Search results for "cadherin"

showing 10 items of 112 documents

Dissecting the role of ADAM10 as a mediator of Staphylococcus aureus α-toxin action

2016

Staphylococcus aureus is a leading cause of bacterial infections in humans, including life-threatening diseases such as pneumonia and sepsis. Its small membrane-pore-forming α-toxin is considered an important virulence factor. By destroying cell–cell contacts through cleavage of cadherins, the metalloproteinase ADAM10 (a disintegrin and metalloproteinase 10) critically contributes to α-toxin-dependent pathology of experimental S. aureus infections in mice. Moreover, ADAM10 was proposed to be a receptor for α-toxin. However, it is unclear whether the catalytic activity or specific domains of ADAM10 are involved in mediating binding and/or subsequent cytotoxicity of α-toxin. Also, it is not k…

0301 basic medicineStaphylococcus aureusADAM10Bacterial Toxinsmedicine.disease_causeBiochemistryVirulence factorADAM10 ProteinHemolysin ProteinsMice03 medical and health sciencesCatalytic DomainmedicineDisintegrinAnimalsMolecular BiologyFurinCells CulturedMice KnockoutMetalloproteinasebiologyCadherinCell MembraneCell BiologyStaphylococcal InfectionsCadherinsCell biology030104 developmental biologyBiochemistryStaphylococcus aureusbiology.proteinCalciumIntracellularProtein BindingBiochemical Journal
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Impact of the Usher syndrome on olfaction

2015

Usher syndrome is a genetically and clinically heterogeneous disease in humans, characterized by sensorineural hearing loss, retinitis pigmentosa and vestibular dysfunction. This disease is caused by mutations in genes encoding proteins that form complex networks in different cellular compartments. Currently, it remains unclear whether the Usher proteins also form networks within the olfactory epithelium (OE). Here, we describe Usher gene expression at the mRNA and protein level in the OE of mice and showed interactions between these proteins and olfactory signaling proteins. Additionally, we analyzed the odor sensitivity of different Usher syndrome mouse models using electro-olfactogram re…

0301 basic medicineUsher syndromeCell Cycle ProteinsMice TransgenicNerve Tissue ProteinsOlfactionMyosinsBiologyCell LineMice03 medical and health sciencesOlfactory MucosaGene expressionRetinitis pigmentosaotorhinolaryngologic diseasesGeneticsmedicineAnimalsHumansCiliaMolecular BiologyGeneGenetics (clinical)GeneticsExtracellular Matrix ProteinsMessenger RNAGene Expression ProfilingEpithelial CellsGeneral MedicineCadherinsmedicine.diseaseeye diseasesSmellCytoskeletal ProteinsDisease Models Animal030104 developmental biologymedicine.anatomical_structureGene Expression RegulationMyosin VIIaMutationOdorantsSignal transductionCarrier ProteinsUsher SyndromesOlfactory epitheliumSignal TransductionHuman Molecular Genetics
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Vitamin A Deficiency and the Lung.

2018

Vitamin A (all-trans-retinol) is a fat-soluble micronutrient which together with its natural derivatives and synthetic analogues constitutes the group of retinoids. They are involved in a wide range of physiological processes such as embryonic development, vision, immunity and cellular differentiation and proliferation. Retinoic acid (RA) is the main active form of vitamin A and multiple genes respond to RA signalling through transcriptional and non-transcriptional mechanisms. Vitamin A deficiency (VAD) is a remarkable public health problem. An adequate vitamin A intake is required in early lung development, alveolar formation, tissue maintenance and regeneration. In fact, chronic VAD has b…

0301 basic medicineVitamincollagenLung DiseasesEpithelial-Mesenchymal Transitionextracellular matrixRetinoic acidlcsh:TX341-641Reviewepithelial–mesenchymal transitionlungExtracellular matrix03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRisk Factorsretinoic acidMedicineAnimalsHumans030212 general & internal medicineVitamin AN-cadherinpulmonary diseaseNutrition and DieteticsLungbusiness.industryVitamin A DeficiencyRegeneration (biology)RetinolE-cadherinMicronutrientmedicine.diseaseVitamin A deficiency030104 developmental biologymedicine.anatomical_structureE-cadherin N-cadherin Vitamin A deficiency collagen epithelial–mesenchymal transition extracellular matrix lung pulmonary disease retinoic acid retinolchemistryImmunologyAirway Remodelingbusinesslcsh:Nutrition. Foods and food supplyFood ScienceretinolSignal Transduction
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GDF11 exhibits tumor suppressive properties in hepatocellular carcinoma cells by restricting clonal expansion and invasion.

2019

Growth differentiation factor 11 (GDF11) has been characterized as a key regulator of differentiation in cells that retain stemness features, despite some controversies in age-related studies. GDF11 has been poorly investigated in cancer, particularly in those with stemness capacity, such as hepatocellular carcinoma (HCC), one of the most aggressive cancers worldwide. Here, we focused on investigating the effects of GDF11 in liver cancer cells. GDF11 treatment significantly reduced proliferation, colony and spheroid formation in HCC cell lines. Consistently, down-regulation of CDK6, cyclin D1, cyclin A, and concomitant upregulation of p27 was observed after 24 h of treatment. Interestingly,…

0301 basic medicine[SDV]Life Sciences [q-bio]Cyclin ACellChick EmbryoChorioallantoic Membrane0302 clinical medicineCell MovementCyclin D1HCCbiologyNeovascularization PathologicCell DifferentiationHep G2 CellsCell cycleCadherinsHuh7 cells3. Good health[SDV] Life Sciences [q-bio]Gene Expression Regulation NeoplasticGrowth Differentiation Factorsmedicine.anatomical_structure030220 oncology & carcinogenesisBone Morphogenetic ProteinsMolecular MedicineLiver cancerCyclin-Dependent Kinase Inhibitor p27Signal Transduction[SDV.CAN]Life Sciences [q-bio]/CancerCyclin ACell cycleHep3B cells03 medical and health sciencesCyclin D1Downregulation and upregulation[SDV.CAN] Life Sciences [q-bio]/CancerAntigens CDCell Line TumorOccludinSpheroids CellularmedicineAnimalsHumansViability assayMolecular BiologyCell Proliferation[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyCyclin-Dependent Kinase 6[SDV.MHEP.HEG] Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology030104 developmental biologyCell cultureGDF11biology.proteinCancer researchCyclin-dependent kinase 6Snail Family Transcription FactorsBiochimica et biophysica acta. Molecular basis of disease
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Alterations in Tight- and Adherens-Junction Proteins Related to Glaucoma Mimicked in the Organotypically Cultivated Mouse Retina Under Elevated Press…

2020

Purpose To scrutinize alterations in cellular interactions and cell signaling in the glaucomatous retina, mouse retinal explants were exposed to elevated pressure. Methods Retinal explants were prepared from C57bl6 mice and cultivated in a pressure chamber under normotensive (atmospheric pressure + 0 mm Hg), moderately elevated (30 mm Hg), and highly elevated (60 mm Hg) pressure conditions. The expression levels of proteins involved in the formation of tight junctions (zonula occludens 1 [ZO-1], occludin, and claudin-5) and adherens junctions (VE-cadherin and β-catenin) and in cell-signaling cascades (Cdc42 and activated Cdc42 kinase 1 [ACK1]), as well as the expression levels of the growth…

0301 basic medicineelevated pressureBlotting WesternVimentinReal-Time Polymerase Chain ReactionOccludinRetinaTight JunctionsAdherens junctionMice03 medical and health scienceschemistry.chemical_compoundOrgan Culture Techniques0302 clinical medicineAntigens CDOccludinmedicinecell signalingAnimalscell contactsEye Proteinscdc42 GTP-Binding ProteinReceptorretina explantsmousebeta CateninRetinabiologyTight junctionGlial fibrillary acidic proteinChemistryGlaucomaRetinalAdherens JunctionsProtein-Tyrosine KinasesCadherinsImmunohistochemistryCell biologyMice Inbred C57BLAtmospheric Pressure030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisZonula Occludens-1 Proteinbiology.proteinInvestigative Opthalmology & Visual Science
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Estudio de la quiescencia y activación de las células madre neurales adultas por uniones adherentes: papel de la N-cadherina.

2017

El descubrimiento de poblaciones de células madre en el cerebro adulto (NSCs) de los mamíferos ha cambiado nuestra visión del sistema nervioso, añadiendo el concepto de plasticidad celular al de plasticidad neural. El conocimiento detallado de los mecanismos que permiten a las NSCs mantenerse indiferenciadas, dividirse de manera asimétrica para auto-perpetuarse mientras generan progenie diferenciada, y activarse para proliferar contribuyendo así a la renovación de ciertas poblaciones de neuronas durante toda la vida se ha convertido en un campo de investigación en continuo avance. El desarrollo de técnicas que permiten la posibilidad de expandir las NSCs in vitro y de estudiarlas en su micr…

:CIENCIAS DE LA VIDA::Biología celular [UNESCO]zona subependimarianeurogénesiscélulas madre neurales adultasUNESCO::CIENCIAS DE LA VIDA::Neurociencias:CIENCIAS DE LA VIDA::Neurociencias [UNESCO]UNESCO::CIENCIAS DE LA VIDA::Biología celularn-cadherinaproliferación
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Epigenetic dysregulation in the developing Down syndrome cortex

2016

Using Illumina 450K arrays, 1.85% of all analyzed CpG sites were significantly hypermethylated and 0.31% hypomethylated in fetal Down syndrome (DS) cortex throughout the genome. The methylation changes on chromosome 21 appeared to be balanced between hypo- and hyper-methylation, whereas, consistent with prior reports, all other chromosomes showed 3–11 times more hyper- than hypo-methylated sites. Reduced NRSF/REST expression due to upregulation of DYRK1A (on chromosome 21q22.13) and methylation of REST binding sites during early developmental stages may contribute to this genome-wide excess of hypermethylated sites. Upregulation of DNMT3L (on chromosome 21q22.4) could lead to de novo methyl…

Adult0301 basic medicineCancer ResearchDown syndromeDown syndromeNeuronal OutgrowthDNMT3BProtein Serine-Threonine KinasesBiologyDNA Methyltransferase 3AEpigenesis Genetic03 medical and health sciencesfetal brain developmentddc:570medicineHumansDNA (Cytosine-5-)-MethyltransferasesEpigeneticsddc:610Molecular BiologyCerebral CortexGeneticsDNA methylationfrontal cortexGene Expression Regulation DevelopmentalChromosomeMethylationProtein-Tyrosine KinasesCadherinsmedicine.diseaseMolecular biologyprotocadherin gamma cluster030104 developmental biologyCpG siteDNA methylationChromosome 21Research Paper
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The transcription factor ZEB1 (deltaEF1) promotes tumour cell dedifferentiation by repressing master regulators of epithelial polarity.

2007

Epithelial to mesenchymal transition (EMT) is implicated in the progression of primary tumours towards metastasis and is likely caused by a pathological activation of transcription factors regulating EMT in embryonic development. To analyse EMT-causing pathways in tumouri-genesis, we identified transcriptional targets of the E-cadherin repressor ZEB1 in invasive human cancer cells. We show that ZEB1 repressed multiple key determinants of epithelial differentiation and cell–cell adhesion, including the cell polarity genes Crumbs3, HUGL2 and Pals1-associated tight junction protein. ZEB1 associated with their endogenous promoters in vivo, and strongly repressed promotor activities in reporter …

AdultCancer ResearchChromatin ImmunoprecipitationCellular differentiationImmunoblottingDown-RegulationBreast NeoplasmsBiologymedicine.disease_causeEpitheliumArticleCell polarityGeneticsmedicineTumor Cells CulturedHumansNeoplasm InvasivenessEpithelial–mesenchymal transitionCell adhesionPromoter Regions GeneticMolecular BiologyTranscription factorEpithelial polarityAgedOligonucleotide Array Sequence AnalysisHomeodomain ProteinsMembrane GlycoproteinsReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingCell PolarityMembrane ProteinsZinc Finger E-box-Binding Homeobox 1Cell DifferentiationMiddle AgedCadherinsCytoskeletal ProteinsMicroscopy FluorescenceCancer cellColonic NeoplasmsCancer researchDisease ProgressionSnail Family Transcription FactorsCarcinogenesisNucleoside-Phosphate KinaseTranscription FactorsOncogene
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Genome-wide Association Study of Alcohol Dependence

2009

Context Alcohol dependence is a serious and common public health problem. It is well established that genetic factors play a major role in the development of this disorder. Identification of genes that contribute to alcohol dependence will improve our understanding of the mechanisms that underlie this disorder. Objective To identify susceptibility genes for alcohol dependence through a genome-wide association study (GWAS) and a follow-up study in a population of German male inpatients with an early age at onset. Design The GWAS tested 524 396 single-nucleotide polymorphisms (SNPs). All SNPs with P −4 were subjected to the follow-up study. In addition, nominally significant SNPs from genes t…

AdultGenetic MarkersMaleGenotypeGenetic LinkagePopulationContext (language use)Single-nucleotide polymorphismGenome-wide association studyBiologyPolymorphism Single NucleotideGenetic determinismArticleAlcohol Withdrawal DeliriumYoung AdultArts and Humanities (miscellaneous)Genetic linkageAnimalsHumansAlleleAge of OnseteducationAllelesGeneticseducation.field_of_studyGene Expression ProfilingAlcohol dependenceAlcohol DehydrogenasePutamenRats Inbred StrainsAmygdalaCadherinsRatsHospitalizationPsychiatry and Mental healthAlcoholismPhenotypeGene Expression RegulationCase-Control StudiesChromosomes Human Pair 2Caudate NucleusLod ScoreFollow-Up StudiesGenome-Wide Association Study
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Recurrence of pleomorphic adenoma of the parotid gland-predictive value of cadherin-11 and fascin

2008

The predictive value of cadherin-11, tenascin, fascin, and mucin-1 as markers for the likelihood of recurrence in pleomorphic adenoma of the parotid gland was examined. In this retrospective study we analysed 20 tumours from16 patients by immunohistochemistry. Staining intensities were measured using a semiquantitative scoring approach; localisation (tumour centre vs border) as well as clinical data were analysed and correlated with follow-up. Cadherin-11 was increased in recurrent tumours. However, no changes of fascin, tenascin or mucin-1 were observed. Cadherin-11 and fascin were increased in primary tumours of patients with later recurrence, with fascin upregulation restricted to the tu…

AdultMaleMicrobiology (medical)Pathologymedicine.medical_specialtyAdolescentAdenoma PleomorphicTenascinmacromolecular substancesPathology and Forensic MedicinePleomorphic adenomaDownregulation and upregulationBiomarkers TumormedicineHumansParotid GlandImmunology and AllergyRetrospective StudiesFascinbiologyCadherinMicrofilament ProteinsMucin-1MucinTenascinGeneral MedicineMiddle AgedCadherinsPrognosismedicine.diseaseImmunohistochemistryParotid NeoplasmsParotid glandmedicine.anatomical_structurebiology.proteinImmunohistochemistryFemaleNeoplasm Recurrence LocalCarrier ProteinsAPMIS
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