Search results for " Notch2"

showing 5 items of 5 documents

Notch and TLR signaling coordinate monocyte cell fate and inflammation

2020

AbstractConventional Ly6Chi monocytes have developmental plasticity for a spectrum of differentiated phagocytes. Here we show, using conditional deletion strategies in a mouse model of Toll-like receptor (TLR) 7-induced inflammation, that the spectrum of developmental cell fates of Ly6Chi monocytes, and the resultant inflammation, is coordinately regulated by TLR and Notch signaling. Cell-intrinsic Notch2 and TLR7-Myd88 pathways independently and synergistically promote Ly6Clo patrolling monocyte development from Ly6Chi monocytes under inflammatory conditions, while impairment in either signaling axis impairs Ly6Clo monocyte development. At the same time, TLR7 stimulation in the absence of …

0301 basic medicineMouseQH301-705.5ScienceNotch signaling pathwayInflammationSpleenBiologyCell fate determinationSystemic inflammationGeneral Biochemistry Genetics and Molecular BiologyMonocytesimmunology03 medical and health sciencesMice0302 clinical medicineImmunology and InflammationmedicineAnimalsReceptor Notch2Biology (General)Receptormousemacrophage differentiationInflammationMembrane GlycoproteinsGeneral Immunology and MicrobiologyGeneral NeuroscienceMonocyteQRCell DifferentiationTLR signalingGeneral MedicineTLR7notch signalingCell biology030104 developmental biologymedicine.anatomical_structureToll-Like Receptor 7inflammationmonocytes and macrophagesMedicinemedicine.symptom030215 immunologySignal TransductionResearch Article
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Truncating mutations in the last exon of NOTCH2 cause a rare skeletal disorder with osteoporosis.

2010

Hajdu-Cheney syndrome is a rare autosomal dominant skeletal disorder with facial anomalies, osteoporosis and acro-osteolysis. We sequenced the exomes of six unrelated individuals with this syndrome and identified heterozygous nonsense and frameshift mutations in NOTCH2 in five of them. All mutations cluster to the last coding exon of the gene, suggesting that the mutant mRNA products escape nonsense-mediated decay and that the resulting truncated NOTCH2 proteins act in a gain-of-function manner.

AdultMaleHeterozygoteHajdu–Cheney syndromeAdolescentmedia_common.quotation_subjectNonsenseMolecular Sequence DataBiologymedicine.disease_causeHajdu-Cheney SyndromeFrameshift mutationExonYoung AdultRare DiseasesSkeletal disorderGeneticsmedicineHumansAmino Acid SequenceReceptor Notch2Frameshift MutationGeneExome sequencingmedia_commonGeneticsMutationBase SequenceDNAExonsMiddle Agedmedicine.diseasePedigreeCodon NonsenseChild PreschoolMutationFemaleSignal TransductionNature genetics
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Associations between Notch-2, Akt-1 and HER2/neu expression in invasive human breast cancer: a tissue microarray immunophenotypic analysis on 98 pati…

2007

<i>Objective:</i> We aimed to investigate the existence of associations between well-established and newly recognized biological and phenotypic features of breast cancer involved in tumor progression and prognosis. <i>Methods:</i> Ninety-eight cases of invasive breast cancer were assessed for the immunohistochemical expression of estrogen and progesterone receptors, Ki-67, HER2, Akt-1, and Notch-2, using the tissue microarray technique. Data regarding tumor histotype, histological grade, tumor size and lymph node status were collected for each patient and included in the analysis. <i>Results:</i> Several significant associations between histological and/o…

AdultOncologyCA15-3medicine.medical_specialtybreast cancer immunophenotypic analysis Notch-2 Akt-1 HER2/neuReceptor ErbB-2Breast NeoplasmsSettore MED/08 - Anatomia PatologicaHER2/neuImmunophenotypingPathology and Forensic MedicineBreast cancerImmunophenotypingInternal medicineBiomarkers TumormedicineHumansReceptor Notch2Notch 2Molecular BiologyProtein kinase BAgedAged 80 and overTissue microarraybiologybusiness.industryCancerCell BiologyGeneral MedicineMiddle Agedmedicine.diseaseReceptors EstrogenTissue Array Analysisbiology.proteinFemaleReceptors ProgesteronebusinessProto-Oncogene Proteins c-akt
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Intraovarian regulation of gonadotropin-dependent folliculogenesis depends on notch receptor signaling pathways not involving Delta-like ligand 4 (Dl…

2013

Background In-situ hybridisation studies demonstrate that Notch receptors and ligands are expressed in granulosa cells (GCs) and in the theca layer vasculature of growing follicles. Notch signaling involves cell-to-cell interaction mediated by transmembrane receptors and ligands. This signaling pathway may represent a novel intraovarian regulator of gonadotropin-dependent follicular development to the preovulatory stage. We hypothesized that blocking Notch pathways would disrupt follicular maturation in the mouse ovary. Methods Hypophysectomized CD21 female mice were administered pregnant mare serum gonadotropin (PMSG) for 3 days to stimulate follicular development. In one experiment, a pan…

Gonadotropins EquineYW152FMiceEndocrinologyOvarian FolliclePregnancyFollicular phaseReceptor Notch2Receptor Notch1Receptor Notch4Receptor Notch3education.field_of_studyReceptors NotchIntracellular Signaling Peptides and ProteinsObstetrics and GynecologyImmunohistochemistryFolliculogenesisObstetricsmedicine.anatomical_structureNotch proteinsThecaTheca Cellscardiovascular systemFemaleJaggedFolliculogenesisSignal Transductionendocrine systemmedicine.medical_specialtyNotchGamma-secretase inhibitorNotch signaling pathwayDll4BiologyProto-Oncogene ProteinsInternal medicineGeneticsmedicineAnimalsHorsesOvarian follicleAntibodies BlockingeducationGranulosa CellsDelta-like ligand 4ResearchOvaryEndothelial CellsMembrane ProteinsMuscle SmoothEstradiol secretionEndocrinologyReproductive MedicineGynecologyFOS: Biological sciencesDevelopmental BiologyReproductive Biology and Endocrinology
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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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