Search results for "N 1"

showing 10 items of 1053 documents

« Un Autrichien à Paris en 1900 : Les visions plurielles de Rudolf Kassner »

2021

International audience

[SHS.LITT] Humanities and Social Sciences/LiteratureRudolf KassnerWien 1900Imagologie Frankreich ÖsterreichImagologie France Autriche[SHS.LITT]Humanities and Social Sciences/LiteratureVienne 1900ComputingMilieux_MISCELLANEOUS
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Folie et présence de l’origine dans la littérature romantique

2011

International audience; Emmanuel Kant, dans son « Esthétique transcendantale », affirme que le temps est à la fois subjectif et universel. Le temps n'est pas une donnée du monde objectif, mais il est néanmoins universellement nécessaire à la représentation humaine du monde. Les auteurs romantiques, en mettant en scène des fous, s'accordent sur le premier point, mais récusent le second. Les héros de Princesse Brambilla de E. T. A. Hoffmann, de La Félicité de la Folie de Nicolas Polévoï et d'Aurélia de Gérard de Nerval vivent dans un rapport au temps qui leur est propre. Cyclique et non linéaire, il conduit à superposer plusieurs temporalités, qui nient ainsi le principe de succession. Ce rap…

[SHS.LITT] Humanities and Social Sciences/Literature[SHS.LITT]Humanities and Social Sciences/LiteratureErnst Theodor Amadeus Hoffmann 1776-1822Littérature comparéeFolie dans la littérature
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Der Deutsche Gewerkschaftsbund und der Schuman-Plan (1949-1951)

1998

ammattiyhdistysliikeSchumanin suunnitelmaDGBMitbestimmungAdenauerin 1. hallitusSaksan liittotasavaltaRuhrin alue
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Distinct 5' SCL enhancers direct transcription to developing brain, spinal cord, and endothelium: neural expression is mediated by GATA factor bindin…

1999

The SCL gene encodes a basic helix-loop-helix transcription factor with a pivotal role in the development of endothelium and of all hematopoietic lineages. SCL is also expressed in the central nervous system, although its expression pattern has not been examined in detail and its function in neural development is unknown. In this article we present the first analysis of SCL transcriptional regulation in vivo. We have identified three spatially distinct regulatory modules, each of which was both necessary and sufficient to direct reporter gene expression in vivo to three different regions within the normal SCL expression domain, namely, developing endothelium, midbrain, and hindbrain/spinal …

animal structuresEmbryo NonmammalianTranscription GeneticHindbrainMice TransgenicChick EmbryoBiologybehavioral disciplines and activities03 medical and health sciencesMice0302 clinical medicineTranscription (biology)Genes Reporterhemic and lymphatic diseasesProto-Oncogene ProteinsBasic Helix-Loop-Helix Transcription FactorsAnimalsTissue DistributionEndotheliumEnhancerMolecular BiologyTranscription factorGeneIn Situ HybridizationT-Cell Acute Lymphocytic Leukemia Protein 1Zebrafish030304 developmental biologyRegulation of gene expressionGenetics0303 health sciencesReporter geneModels GeneticfungiBrainCell BiologyZebrafish ProteinsEmbryo MammalianCell biologyDNA-Binding ProteinsLac OperonSpinal CordNeural development030217 neurology & neurosurgeryDevelopmental BiologyTranscription FactorsDevelopmental biology
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Procollagen C-proteinase Enhancer Stimulates Procollagen Processing by Binding to the C-propeptide Region Only*

2011

Background: Procollagen C-proteinase enhancer-1 (PCPE-1) is an extracellular glycoprotein that increases activity of certain zinc metalloproteinases involved in tissue development and repair. Results: PCPE-1 binds uniquely to the C-propeptide region of the procollagen molecule. Conclusion: PCPE-1 enhances proteolysis by binding solely to the procollagen C-propeptides. Significance: These data may lead to future applications in the development of antifibrotic therapies.

animal structuresGlycosylationBiologyBiochemistryBone morphogenetic protein 1Protein Structure SecondaryBone Morphogenetic Protein 103 medical and health scienceschemistry.chemical_compoundMetalloprotease0302 clinical medicineHumansBinding siteEnhancerMolecular Biology030304 developmental biologyCell Line TransformedGlycoproteinschemistry.chemical_classification0303 health sciencesMetalloproteinaseExtracellular Matrix ProteinsBinding Sitesintegumentary systemCell BiologyEnzymatic ProcessingFibrosisExtracellular MatrixProcollagen peptidaseCollagen Type IIIchemistryBiochemistry030220 oncology & carcinogenesisembryonic structuresEnzymologyCollagenGlycoproteinProtein Processing Post-TranslationalTriple helixThe Journal of Biological Chemistry
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Smad7 controls resistance of colitogenic T cells to regulatory T cell-mediated suppression.

2008

Background & Aims Foxp3-expressing regulatory T cells (Tregs) play a key role in the maintenance of the gut immune homeostasis, and an intact transforming growth factor (TGF)-β signaling is required for their function. In inflammatory bowel disease (IBD), the TGF-β signaling is impaired because of high expression of the inhibitory molecule Smad7. Although no intrinsic defects in Tregs function have been shown in IBD, it is still unknown whether colitogenic T cells are susceptible to Treg-mediated suppression. In this study, we have investigated whether IBD mucosal CD4+ T cells are resistant to Tregs and whether Smad7 is involved in this process. Methods IBD lamina propria mononuclear cells …

antisense oligonucleotideCD4-Positive T-LymphocytesAdoptive cell transferT-Lymphocytesanimal cellCell CommunicationInbred C57BLT-Lymphocytes RegulatoryTransgenicMiceregulatory T lymphocyteCrohn DiseaseTransforming Growth Factor betamononuclear cellRAG1 proteinIntestinal MucosaenteritisCells CulturedMice KnockoutSettore MED/12 - GastroenterologiaCulturedintegumentary systemmedicine.diagnostic_testarticleGastroenterologyInterleukinhemic and immune systemsT helper cellColitisRegulatoryUp-Regulationmedicine.anatomical_structurepriority journalgamma interferonSignal TransductionRegulatory T cellColonCellsKnockoutanimal experimentinterleukin 6chemical and pharmacologic phenomenaMice TransgenicBiologyinterleukin 2Recombination-activating geneFlow cytometryProinflammatory cytokineSmad7 ProteinmedicineAnimalsHumanscontrolled studyhumanlamina propriamouseCell ProliferationHomeodomain ProteinsCD4+ T lymphocytenonhumanHepatologyAnimalflow cytometryhuman cellanimal cell culturetransgenic mouseMice Inbred C57BLDisease Models Animalantisense oligonucleotide; gamma interferon; interleukin 17; interleukin 2; interleukin 6; RAG1 protein; Smad7 protein; animal cell; animal cell culture; animal experiment; article; CD4+ T lymphocyte; cell proliferation; colitis; controlled study; enteritis; flow cytometry; human; human cell; knockout mouse; lamina propria; mononuclear cell; mouse; nonhuman; priority journal; regulatory T lymphocyte; transgenic mouse; Animals; CD4-Positive T-Lymphocytes; Cell Communication; Cell Proliferation; Cells Cultured; Colitis; Colon; Crohn Disease; Disease Models Animal; Homeodomain Proteins; Humans; Intestinal Mucosa; Mice; Mice Inbred C57BL; Mice Knockout; Mice Transgenic; Signal Transduction; Smad7 Protein; T-Lymphocytes Regulatory; Transforming Growth Factor beta; Up-RegulationDisease ModelsImmunologyinterleukin 17knockout mouseTransforming growth factorGastroenterology
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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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Novel Insights into the Cellular Localization and Regulation of the Autophagosomal Proteins LC3A, LC3B and LC3C

2020

Macroautophagy is a conserved degradative process for maintaining cellular homeostasis and plays a key role in aging and various human disorders. The microtubule-associated protein 1A/1B light chain 3B (MAP1LC3B or LC3B) is commonly analyzed as a key marker for autophagosomes and as a proxy for autophagic flux. Three paralogues of the LC3 gene exist in humans: LC3A, LC3B and LC3C. The molecular function, regulation and cellular localization of LC3A and LC3C have not been investigated frequently, even if a similar function to that described for LC3B appears likely. Here, we have selectively decapacitated LC3B by three separate strategies in primary human fibroblasts and analyzed the evoked e…

autophagysequestosome 1 (p62)LC3CATG8GABARAPGABARAPCellular homeostasisProtein lipidationsirtuin 1ArticleCell LineAntibody SpecificityHumansSirtuinsAmino Acid SequenceLC3BRNA Small InterferingLC3Alcsh:QH301-705.5PhylogenyCellular localizationCell NucleusBinding SitesbiologyChemistrySirtuin 1AutophagosomesAutophagy-Related Protein 8 FamilyGeneral MedicineFibroblastsLipidsCell biologyProtein Transportlcsh:Biology (General)Gene Knockdown TechniquesSirtuinbiology.proteinApoptosis Regulatory ProteinsMicrotubule-Associated ProteinsATG8MAP1LC3BSubcellular FractionsCells
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Vecchi e nuovi problemi in tema di intervento dei creditori nell’esecuzione (note a margine di Cass. S.U. n. 61 del 7 gennaio 2014)

2015

Nel contributo in oggetto l'autore, muovendo dalla decisione delle Sezioni Unite della Cassazione n. 61 del 7 gennaio 2014, coglie l'occasione per riesaminare le vecchie e nuove problematiche sottese all’intervento dei creditori nel processo esecutivo. Il primo tema affrontato è quello della par condicio creditorum, che viene esaminata nella sua storia evolutiva dal Code Napoleon, al suo periodo di massima estensione, dato dal codice del 1940, fino al suo ridimensionamento a seguito delle riforme del 2005. Esamina quindi la possibilità del possibile superamento quoad effectum della distinzione tra intervento di creditori con titolo e senza titolo, alla luce delle evoluzioni della giurisprud…

b) the same par condicio creditorum principle and the consequent possibility of intervention of third party in the execution. It concludes however that a revolution like the aforesaid explained would be only apparently advantageouOld and new problems related to the intervention of creditors in the expropriation (marginal notes at Cass. Sez. Un. January 7 2014 n. 61) Moving from the decision of the Sezioni Unite n. 61/2014 the author takes the opportunity to re-examine old and new problems related to the intervention of creditors in the forceable execution. The first major theme concerns par condicio creditorum which is examined in its evolutionary history since the Code Napoleon through its period of maximum extension (the Code of 1940) until its reduction as a result of the reforms of 2005. The author examines the possibility to overcome quoad effectum the distinction between sine titulo et cum titulo interveners in light of jurisprudence’s evolution between 1978 2009 and 2014. The possibility in particular concerns those creditors sine titulo the where credit has not been contested (ex art. 499 c.p.c.) by the debtor seek payment and partecipate to distribution. In the last section the author examines the possibilities for other creditors to contest the intervention of the creditor sine titulo ex art. 499 c.p.c. (utendo iuribus in subrogation in case of inaction of the debtor) or in the distribution phase ex art. 512 c.p.c. He concludes that the only person that will be really damaged if he doesn’t contest - ex art. 499 c.p.c. - the credit it is precisely the debtor. He also notes that in the legislation of the last decade the apparent effort to reduce the numbers of judicial enquiry incidental to forceable execution will never be achieved unless it’s eliminated in radice: a) the existence in our system of extrajudicial enforcement titulaSettore IUS/15 - Diritto Processuale Civilesince it would lead to increase autonomous expropriations (one for each creditor who can today intervene) and to increment judicial enquiries in order to form enforceable judgments
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The effects of α-secretase ADAM10 on the proteolysis of neuregulin-1

2009

Although ADAM10 is a major alpha-secretase involved in non-amyloidogenic processing of the amyloid precursor protein, several additional substrates have been identified, most of them in vitro. Thus, therapeutical approaches for the prevention of Alzheimer's disease by upregulation of this metalloproteinase may have severe side effects. In the present study, we examined whether the ErbB receptor ligand neuregulin-1, which is essential for myelination and other important neuronal functions, is cleaved by ADAM10. Studies with beta- and gamma-secretase inhibitors, as well as with the metalloproteinase inhibitor GM6001, revealed an inhibition of neuregulin-1 processing in human astroglioma cell …

biologyADAM10Cell BiologySheddaseBiochemistryDownregulation and upregulationErbBIn vivoAmyloid precursor proteinbiology.proteinCancer researchAstrogliomaNeuregulin 1Molecular BiologyFEBS Journal
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