Search results for " alpha"

showing 10 items of 1610 documents

A Computational Assay of Estrogen Receptor α Antagonists Reveals the Key Common Structural Traits of Drugs Effectively Fighting Refractory Breast Can…

2017

AbstractSomatic mutations of the Estrogen Receptor α (ERα) occur with an up to 40% incidence in ER sensitive breast cancer (BC) patients undergoing prolonged endocrine treatments. These polymorphisms are implicated in acquired resistance, disease relapse, and increased mortality rates, hence representing a current major clinical challenge. Here, multi-microseconds (12.5 µs) molecular dynamics simulations revealed that recurrent ERα polymorphisms (i. e. L536Q, Y537S, Y537N, D538G) (mERα) are constitutively active in their apo form and that they prompt the selection of an agonist (active)-like conformation even upon antagonists binding. Interestingly, our simulations rationalize, for the firs…

0301 basic medicineAgonistModels MolecularBreast cancerComputational chemistryMolecular dynamicsSomatic cellmedicine.drug_classlcsh:MedicineEstrogen receptorBreast Neoplasms-Molecular Dynamics SimulationPolymorphism Single NucleotideArticleProtein Structure SecondaryEstrogen Receptor Antagonists03 medical and health sciences0302 clinical medicineBreast cancermedicineEndocrine systemHumanslcsh:ScienceMultidisciplinarybusiness.industrylcsh:REstrogen Receptor alphamedicine.diseaseEstrogen Receptor Antagonist030104 developmental biologySelective estrogen receptor modulator030220 oncology & carcinogenesisCancer researchlcsh:QFemaleEstrogen Receptor AntagonistsbusinessEstrogen receptor alphaBreast NeoplasmHuman
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TRAIL–NP hybrids for cancer therapy: a review

2017

IF 7.367; International audience; Cancer is a worldwide health problem. It is now considered as a leading cause of morbidity and mortality in developed countries. In the last few decades, considerable progress has been made in anti-cancer therapies, allowing the cure of patients suffering from this disease, or at least helping to prolong their lives. Several cancers, such as those of the lung and pancreas, are still devastating in the absence of therapeutic options. In the early 90s, TRAIL (Tumor Necrosis Factor-related apoptosis-inducing ligand), a cytokine belonging to the TNF superfamily, attracted major interest in oncology owing to its selective anti-tumor properties. Clinical trials u…

0301 basic medicineAgonistmedicine.drug_classmedicine.medical_treatmentApoptosis[SDV.CAN]Life Sciences [q-bio]/Cancer02 engineering and technologyDiseaseCD8-Positive T-Lymphocytes[ SDV.CAN ] Life Sciences [q-bio]/CancerTNF-Related Apoptosis-Inducing Ligand03 medical and health sciences[SDV.CAN] Life Sciences [q-bio]/CancerNeoplasmsHumansMedicineGeneral Materials Science[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyAnti-cancer therapiesReceptor[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyComputingMilieux_MISCELLANEOUSbiologybusiness.industryCancer021001 nanoscience & nanotechnologymedicine.disease3. Good healthKiller Cells NaturalReceptors TNF-Related Apoptosis-Inducing LigandAntitumoral properties030104 developmental biologyCytokineImmunologyCancer researchbiology.proteinNanoparticlesTumor necrosis factor alphaAntibody0210 nano-technologybusinessCD8
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Estradiol, acting through ERα, induces endothelial non-classic renin-angiotensin system increasing angiotensin 1–7 production

2016

Intracellular renin-angiotensin system (RAS) can operate independently of the circulating RAS. Estrogens provide protective effects by modulating the RAS. Our aim was to investigate the effect of estradiol (E2) on angiotensin converting enzymes (ACE) 1 and ACE2 expression and activities in human endothelial cells (HUVEC), and the role of estrogen receptors (ER). The results confirmed the presence of active intracellular RAS in HUVEC. Physiological concentrations of E2 induced a concentration-dependent increase of ACE1 and ACE2 mRNA expression and ACE1, but not ACE2, protein levels. ACE1 and ACE2 enzymatic activities were also induced with E2. These effects were mediated through ERα activati…

0301 basic medicineAgonistmedicine.medical_specialtymedicine.drug_classEstrogen receptorPeptidyl-Dipeptidase A030204 cardiovascular system & hematologyBiologyBiochemistryEstrogen Receptor AntagonistsCiencias Biológicas03 medical and health sciences0302 clinical medicineEndocrinologyPiperidinesInternal medicineRenin–angiotensin systemHuman Umbilical Vein Endothelial CellsmedicineHumansFulvestrantMolecular BiologyESTROGEN RECEPTORDose-Response Relationship DrugEstradiolEstrogen Receptor alphaANGIOTENSIN CONVERTING ENZYMESBioquímica y Biología MolecularRENIN ANGIOTENSIN SYSTEMPeptide FragmentsEndothelial stem cellESTROGEN030104 developmental biologyEndocrinologyGene Expression RegulationEstrogenENDOTHELIAL CELLPyrazolesAngiotensin-Converting Enzyme 2Estrogen Receptor AntagonistsAngiotensin IEstrogen receptor alphaCIENCIAS NATURALES Y EXACTAShormones hormone substitutes and hormone antagonistsIntracellularMolecular and Cellular Endocrinology
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The Role of Osteoprotegerin and Its Ligands in Vascular Function

2019

International audience; The superfamily of tumor necrosis factor (TNF) receptors includes osteoprotegerin (OPG) and its ligands, which are receptor activators of nuclear factor kappa-B ligand (RANKL) and TNF-related apoptosis-inducing ligand (TRAIL). The OPG/RANKL/RANK system plays an active role in pathological angiogenesis and inflammation as well as cell survival. It has been demonstrated that there is crosstalk between endothelial cells and osteoblasts during osteogenesis, thus establishing a connection between angiogenesis and osteogenesis. This OPG/RANKL/RANK/TRAIL system acts on specific cell surface receptors, which are then able to transmit their signals to other intracellular comp…

0301 basic medicineAngiogenesismedicine.medical_treatmentReview030204 cardiovascular system & hematologyLigandslcsh:ChemistryTNF-Related Apoptosis-Inducing Ligand0302 clinical medicineReceptorlcsh:QH301-705.5Cellular SenescenceSpectroscopyReceptor Activator of Nuclear Factor-kappa BbiologyChemistryvascular diseaseGeneral MedicineComputer Science ApplicationsProtein Transportmedicine.anatomical_structureCytokineRANKLTumor necrosis factor alphaDisease Susceptibilitymedicine.symptomProtein BindingSignal Transductionmusculoskeletal diseasesProteasome Endopeptidase ComplexEndotheliumendotheliumNeovascularization PhysiologicInflammationCatalysisInorganic ChemistryStructure-Activity Relationship03 medical and health sciencesOsteoprotegerin[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemmedicineAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologyMyocardiumRANK LigandOrganic ChemistryEndothelial Cells030104 developmental biologylcsh:Biology (General)lcsh:QD1-999osteoprotegerinOPG/RANKL/RANKCancer researchbiology.proteinBlood VesselsBiomarkers
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Crosstalk between angiotensin and the nonamyloidogenic pathway of Alzheimer's amyloid precursor protein.

2017

The association between hypertension and an increased risk for Alzheimer's disease (AD) and dementia is well established. Many data suggest that modulation of the renin-angiotensin system may be meaningful for the prevention and therapy of neurodegenerative disorders, in particular AD. Proteolytic cleavage of the amyloid precursor protein (APP) by α-secretase precludes formation of neurotoxic Aβ peptides and is expected to counteract the development of AD. An established approach for the up-regulation of α-secretase cleavage is the activation of G protein-coupled receptors (GPCRs). Therefore, our study aimed to analyze whether stimulation of angiotensin AT1 or AT2 receptors stably expressed…

0301 basic medicineAngiotensin receptorAngiotensinsBiochemistryReceptor Angiotensin Type 2Receptor Angiotensin Type 103 medical and health sciencesAmyloid beta-Protein PrecursorAlzheimer DiseaseCyclohexanesGTP-Binding Protein gamma SubunitsAmyloid precursor proteinHumansMolecular Biologybeta-ArrestinsG protein-coupled receptorAngiotensin II receptor type 1biologyChemistryGTP-Binding Protein beta SubunitsP3 peptideCell BiologyAmyloidosisAngiotensin IIGTP-Binding Protein alpha SubunitsBiochemistry of Alzheimer's diseaseCell biology030104 developmental biologyHEK293 CellsPyrazinesProteolysisbiology.proteinAmyloid Precursor Protein SecretasesAmyloid precursor protein secretaseThe FEBS journal
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Pinolenic acid ameliorates oleic acid-induced lipogenesis and oxidative stress via AMPK/SIRT1 signaling pathway in HepG2 cells

2019

Pinolenic acid (PLA), a natural compound isolated from pine nut oil, has been reported to exert bioactivity against lipid anabolism. Nonetheless, the underlying mechanisms still poorly elucidated. The aim of this study is to comprehensively demonstrate the effects of PLA on oleic acid (OA)-induced non-alcoholic fatty liver disease (NAFLD) and their relationship with the lipid metabolic regulation. The results demonstrated that treatment with PLA dramatically inhibited lipid accumulation, oxidative stress as well as inflammatory responses induced by oleic acid in HepG2 cells. PLA also obviously decreased the levels of cellular triglyceride (TG), total cholesterol (TC), malondialdehyde (MDA),…

0301 basic medicineAntioxidantLinolenic Acidsmedicine.medical_treatmentPinolenic acidAMP-Activated Protein KinasesNitric Oxidemedicine.disease_causePine nut oil03 medical and health scienceschemistry.chemical_compound0302 clinical medicineSirtuin 1medicineHumansPPAR alphaPharmacologybiologyLipogenesisAMPKHep G2 CellsOxidative StressFatty acid synthaseOleic acid030104 developmental biologyGene Expression RegulationchemistryBiochemistryLipogenesisbiology.proteinlipids (amino acids peptides and proteins)030217 neurology & neurosurgeryOxidative stressOleic AcidSignal TransductionEuropean Journal of Pharmacology
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Evaluation of Antioxidant, Anti-Inflammatory and Cytoprotective Properties of Ethanolic Mint Extracts from Algeria on 7-Ketocholesterol-Treated Murin…

2018

The present study consisted in evaluating the antioxidant, anti-inflammatory and cytoprotective properties of ethanolic extracts from three mint species (Mentha spicata L. (MS), Mentha pulegium L. (MP) and Mentha rotundifolia (L.) Huds (MR)) with biochemical methods on murine RAW 264.7 macrophages (a transformed macrophage cell line isolated from ascites of BALB/c mice infected by the Abelson leukemia virus). The total phenolic, flavonoid and carotenoid contents were determined with spectrophotometric methods. The antioxidant activities were quantified with the Kit Radicaux Libres (KRLTM), the ferric reducing antioxidant power (FRAP) and the 2,2-diphenyl-1-picrylhydrazyl (DPPH) assays. The …

0301 basic medicineAntioxidantLipopolysaccharidePhysiologymedicine.drug_classDPPHmedicine.medical_treatmentClinical BiochemistryFlavonoidantioxidant activityphenolic compoundsPharmacologyBiochemistryArticleAnti-inflammatory03 medical and health scienceschemistry.chemical_compoundcytoprotectionmedicineanti-inflammatory activityMolecular Biology7-ketocholesterolchemistry.chemical_classificationMentha sp. ethanolic extractslcsh:RM1-950<i>Mentha</i> sp. ethanolic extractscarotenoidsInterleukinCell Biologylcsh:Therapeutics. Pharmacology030104 developmental biologychemistryflavonoidsCytokine secretionTumor necrosis factor alphaAntioxidants
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Mutant p53 induces Golgi tubulo-vesiculation driving a prometastatic secretome

2020

TP53 missense mutations leading to the expression of mutant p53 oncoproteins are frequent driver events during tumorigenesis. p53 mutants promote tumor growth, metastasis and chemoresistance by affecting fundamental cellular pathways and functions. Here, we demonstrate that p53 mutants modify structure and function of the Golgi apparatus, culminating in the increased release of a pro-malignant secretome by tumor cells and primary fibroblasts from patients with Li-Fraumeni cancer predisposition syndrome. Mechanistically, interacting with the hypoxia responsive factor HIF1α, mutant p53 induces the expression of miR-30d, which in turn causes tubulo-vesiculation of the Golgi apparatus, leading …

0301 basic medicineBiopsyGeneral Physics and AstronomyGolgi ApparatusAnimals Biopsy Breast Neoplasms Cell Line Tumor Cell Transformation Neoplastic Female Fibroblasts Gene Expression Regulation Neoplastic Golgi Apparatus Humans Hypoxia-Inducible Factor 1 alpha Subunit Li-Fraumeni Syndrome Mice MicroRNAs Microtubules Mutation Primary Cell Culture Secretory Vesicles Signal TransductionSkin Tumor Microenvironment Tumor Suppressor Protein p53 Xenograft Model Antitumor Assays02 engineering and technologymedicine.disease_causeCell TransformationMicrotubulesSettore BIO/09 - FisiologiaMetastasisLi-Fraumeni SyndromeMiceTumor MicroenvironmentGolgisecretory machinerySuper-resolution microscopyAnimals; Biopsy; Breast Neoplasms; Cell Line Tumor; Cell Transformation Neoplastic; Female; Fibroblasts; Gene Expression Regulation Neoplastic; Golgi Apparatus; Humans; Hypoxia-Inducible Factor 1 alpha Subunit; Li-Fraumeni Syndrome; Mice; MicroRNAs; Microtubules; Mutation; Primary Cell Culture; Secretory Vesicles; Signal Transduction; Skin; Tumor Microenvironment; Tumor Suppressor Protein p53; Xenograft Model Antitumor Assayslcsh:ScienceSkinMultidisciplinaryTumorChemistrymutant p53QCell migrationMicroRNASecretomics021001 nanoscience & nanotechnologyCell biologyGene Expression Regulation NeoplasticCell Transformation NeoplasticsymbolsFibroblastmiR-30dFemaleHypoxia-Inducible Factor 10210 nano-technologyBreast NeoplasmHumanSignal TransductionCancer microenvironmentStromal cellSecretory VesicleSciencePrimary Cell CultureBreast NeoplasmsMicrotubuleGolgi ApparatuSettore MED/08 - Anatomia Patologicaalpha SubunitGeneral Biochemistry Genetics and Molecular BiologyArticleCell Line03 medical and health sciencessymbols.namesakeCell Line TumormedicineAnimalsHumansSettore MED/05 - Patologia ClinicaSecretionTumor microenvironmentNeoplasticAnimalSecretory VesiclesGeneral ChemistryOncogenesGolgi apparatusHDAC6FibroblastsMicroreviewHypoxia-Inducible Factor 1 alpha SubunitmicroenvironmentXenograft Model Antitumor AssaysMicroRNAs030104 developmental biologyGene Expression RegulationMutationlcsh:QTumor Suppressor Protein p53Carcinogenesis
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H-ferritin and proinflammatory cytokines are increased in the bone marrow of patients affected by macrophage activation syndrome

2017

Summary Macrophage activation syndrome (MAS) is hyperinflammatory life-threatening syndrome, associated typically with high levels of serum ferritin. This is an iron storage protein including heavy (H) and light (L) subunits, categorized on their molecular weight. The H-/L subunits ratio may be different in tissues, depending on the specific tissue and pathophysiological status. In this study, we analysed the bone marrow (BM) biopsies of adult MAS patients to assess the presence of: (i) H-ferritin and L-ferritin; (ii) CD68+/H-ferritin+ and CD68+/L-ferritin+; and (iii) interleukin (IL)-1β, tumour necrosis factor (TNF) and interferon (IFN)-γ. We also explored possible correlations of these re…

0301 basic medicineBiopsymedicine.medical_treatment0302 clinical medicineBone MarrowcytokineImmunology and AllergyInterleukinBlood ProteinsSyndromeMiddle AgedC-Reactive ProteinCytokinemedicine.anatomical_structureCytokinesTumor necrosis factor alphaInflammation Mediatorsmedicine.symptommacrophage activation syndromeAdultImmunologyAntigens Differentiation MyelomonocyticInflammationmacrophageBiologyProinflammatory cytokine03 medical and health sciencesAntigens CDmedicineHumansAgedRetrospective StudiesInflammation030203 arthritis & rheumatologyMacrophagesferritinOriginal ArticlesMacrophage Activationmedicine.diseaseFerritinSettore MED/16 - Reumatologia030104 developmental biologyMacrophage activation syndromeApoferritinsImmunologybiology.proteinBone marrowCytokine; Ferritin; Hyperferritinaemic syndrome; Macrophage; Macrophage activation syndrome; Immunology and Allergy; Immunologycytokine; ferritin; hyperferritinaemic syndrome; macrophage; macrophage activation syndromehyperferritinaemic syndrome
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Mast cells contribute to autoimmune diabetes by releasing interleukin-6 and failing to acquire a tolerogenic IL-10+ phenotype

2017

Mast cells (MCs) are innate immune cells that exert positive and negative immune modulatory functions capable to enhance or limit the intensity and/or duration of adaptive immune responses. Although MCs are crucial to regulate T cell immunity, their action in the pathogenesis of autoimmune diseases is still debated. Here we demonstrate that MCs play a crucial role in T1D pathogenesis so that their selective depletion in conditional MC knockout NOD mice protects them from the disease. MCs of diabetic NOD mice are overly inflammatory and secrete large amounts of IL-6 that favors differentiation of IL-17-secreting T cells at the site of autoimmunity. Moreover, while MCs of control mice acquire…

0301 basic medicineBlood GlucoseAutoimmune diabeteAutoimmunityNodmedicine.disease_causeT-Lymphocytes RegulatoryAutoimmunityImmune toleranceSettore MED/13 - EndocrinologiaMiceAutoimmune diabetes0302 clinical medicineMice Inbred NODImmunology and AllergyNOD miceMice KnockoutInterleukin-17Forkhead Transcription FactorsFlow CytometryImmunohistochemistryhumanitiesInterleukin-10Interleukin 10Tumor necrosis factor alphaImmunologySettore MED/50 - Scienze Tecniche Mediche ApplicateMice TransgenicLaser Capture MicrodissectionReal-Time Polymerase Chain Reactionbehavioral disciplines and activities03 medical and health sciencesIslets of LangerhansImmune systemChymasesmedicineAnimalsInflammationInnate immune systembusiness.industryInterleukin-6Immune toleranceSettore MED/46 - Scienze Tecniche di Medicina di LaboratorioAutoimmune diabetes; Immune tolerance; Interleukin-10; Interleukin-6; Mast cells030104 developmental biologyDiabetes Mellitus Type 1ImmunologyMast cellsTh17 CellsMast cells; Autoimmune diabetes; Interleukin-6; Immune tolerance; Interleukin-10business030215 immunology
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