Search results for " ACTIVATION"

showing 10 items of 1535 documents

No effect of C-reactive protein on early atherosclerosis in LDLR-/- / human C-reactive protein transgenic mice

2008

summaryThe association between increased concentrations of C-reactive protein (CRP) and future cardiovascular events is well established. However, it is currently unclear whether this clinical observation represents an epiphenomenon or whether the pentraxin may actively promote the development of atherosclerosis. Experimental studies with knockout mice with a defect in apolipoprotein E (ApoE-/-) have been used to investigate the role of CRP in atherogenesis, but the results obtained have been contradictory so far. Since knockout mice with a defect in low density lipoprotein receptor (LDLR-/-) may represent a better model of atherogenesis compared to ApoE-/- animals, we undertook experiments…

Genetically modified mouseApolipoprotein ETime FactorsGenotypeLipoproteinsTransgeneMice TransgenicBiologyLesionMicemedicineAnimalsHumansComplement ActivationAortaCrosses GeneticMice KnockoutC-reactive proteinAcute-phase proteinHematologyAtherosclerosisDietary FatsLipidsDisease Models AnimalC-Reactive ProteinPhenotypeReceptors LDLImmunologyLDL receptorKnockout mousebiology.proteinlipids (amino acids peptides and proteins)medicine.symptomThrombosis and Haemostasis
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A disintegrin-metalloproteinase prevents amyloid plaque formation and hippocampal defects in an Alzheimer disease mouse model

2004

Alzheimer disease (AD) is characterized by excessive deposition of amyloid beta-peptides (A beta peptides) in the brain. In the nonamyloidogenic pathway, the amyloid precursor protein (APP) is cleaved by the alpha-secretase within the A beta peptide sequence. Proteinases of the ADAM family (adisintegrin and metalloproteinase) are the main candidates as physiologically relevant alpha-secretases, but early lethality of knockout animals prevented a detailed analysis in neuronal cells. To overcome this restriction, we have generated transgenic mice that overexpress either ADAM10 or a catalytically inactive ADAM10 mutant. In this report we show that a moderate neuronal overexpression of ADAM10 i…

Genetically modified mousePathologymedicine.medical_specialtyAmyloidAmyloidADAM10BACE1-ASGene ExpressionMice TransgenicHippocampusArticleAmyloid beta-Protein PrecursorMiceAlzheimer DiseaseEndopeptidasesAmyloid precursor proteinmedicineAnimalsAspartic Acid EndopeptidasesHumansbiologybusiness.industryP3 peptideAmyloidosisGeneral Medicinemedicine.diseaseCell biologyEnzyme ActivationDisease Models AnimalCommentarybiology.proteinErratumAlzheimer's diseaseAmyloid Precursor Protein SecretasesbusinessAmyloid precursor protein secretaseJournal of Clinical Investigation
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C1q acts in the tumour microenvironment as a cancer-promoting factor independently of complement activation

2015

Complement C1q is the activator of the classical pathway. However, it is now recognized that C1q can exert functions unrelated to complement activation. Here we show that C1q, but not C4, is expressed in the stroma and vascular endothelium of several human malignant tumours. Compared with wild-type (WT) or C3- or C5-deficient mice, C1q-deficient (C1qa−/−) mice bearing a syngeneic B16 melanoma exhibit a slower tumour growth and prolonged survival. This effect is not attributable to differences in the tumour-infiltrating immune cells. Tumours developing in WT mice display early deposition of C1q, higher vascular density and an increase in the number of lung metastases compared with C1qa−/− mi…

Genetics and Molecular Biology (all)0301 basic medicinePROTEINGeneral Physics and AstronomyMELANOMAApoptosisInbred C57BLBiochemistryDISEASEAnimals; Apoptosis; Cell Line Tumor; Cell Movement; Cell Proliferation; Complement Activation; Complement C1q; Complement C3; Complement C5; Humans; Mice; Mice Inbred C57BL; Mice Knockout; Neoplasms; Biochemistry Genetics and Molecular Biology (all); Chemistry (all); Physics and Astronomy (all)Micefluids and secretionsCell Movementimmune system diseasesNeoplasmsIMMUNE-RESPONSEskin and connective tissue diseasesComplement ActivationComplement C1qMice KnockoutComplement component 5TumorMultidisciplinaryQChemistry (all)Complement C5Complement C33. Good healthCell biologyMultidisciplinary SciencesDEFICIENCYmedicine.anatomical_structureScience & Technology - Other TopicsHumanKnockoutSciencechemical and pharmacologic phenomenaBiologyArticleGeneral Biochemistry Genetics and Molecular BiologyTROPHOBLAST INVASIONMECHANISMSCell LinePhysics and Astronomy (all)03 medical and health sciencesClassical complement pathwayImmune systemINFLAMMATIONCell Line TumormedicineAnimalsHumansCell ProliferationScience & TechnologyBiochemistry Genetics and Molecular Biology (all)AnimalCell growthEFFECTOR SYSTEMComplement C1qApoptosiGeneral ChemistryComplement systemMice Inbred C57BL030104 developmental biologyCancer cellNeoplasmBone marrowANTIBODY THERAPYNature Communications
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Drp1 Controls Effective T Cell Immune-Surveillance by Regulating T Cell Migration, Proliferation, and cMyc-Dependent Metabolic Reprogramming

2018

Summary Mitochondria are key players in the regulation of T cell biology by dynamically responding to cell needs, but how these dynamics integrate in T cells is still poorly understood. We show here that the mitochondrial pro-fission protein Drp1 fosters migration and expansion of developing thymocytes both in vitro and in vivo. In addition, we find that Drp1 sustains in vitro clonal expansion and cMyc-dependent metabolic reprogramming upon activation, also regulating effector T cell numbers in vivo. Migration and extravasation defects are also exhibited in Drp1-deficient mature T cells, unveiling its crucial role in controlling both T cell recirculation in secondary lymphoid organs and acc…

Genetics and Molecular Biology (all)0301 basic medicinecell migrationT-LymphocytesCellCell CountMitochondrionLymphocyte ActivationBiochemistryCell MovementHomeostasismetabolic reprogrammingcell migration; cell proliferation; cMyc; Drp1; exhaustion; metabolic reprogramming; mitochondrial dynamics; T cells; thymocytes; tumor immune-surveillance; Biochemistry Genetics and Molecular Biology (all)lcsh:QH301-705.5cMycImmunologic SurveillanceMice KnockoutThymocytesEffectorDrp1; T cells; cMyc; cell migration; cell proliferation; exhaustion; metabolic reprogramming; mitochondrial dynamics; thymocytes; tumor immune-surveillanceCell migrationCell DifferentiationCell biologymedicine.anatomical_structurePhenotypeDynaminsendocrine systemSettore BIO/06Cell SurvivalLymphoid TissueMAP Kinase Signaling SystemT cellT cellsReceptors Antigen T-CellDrp1BiologyGeneral Biochemistry Genetics and Molecular BiologyArticleProto-Oncogene Proteins c-myc03 medical and health sciencestumor immune-surveillancemitochondrial dynamicexhaustionHomeostasimedicineAnimalsCell ProliferationTumor microenvironmentBiochemistry Genetics and Molecular Biology (all)Cell growthAnimalT cellthymocytemitochondrial dynamicsDynamin030104 developmental biologylcsh:Biology (General)T-LymphocyteT cell migration
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Interventions to Slow Aging in Humans: Are We Ready?

2015

The workshop entitled 'Interventions to Slow Aging in Humans: Are We Ready?' was held in Erice, Italy, on October 8-13, 2013, to bring together leading experts in the biology and genetics of aging and obtain a consensus related to the discovery and development of safe interventions to slow aging and increase healthy lifespan in humans. There was consensus that there is sufficient evidence that aging interventions will delay and prevent disease onset for many chronic conditions of adult and old age. Essential pathways have been identified, and behavioral, dietary, and pharmacologic approaches have emerged. Although many gene targets and drugs were discussed and there was not complete consens…

GerontologyAgingDisease onsetPrescription DrugsLongevityPsychological interventionReviewsBiologyAMP-Activated Protein KinasesGrowth hormoneAging; Anti-aging; Centenarians; Dietary restriction; Lifespan studies; Longevity gene; Longevity regulation; Cell Biology; AgingDietary interventionsBiological FactorsMicelongevity geneSettore BIO/13 - Biologia ApplicataAnimalsHumansSirtuinsProtein restrictionCentenarianInsulin-Like Growth Factor ILifespan studieCaloric RestrictionSettore MED/04 - Patologia GeneraleGeroscienceGene targetsRibosomal Protein S6 KinasesTOR Serine-Threonine Kinasesanti-agingdietary restrictionCell Biologydietary restriction ; lifespan studies ; longevity gene ; centenarians ; anti-aging ; longevity regulation ; aginglongevity regulation3. Good healthDietEnzyme ActivationGene Expression RegulationGrowth HormoneGenetics of agingcentenariansaging; anti-aging; centenarians; dietary restriction; lifespan studies; longevity gene; longevity regulationSignal Transductionlifespan studies
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Gpibα Engagement Induces Activation of Human Platelet TF and Association with Constitutively Platelet Surface-Bound FVIIa

2019

The membranes of activated platelets assemble clotting protein complexes and enzymatic reactions needed for hemostasis and causing pathological thrombosis. Several reports have shown that human platelets contain TF, but controversies remain on the functional contributions of platelet TF to coagulation initiation. Here, we delineate the mechanism that converts platelet-associated TF to a procoagulant molecule. By combining specific inhibitors with human platelets from normal probands or patients with Glanzmann thrombasthenia or homozygous GPVI deficiency, we analyzed the procoagulant activation of platelet TF by biochemical methods, confocal microscopy, platelet adhesion under flow on VWF an…

Glanzmann's thrombastheniaChemistryImmunologyCell BiologyHematologymedicine.diseaseBiochemistryCell biologychemistry.chemical_compoundTissue factor pathway inhibitorThrombinCoagulationmedicinePlateletPlatelet activationGPVIRistocetinmedicine.drugBlood
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IκB kinase-driven nuclear factor-κB activation in patients with asthma and chronic obstructive pulmonary disease.

2011

Background Nuclear factor-κB (NF-κB) is a transcriptional factor of different inflammatory patterns involved in asthma and chronic obstructive pulmonary disease (COPD) that is tightly controlled by IκB kinase (IKK) complex. Objective We investigated the dysregulation of IKK-driven NF-κB activation in patients with asthma and COPD. Methods We assessed IKKα and IKKβ expression and activation, their regulation by glucocorticosteroids, and their involvement in IL-8 synthesis in PBMCs isolated from asthmatic patients, healthy smokers (HSs), patients with COPD, and control subjects. PBMCs from control subjects were stimulated with TNF-α and cigarette smoke extract in the presence or absence of fl…

Glutathione-S-transferaseAdultMaleImmunologyInflammationIκB kinaseFluticasone propionateFEV1/FVC ratioPulmonary Disease Chronic ObstructiveImmunopathologymedicineImmunology and AllergyHumansInterleukin 8COPD CSE Fluticasone propionateIKK IκB kinaseGlucocorticoidsAsthmaHDACCOPDbusiness.industryInterleukin-8SmokingNF-kappa BMiddle Agedmedicine.diseaseAsthmaBronchodilator AgentsI-kappa B KinaseEnzyme ActivationGene Expression RegulationNF-κBImmunologyLeukocytes MononuclearFemalemedicine.symptombusinessmedicine.drugThe Journal of allergy and clinical immunology
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Amino acid activation in Ciona ovary and developing egg

1964

E stata studiata la attivazione di alcuni amini acidi negli ovociti nell'uovo vergine e nell'uovo fecondato diCiona intestinalis. L'andamento della attivazione della glicina e stato seguito sino alla neurulazione. Il quantitativo di amino acidi attivati e minimo nell'uovo vergine, esso aumenta rapidamente dopo la fecondazione. Durante la gastrulazione la attivazione della glicina raggiunge i valori maggiori.

GlycineOvaryIn Vitro TechniquesBiologyArginineCellular and Molecular NeuroscienceChordata NonvertebrateLeucinemedicineAnimalsHistidineMolecular BiologyOvumPharmacologyAmino acid activationAlanineOvaryCell Biologybiology.organism_classificationMolecular biologyCionamedicine.anatomical_structureBiochemistryProtein BiosynthesisTyrosineMolecular MedicineFemaleExperientia
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Role of the Netrin-like Domain of Procollagen C-Proteinase Enhancer-1 in the Control of Metalloproteinase Activity

2010

The netrin-like (NTR) domain is a feature of several extracellular proteins, most notably the N-terminal domain of tissue inhibitors of metalloproteinases (TIMPs), where it functions as a strong inhibitor of matrix metalloproteinases and some other members of the metzincin superfamily. The presence of a C-terminal NTR domain in procollagen C-proteinase enhancers (PCPEs), proteins that stimulate the activity of astacin-like tolloid proteinases, raises the possibility that this might also have inhibitory activity. Here we show that both long and short forms of the PCPE-1 NTR domain, the latter beginning at the N-terminal cysteine known to be critical for TIMP activity, show no inhibition, at …

Glycobiology and Extracellular MatricesMatrix metalloproteinaseBiochemistryBONE MORPHOGENETIC PROTEIN-1AdamalysinFIBRILLAR PROCOLLAGENSTolloid ProteinaseExtracellular Matrix Proteins0303 health sciencesADAMTSFRIZZLED-RELATED PROTEINS030302 biochemistry & molecular biologyTissue Inhibitor of Metalloproteinases11 Medical And Health SciencesALPHA-CONVERTING-ENZYMEI PROCOLLAGENADAM ProteinsExtracellular MatrixPLASMINOGEN ACTIVATIONBiochemistryCollagen03 Chemical SciencesLife Sciences & BiomedicineProcollagenBiochemistry & Molecular BiologyTERMINAL DOMAINTolloid-Like MetalloproteinasesADAMTSBiologyBone morphogenetic protein 1Cell Line03 medical and health sciencesDisintegrinHumansHUMAN TISSUE INHIBITORMatrix MetalloproteinaseMolecular BiologyGlycoproteins030304 developmental biologyThrombospondinScience & TechnologyHeparinADAMCell Biology06 Biological SciencesMATRIX-METALLOPROTEINASESProtein Structure TertiaryADAM ProteinsProcollagen peptidaseSULFATED GLYCOSAMINOGLYCANSEnzymologybiology.proteinJournal of Biological Chemistry
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Design, Synthesis and Biological Evaluation of 7-Chloro-9

2019

Glycogen synthase kinase-3β (GSK-3β) represents a relevant drug target for the treatment of neurodegenerative pathologies including Alzheimer’s disease. We herein report on the optimization of a novel class of GSK-3β inhibitors based on the tofacitinib-derived screen hit 3-((3R,4R)-3-((7-chloro-9H-pyrimido[4,5-b]indol-4-yl)(methyl)amino)-4-methylpiperidin-1-yl)-3-oxopropanenitrile (1). We synthesized a series of 19 novel 7-chloro-9H-pyrimido[4,5-b]indole-based derivatives and studied their structure–activity relationships with focus on the cyanoacetyl piperidine moiety. We unveiled the crucial role of the nitrile group and its importance for the activity of this compound series. A successfu…

Glycogen synthase kinase-3βBinding SitesGlycogen Synthase Kinase 3 betatofacitinibDose-Response Relationship DrugMolecular Structurekinase inhibitorMolecular Conformationprotein kinaseChemistry Techniques SyntheticMolecular Dynamics SimulationArticle7-chloro-9H-pyrimido[45-b]indoleEnzyme ActivationMolecular Docking SimulationStructure-Activity RelationshipAdenosine TriphosphateDrug DesignHumansEnzyme InhibitorsHydrophobic and Hydrophilic InteractionsProtein Kinase InhibitorsProtein BindingMolecules (Basel, Switzerland)
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