), induces mitochondrial oxidative stress. We focused on dysregulations of ubiquitin ligases in Alzheimer’s and their relation to oxidative stress. The anaphase-promoting complex/cyclosome (APC/C)-Cdh1 ubiquitin ligase has a role as cell cycle regulator in proliferating cells and, recently another role in the regulation the degradation of key glycolytic enzyme 6-phosphofructo-2-kinase/fructose-2, 6-bisphosphatase-3 has been found (Almeida et al., 2012). Herrero-Mendez et al. observed in 2009 that inhibition of Cdh1 leads to an upregulation of Pfkfb3 in neurons and that this results in the activ…

biologyGlutaminaseAmyloid betaGlutamate receptorExcitotoxicityPentose phosphate pathwaymedicine.disease_causeBiochemistryUbiquitin ligaseCell biologyBiochemistryUbiquitinPhysiology (medical)biology.proteinmedicineOxidative stressFree Radical Biology and Medicine
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The ATXN1 and TRIM31 genes are related to intelligence in an ADHD background: evidence from a large collaborative study totaling 4,963 subjects

2010

Contains fulltext : 96400.pdf (Publisher’s version ) (Closed access) Intelligence is a highly heritable trait for which it has proven difficult to identify the actual genes. In the past decade, five whole-genome linkage scans have suggested genomic regions important to human intelligence; however, so far none of the responsible genes or variants in those regions have been identified. Apart from these regions, a handful of candidate genes have been identified, although most of these are in need of replication. The recent growth in publicly available data sets that contain both whole genome association data and a wealth of phenotypic data, serves as an excellent resource for fine mapping and …

cognitionCandidate genegenetic associationUbiquitin-Protein LigasesEuropean Continental Ancestry GroupIntelligencePopulationMedizinNerve Tissue ProteinsSingle-nucleotide polymorphismGenomic disorders and inherited multi-system disorders Functional Neurogenomics [IGMD 3]Quantitative trait locusBiologyPolymorphism Single NucleotideGenomeWhite PeopleNuclear FamilyGenomic disorders and inherited multi-system disorders [IGMD 3]Tripartite Motif ProteinsCohort Studies03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineMeta-Analysis as TopicADHDHumansddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und JugendalterseducationAtaxin-1Genetics (clinical)030304 developmental biologyGenetic associationGeneticsMental Health [NCEBP 9]0303 health scienceseducation.field_of_studyIntelligence quotientHuman intelligenceNuclear ProteinsALSPACPsychiatry and Mental healthPhenotypeAtaxinsAttention Deficit Disorder with Hyperactivitycandidate genesFunctional Neurogenomics [DCN 2]030217 neurology & neurosurgeryResearch Article
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Aging of the musculoskeletal system: How the loss of estrogen impacts muscle strength.

2019

Skeletal muscle weakness occurs with aging and in females this is compounded by the loss of estrogen with ovarian failure. Estrogen deficiency mediates decrements in muscle strength from both inadequate preservation of skeletal muscle mass and decrements in the quality of the remaining skeletal muscle. Processes and components of skeletal muscle that are affected by estrogens are beginning to be identified. This review focuses on mechanisms that contribute to the loss of muscle force generation when estrogen is low in females, and conversely the maintenance of strength by estrogen. Evidence is accumulating that estrogen deficiency induces apoptosis in skeletal muscle contributing to loss of…

estrogeenit0301 basic medicinemedicine.medical_specialtyAgingProteasome Endopeptidase ComplexHistologyPhysiologymedicine.drug_classEndocrinology Diabetes and Metabolism030209 endocrinology & metabolismApoptosisArticle03 medical and health sciences0302 clinical medicineInternal medicineestrogenmedicineHumansMuscle Strengthskeletal muscleta315Muscle SkeletalMuscle forcebusiness.industryagingOvarian failureUbiquitinationSkeletal muscleta3141Estrogensmedicine.diseaseGenerating capacityikääntyminen030104 developmental biologymedicine.anatomical_structureEndocrinologyEstrogenSarcopeniaMuscle strengthEstrogenic EffectsFemalestrengthbusinesshormones hormone substitutes and hormone antagonistslihasvoimaBone
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