Search results for "NOTCH1"

showing 10 items of 13 documents

Notch-1 decreased expression contributes to leptin receptor downregulation in nasal epithelium from allergic turbinates

2019

Abstract BACKGROUND: Allergic rhinitis is characterized by a remodeling of nasal epithelium. Since the Notch and TGF-β signaling pathways are known to be involved in cell differentiation and remodeling processes and leptin adipokine has already been identified as a marker for homeostasis in human bronchial and nasal epithelial cells of asthmatics, roles played by these pathways have been investigated for chronic allergic rhinitis. METHODS: The leptin/leptin receptor expression has been investigated in a study with 40 biopsies from allergic (AR, n = 18) and non-allergic (C, n = 22) inferior turbinates, using immunohistochemistry, immunofluorescence staining and RT-PCR. In addition, extracts …

0301 basic medicineAdultLeptinMalemedicine.medical_specialtyBiopsyPrimary Cell CultureAdipokineTurbinatesCell LineTransforming Growth Factor beta103 medical and health sciences0302 clinical medicineDownregulation and upregulationInternal medicinemedicineHomeostasisHumansRNA MessengerReceptor Notch1610 Medicine & healthReceptorMolecular BiologyNotch 1Leptin receptorChemistryLeptindigestive oral and skin physiologyEpithelial CellsMiddle AgedRhinitis AllergicAllergic rhinitis Epithelium Leptin NotchEpitheliumNasal Mucosa030104 developmental biologyEndocrinologymedicine.anatomical_structureGene Expression Regulation030220 oncology & carcinogenesisCase-Control StudiesMolecular MedicineReceptors LeptinFemaleSignal transductionSignal Transduction
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Human Papilloma Virus-Dependent HMGA1 Expression Is a Relevant Step in Cervical Carcinogenesis

2008

HMGA1 is a member of a small family of architectural transcription factors involved in the coordinate assembly of multiprotein complexes referred to as enhanceosomes. In addition to their role in cell proliferation, differentiation, and development, high-mobility group proteins of the A type (HMGA) family members behave as transforming protoncogenes either in vitro or in animal models. Recent reports indicated that HMGA1 might counteract p53 pathway and provided an interesting hint on the mechanisms determining HMGA's transforming potential. HMGA1 expression is deregulated in a very large array of human tumors, including cervical cancer, but very limited information is available on the mole…

Uterine Cervical NeoplasmCancer ResearchDNA-Binding ProteinBiologyHeLa Celllcsh:RC254-282DNA-binding proteinRNA interferenceCell Line TumorHMGA1a ProteinRNA MessengerReceptor Notch1PapillomaviridaePapillomavirus InfectionPsychological repressionTranscription factorCell ProliferationReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingHMGAOncogene Proteins ViralCell Transformation Virallcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensHMGA1Gene Expression Regulation NeoplasticGene expression profilingCancer cellCancer researchbiology.proteinFemaleTumor Suppressor Protein p53HumanNeoplasia
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Biomarkers for vascular ageing in aorta tissues and blood samples.

2019

Abstract Objectives Functional and quantitative alterations and senescence of circulating and expanded endothelial progenitor cells (EPC), as well as systemic and tissue modifications of angiogenetic and inflammatory molecules, were evaluated for predicting age-related vessel wall remodeling, correlating them to intima media thickness (IMT) in the common carotid artery (CCA), a biomarker of early cardiovascular disease and aortic root dilation. Populations and methods A homogenous Caucasian population was included in the study, constituted by 160 healthy subjects (80 old subjects, mean age 72 ± 6.4, range 66–83 years; and 80 younger blood donors, mean age 26.2 ± 3.4, range 21–33 years), and…

0301 basic medicineMaleVascular Endothelial Growth Factor AAgingPhysiologySystemic inflammationBiochemistryCarotid Intima-Media Thickness0302 clinical medicineEndocrinologySA-β-Gal activityp21 and p16 genesMedicineTP53Receptor Notch1AortaEndothelial Progenitor CellsAged 80 and overeducation.field_of_studyChemotaxisInflammatory cytokinesmedicine.anatomical_structurecardiovascular systemBiomarker (medicine)Femalemedicine.symptomTP53 p21 and p16 genesSenescenceAdultEndotheliumInflammatory cytokineNotch and TLR4Carotid Artery CommonPopulationProinflammatory cytokine03 medical and health sciencesYoung AdultTP53 p21 and p16 genemedicine.arteryGeneticsHumansEPC cell populationeducationMolecular BiologyEPC cell populationsAgedAortabusiness.industryEndothelium age-related impairmentCell BiologyChemokine CXCL12Toll-Like Receptor 4EPC cell populations; Endothelium age-related impairment; Inflammatory cytokines; Notch and TLR4; SA-β-Gal activity; TP53 p21 and p16 genesSettore MED/23030104 developmental biologyIntima-media thicknessbusiness030217 neurology & neurosurgeryBiomarkersExperimental gerontology
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Deregulation of Notch1 pathway and circulating endothelial progenitor cell (EPC) number in patients with bicuspid aortic valve with and without ascen…

2018

AbstractBicuspid aortic valve (BAV) is frequently associated with the development of ascending aortic aneurysm, even if the underlying mechanisms remain to be clarified. Here, we investigated if a deregulation of Notch1 signaling pathway and endothelial progenitor cells (EPCs) number is associated with BAV disease and an early ascending aortic aneurysm (AAA) onset. For this purpose, 70 subjects with BAV (M/F 50/20; mean age: 58.8 ± 14.8 years) and 70 subjects with tricuspid aortic valve (TAV) (M/F 35/35; mean age: 69.1 ± 12.8 years) and AAA complicated or not, were included. Interestingly, patients with AAA showed a significant increase in circulating Notch1 levels and EPC number than subje…

Male0301 basic medicineAortic valveNotch1 signaling pathwatHeart Valve Diseases030204 cardiovascular system & hematologyAortic aneurysm0302 clinical medicineBicuspid aortic valveBicuspid Aortic Valve DiseaseNotch Signaling Pathwaycirculating EPC populationsReceptor Notch1ReceptorAortaEndothelial Progenitor CellsAged 80 and overMultidisciplinaryQRMiddle AgedAortic Aneurysmmedicine.anatomical_structureAortic Valvecardiovascular systemCardiologyMedicineFemaleTricuspid ValveSignal TransductionAdultmedicine.medical_specialtyBicuspid aortic valveEndothelial Progenitor Cells (EPC)ScienceNotch signaling pathwayBicuspid Aortic Valve (BAV)Endothelial progenitor cellArticleBicuspid aortic valve; Notch1 signaling pathwat; ascending aortic aneurysm03 medical and health sciencesascending aortic aneurysmInternal medicinemedicineHumansIn patientcardiovascular diseasesProgenitor cellNotch 1 signaling pathwayAgedTricuspid Aortic Valve (TAV)Ascending Aorta Aneurysm (AAA)business.industrySettore MED/23 - Chirurgia Cardiacamedicine.disease030104 developmental biologybusiness
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Expression pattern of Notch1, 2 and 3 and Jagged1 and 2 in lymphoid and stromal thymus components: distinct ligand–receptor interactions in intrathym…

1999

The suggested role of Notch1 or its mutants in thymocyte differentiation and T cell tumorigenesis raises the question of how the different members of the Notch family influence distinct steps in T cell development and the role played by Notch ligands in the thymus. We report here that different Notch receptor-ligand partnerships may occur inside the thymus, as we observed differential expression of Notch1, 2 and 3 receptors, their ligands Jagged1 and 2, and downstream intracellular effectors hairy and Enhancer of Split homolog 1 (HES-1) and hairy and Enhancer of Split homolog 5 (HES-5), depending on ontogenetic stage and thymic cell populations. Indeed, while Jagged2 is expressed in both st…

MaleT-LymphocytesLigandsMiceNotch FamilyCell–cell interactionT-Lymphocyte SubsetsBasic Helix-Loop-Helix Transcription FactorsImmunology and AllergySerrate-Jagged ProteinsReceptor Notch2Receptor Notch1Receptor Notch4Receptor Notch3Receptors NotchHelix-Loop-Helix Motifscell-cell interaction; thymic stromal cells; thymocyteCell DifferentiationGeneral MedicineCell biologyDNA-Binding ProteinsThymocytemedicine.anatomical_structureIntercellular Signaling Peptides and ProteinsJagged-2 ProteinSignal TransductionStromal cellLymphoid TissueT cellImmunologyNotch signaling pathwayReceptors Cell SurfaceThymus GlandBiologySerrate-Jagged ProteinsProto-Oncogene ProteinsmedicineAnimalsRNA MessengerHomeodomain ProteinsCalcium-Binding ProteinsMembrane ProteinsProteinsMice Inbred C57BLRepressor ProteinsProtein BiosynthesisTranscription Factor HES-1Jagged-1 ProteinStromal CellsCarrier ProteinsJagged-1 ProteinTranscription FactorsInternational Immunology
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Identification of novel, clonally stable, somatic mutations targeting transcription factors PAX5 and NKX2-3, the epigenetic regulator LRIF1, and BRAF…

2021

Diagnosis of B-cell chronic lymphocytic leukemia (B-CLL) is usually straightforward, involving clinical, immunophenotypic (Matutes score), and (immuno)genetic analyses (to refine patient prognosis for treatment). CLL cases with atypical presentation (e.g., Matutes ≤ 3) are also encountered, and for these diseases, biology and prognostic impact are less clear. Here we report the genomic characterization of a case of atypical B-CLL in a 70-yr-old male patient; B-CLL cells showed a Matutes score of 3, chromosomal translocation t(14;18)(q32;q21) (BCL2/IGH), mutated IGHV, deletion 17p, and mutations in BCL2, NOTCH1 (subclonal), and TP53 (subclonal). Quite strikingly, a novel PAX5 mutation that w…

MaleProto-Oncogene Proteins B-rafChronic lymphocytic leukemiaCell Cycle ProteinsBiologymedicine.disease_causeSomatic evolution in cancerTranslocation GeneticEpigenesis Genetichematological neoplasmClonal Evolutionimmune system diseaseshemic and lymphatic diseasesExome SequencingmedicineHumansEpigeneticsReceptor Notch1neoplasmsLoss functionExome sequencingAgedHomeodomain ProteinsMutationPAX5 Transcription FactorGeneral Medicinemedicine.diseasePrognosisLeukemia Lymphocytic Chronic B-CellProto-Oncogene Proteins c-bcl-2MutationCancer researchPAX5Tumor Suppressor Protein p53IGHV@Rapid Cancer CommunicationTranscription FactorsCold Spring Harbor Molecular Case Studies
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Haploinsufficiency of the NOTCH1 receptor as a cause of Adams-Oliver syndrome with variable cardiac anomalies

2015

Background— Adams–Oliver syndrome (AOS) is a rare disorder characterized by congenital limb defects and scalp cutis aplasia. In a proportion of cases, notable cardiac involvement is also apparent. Despite recent advances in the understanding of the genetic basis of AOS, for the majority of affected subjects, the underlying molecular defect remains unresolved. This study aimed to identify novel genetic determinants of AOS. Methods and Results— Whole-exome sequencing was performed for 12 probands, each with a clinical diagnosis of AOS. Analyses led to the identification of novel heterozygous truncating NOTCH1 mutations (c.1649dupA and c.6049_6050delTC) in 2 kindreds in which AOS was segregat…

MaleModels MolecularProbandreceptorGene ExpressionHaploinsufficiencyNOTCH1Ectodermal DysplasiaMissense mutationExomeReceptor Notch1ChildExomeGenetics (clinical)GeneticsReverse Transcriptase Polymerase Chain ReactionAutosomal dominant traitMiddle AgedPedigreeembryonic structuresheart defectscardiovascular systemFemaleCardiology and Cardiovascular MedicineHaploinsufficiencySignal TransductionAdultHeart Defects CongenitalAdolescentLimb Deformities CongenitalNotch signaling pathwayBiologyArticleYoung AdultAdams-Oliver syndromeGeneticsmedicineHumansGenetic Predisposition to DiseaseGeneFamily HealthBase SequencecongenitalAdams-Oliver syndrome; genetics; haploinsufficiency; heart defects; congenital; receptor; NOTCH1; Cardiology and Cardiovascular Medicine; Genetics (clinical); GeneticsSequence Analysis DNAmedicine.diseaseProtein Structure TertiaryScalp DermatosesHuman medicineAdams–Oliver syndromeCirculation. Cardiovascular genetics
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Notch‐1 signaling activation sustains overexpression of interleukin 33 in the epithelium of nasal polyps

2019

Abstract BACKGROUND: Alterations in the nasal epithelial barrier homeostasis and increased interleukin 33 (IL-33) expression contribute to the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP). AIMS: As Notch-1 signaling is crucial in repair processes of mucosa, the current study assessed Notch-1/Jagged-1 signaling and IL-33 in the epithelium of nasal polyps biopsies from allergic (A-CRSwNP; n = 9) and not allergic (NA-CRSwNP; n = 9) subjects by immunohistochemistry. We also assessed, in a model of nasal epithelial cells, the effects of stimulation of Notch-1 with Jagged-1 on the expression of IL-33 (by flow cytometry, immunofluorescence, and immunocytochemistry), Jagged-1 (…

AdultMale0301 basic medicineendocrine systemPhysiologyClinical BiochemistryImmunocytochemistryStimulationBiologyCell LineFlow cytometryYoung Adult03 medical and health sciencesNasal Polyps0302 clinical medicinestomatognathic systemmedicineHumansNasal polypsPhosphorylationReceptor Notch1SinusitisCyclic AMP Response Element-Binding ProteinNotch 1medicine.diagnostic_testEpithelial CellsCell BiologyMiddle AgedInterleukin-33medicine.diseaseRhinitis AllergicMolecular biologyEpitheliumUp-RegulationInterleukin 33Nasal Mucosa030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisChronic DiseaseIL-33; Notch-1; chronic rhinosinusitis; nasal epithelium; nasal polypsImmunohistochemistryFemaleNOTCH-1 INTERLEUKIN 33 NASAL POLYPSJagged-1 ProteinSignal TransductionJournal of Cellular Physiology
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A Typical Immune T/B Subset Profile Characterizes Bicuspid Aortic Valve: In an Old Status?

2018

Bicuspid valve disease is associated with the development of thoracic aortic aneurysm. The molecular mechanisms underlying this association still need to be clarified. Here, we evaluated the circulating levels of T and B lymphocyte subsets associated with the development of vascular diseases in patients with bicuspid aortic valve or tricuspid aortic valve with and without thoracic aortic aneurysm. We unveiled that the circulating levels of the MAIT, CD4+IL−17A+, and NKT T cell subsets were significantly reduced in bicuspid valve disease cases, when compared to tricuspid aortic valve cases in either the presence or the absence of thoracic aortic aneurysm. Among patients with tricuspid aortic…

Male0301 basic medicineAortic valveAgingT-LymphocytesLymphocyteHeart Valve Diseases030204 cardiovascular system & hematologyBiochemistryImmunoglobulin D0302 clinical medicineBicuspid aortic valveBicuspid Aortic Valve DiseaseBicuspid aortic valve aneurysm B cellsb-cellsnotch1Invariant t-cells; aneurysm formation; angiotensin-ii; signaling pathway; genetic-variants; apoptotic cells; b-cells; mechanisms; mutations; notch1B-Lymphocytesmechanismsbiologylcsh:Cytologyhemic and immune systemsGeneral MedicineMiddle Agedmedicine.anatomical_structureAortic ValveCardiologycardiovascular systemFemaleResearch Articlesignaling pathwaymedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesaneurysm formationInvariant t-cellsArticle SubjectBicuspid aortic valveT cellNaive B cellchemical and pharmacologic phenomenaThoracic aortic aneurysm03 medical and health sciencesBicuspid valveInternal medicinemedicineHumansSettore MED/05 - Patologia Clinicacardiovascular diseaseslcsh:QH573-671angiotensin-iigenetic-variantsB cellsbusiness.industrySettore MED/23 - Chirurgia Cardiacaapoptotic cellsCell Biologymutationsmedicine.disease030104 developmental biologybiology.proteinaneurysmbusinessA Typical Immune T/B Subset Profile Bicuspid Aortic Valve
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An overview of the molecular mechanisms underlying development and progression of bicuspid aortic valve disease

2019

Bicuspid aortic valve (BAV) is a common congenital heart malformation frequently associated with the development of aortic valve diseases and severe aortopathy, such as aortic dilatation, aneurysm and dissection. To date, different genetic loci have been identified in syndromic and non- syndromic forms of BAV. Among these, genes involved in the regulation of extracellular matrix remodelling, epithelial to mesenchymal transition and nitric oxide metabolism appear to be the main contributors to BAV pathogenesis. However, no- single gene model explains BAV inheritance, suggesting that more factors are simultaneously involved. In this regard, characteristic epigenetic and immunological profiles…

0301 basic medicineaneurysm; aortic dilatation; aortic stenosis; aortopathy; bicuspid aortic valve; NOTCH1Aortic stenosibicuspid aortic valveHeart malformationAortic DiseasesHeart Valve Diseasesaortopathy610 Medicine & healthDisease030204 cardiovascular system & hematologyBioinformatics2705 Cardiology and Cardiovascular Medicine11459 Center for Molecular CardiologyPathogenesis03 medical and health sciences0302 clinical medicineAneurysmBicuspid aortic valveNOTCH1Bicuspid Aortic Valve Disease1312 Molecular BiologymedicineSettore MED/05 - Patologia ClinicaAnimalsHumansEpithelial–mesenchymal transitionEpigeneticsMolecular BiologyAortic dilatationbusiness.industryaortic stenosisaortic dilatationmedicine.disease030104 developmental biologyAortic ValveaneurysmDisease Progressioncardiovascular systemCardiology and Cardiovascular MedicinebusinessJournal of Molecular and Cellular Cardiology
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