Search results for "Cadherins"

showing 10 items of 85 documents

Melittin Modulates Keratinocyte Function through P2 Receptor-dependent ADAM Activation

2012

Melittin, the major component of the bee venom, is an amphipathic, cationic peptide with a wide spectrum of biological properties that is being considered as an anti-inflammatory and anti-cancer agent. It modulates multiple cellular functions but the underlying mechanisms are not clearly understood. Here, we report that melittin activates disintegrin-like metalloproteases (ADAMs) and that downstream events likely contribute to the biological effects evoked by the peptide. Melittin stimulated the proteolysis of ADAM10 and ADAM17 substrates in human neutrophil granulocytes, endothelial cells and murine fibroblasts. In human HaCaT keratinocytes, melittin induced shedding of the adhesion molecu…

KeratinocytesCell SurvivalBlotting WesternADAM17 ProteinP2 receptorBiologyModels Biologicalcomplex mixturesBiochemistryMelittinCell LineADAM10 ProteinMicechemistry.chemical_compoundTransactivationAdenosine TriphosphateAnimalsHumansPhosphorylationExtracellular Signal-Regulated MAP KinasesReceptorMolecular BiologyCells CulturedMice KnockoutDose-Response Relationship DrugReverse Transcriptase Polymerase Chain ReactionPurinergic receptorHEK 293 cellstechnology industry and agricultureMembrane ProteinsCell BiologyFibroblastsCadherinsEmbryo MammalianMelittenCell biologyErbB ReceptorsADAM ProteinsHaCaTHEK293 CellschemistryPhosphorylationlipids (amino acids peptides and proteins)Receptors Purinergic P2X7Amyloid Precursor Protein SecretasesJournal of Biological Chemistry
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Induction of Cell Differentiation in Transformed Keratinocytes by Synthetic (Glyco)peptides from the Homophilic Recognition Domain of E-Cadherin

2002

KeratinocytesProtein ConformationCadherinChemistryStereochemistryCellular differentiationMolecular Sequence DataGlycopeptidesCell DifferentiationGeneral ChemistryCadherinsPeptide FragmentsCatalysisGlycopeptideProtein Structure TertiaryDomain (software engineering)Cell biologySolid-phase synthesisMicroscopy FluorescenceHumansAmino Acid SequenceNuclear Magnetic Resonance BiomolecularCell Line TransformedAngewandte Chemie International Edition
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Rottlerin induces a transformed phenotype in human keratinocytes.

2001

PKCdelta plays a fundamental role in cell cycle control. Consistent with its proposed tumour suppressor function, ras transfection of the human keratinocyte cell line HaCaT results in a loss of PKCdelta expression mediated by TGFalpha (Exp. Cell Res., 219, 299, 1995). To get more insight into the role of PKCdelta in keratinocytes, we investigated the effects of Rottlerin, a specific inhibitor of protein kinase Cdelta, in HaCaT cells. After Rottlerin treatment, HaCaT cells lost their cobble-stone morphology and displayed a spindle-shaped, fibroblastic phenotype. Additionally, the establishment of cell-cell contacts was prevented. This was caused by an internalization of E-cadherin and beta-c…

Keratinocytesmedia_common.quotation_subjectCellBiophysicsBiologyBiochemistryCell Linechemistry.chemical_compoundmedicineCell AdhesionHumansBenzopyransEnzyme InhibitorsProtein kinase AInternalizationMolecular BiologyProtein Kinase Cbeta Cateninmedia_commonintegumentary systemContact InhibitionAcetophenonesCell DifferentiationCell BiologyTransfectionCadherinsPhenotypeMolecular biologyCell biologyIsoenzymesHaCaTCytoskeletal ProteinsProtein Kinase C-deltamedicine.anatomical_structureCell Transformation NeoplasticPhenotypechemistryCell cultureTrans-ActivatorsRottlerinBiochemical and biophysical research communications
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Synthetic (glyco-)peptides of the homophilic recognition domain of E-cadherin lead to increased E-cadherin mRNA synthesis and are inductors of cell d…

2010

E-cadherin is one of the critical molecules involved in the metastatic process in many types of cancer. Once combined, E-cadherin exceeds the amount of membranous E-cadherin on the cellular surface by activation of intracellular signaling cascades. Studies on transformed keratinocytes of the HaCat cell line showed induction of differentiation by synthetical partial structures of the homophilic binding region of E-cadherin. The knowledge of effects in lung cancer cells is sparse. Therefore, the effects in primary lung cancer cell lines were investigated. Four primary lung cancer cell lines were incubated for 3, 6, 12, 15, 18, and 24h with synthetic partial structures (peptide and glycopeptid…

Lung NeoplasmsCell SurvivalCellular differentiationCellBiologyPathology and Forensic Medicinechemistry.chemical_compoundCell Line TumorExtracellularmedicineHumansRNA MessengerReverse Transcriptase Polymerase Chain ReactionCadherinGlycopeptidesCell DifferentiationSodium butyrateCell BiologyCadherinsImmunohistochemistryMolecular biologyProtein Structure TertiaryCell biologymedicine.anatomical_structurechemistryTumor progressionCell cultureIntracellularPathology - Research and Practice
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Vezatin, a novel transmembrane protein, bridges myosin VIIA to the cadherin-catenins complex

2000

International audience; Defects in myosin VIIA are responsible for deafness in the human and mouse. The role of this unconventional myosin in the sensory hair cells of the inner ear is not yet understood. Here we show that the C-terminal FERM domain of myosin VIIA binds to a novel transmembrane protein, vezatin, which we identi®ed by a yeast two-hybrid screen. Vezatin is a ubiquitous protein of adherens cell±cell junctions, where it interacts with both myosin VIIA and the cadherin±catenins complex. Its recruitment to adherens junctions implicates the C-terminal region of a-catenin. Taken together, these data suggest that myosin VIIA, anchored by vezatin to the cadherin±catenins complex, cre…

MESH: Cytoskeletal ProteinsMESH: alpha CateninStereocilia (inner ear)[SDV]Life Sciences [q-bio]MESH: Amino Acid SequenceDeafnessMESH: CadherinsMiceMESH: Protein Structure Tertiary0302 clinical medicine[SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseasesMyosinMESH: Hair Cells AuditoryMESH: AnimalsCytoskeleton0303 health sciencesFERM domainGeneral NeuroscienceMESH: Alternative SplicingArticlesCadherinsCell biologymedicine.anatomical_structureIntercellular Junctions[SDV.MP]Life Sciences [q-bio]/Microbiology and ParasitologyMyosin VIIaHair cellMESH: Membrane ProteinsMESH: DyneinsProtein BindingMESH: MutationMacromolecular SubstancesMolecular Sequence DataMESH: Deafnessmacromolecular substancesBiologyIn Vitro TechniquesMyosinsGeneral Biochemistry Genetics and Molecular BiologyCell LineAdherens junction03 medical and health sciencesHair Cells Auditorymedicineotorhinolaryngologic diseasesAnimalsHumansMESH: Myosin VIIaMESH: Protein BindingAmino Acid SequenceMolecular BiologyMESH: Mice030304 developmental biologyMESH: In Vitro TechniquesMESH: Molecular Sequence DataMESH: HumansGeneral Immunology and MicrobiologyCadherinDyneinsMembrane ProteinsMESH: Macromolecular SubstancesMESH: MyosinsActin cytoskeleton[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/BacteriologyProtein Structure TertiaryMESH: Cell LineAlternative SplicingCytoskeletal ProteinsMutationsense organs030217 neurology & neurosurgeryalpha Catenin[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyMESH: Intercellular Junctions
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Detachment of Chain-Forming Neuroblasts by Fyn-Mediated Control of cell–cell Adhesion in the Postnatal Brain

2018

In the rodent olfactory system, neuroblasts produced in the ventricular-subventricular zone of the postnatal brain migrate tangentially in chain-like cell aggregates toward the olfactory bulb (OB) through the rostral migratory stream (RMS). After reaching the OB, the chains are dissociated and the neuroblasts migrate individually and radially toward their final destination. The cellular and molecular mechanisms controlling cell–cell adhesion during this detachment remain unclear. Here we report that Fyn, a nonreceptor tyrosine kinase, regulates the detachment of neuroblasts from chains in the male and female mouse OB. By performing chemical screening andin vivoloss-of-function and gain-of-f…

Male0301 basic medicineanimal structuresRostral migratory streamNerve Tissue ProteinsProto-Oncogene Proteins c-fynAdherens junctionMice03 medical and health sciencesFYNNeural Stem CellsNeuroblastCell MovementCell AdhesionmedicineAnimalsCell adhesionResearch ArticlesChemistryGeneral NeurosciencefungiBrainCateninsCadherinsDAB1Granule cellOlfactory BulbOlfactory bulbCell biology030104 developmental biologymedicine.anatomical_structurenervous systemGene Knockdown Techniquesembryonic structuresFemaleThe Journal of Neuroscience
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Deregulation of ARID1A, CDH1, cMET and PIK3CA and target-related microRNA expression in gastric cancer.

2015

Genetic and epigenetic alterations play an important role in gastric cancer (GC) pathogenesis. Aberrations of the phosphatidylinositol-3-kinase signaling pathway are well described. However, emerging genes have been described such as, the chromatin remodeling gene ARID1A. Our aim was to determine the expression levels of four GC-related genes, ARID1A, CDH1, cMET and PIK3CA, and 14 target-related microRNAs (miRNAs). We compared mRNA and miRNA expression levels among 66 gastric tumor and normal adjacent mucosa samples using quantitative real-time reverse transcription PCR. Moreover, ARID1A, cMET and PIK3CA protein levels were assessed by immunohistochemistry (IHC). Finally, gene and miRNAs as…

MaleARID1AClass I Phosphatidylinositol 3-KinasesReal-Time Polymerase Chain ReactionCDH1Epigenesis GeneticPhosphatidylinositol 3-KinasesAntigens CDStomach NeoplasmsGene expressionmicroRNAmedicineBiomarkers TumorHumansRNA MessengerAgedbiologyReverse Transcriptase Polymerase Chain ReactionGene Expression Profilinggastric cancerCancerNuclear ProteinsbiomarkersMiddle AgedProto-Oncogene Proteins c-metmedicine.diseaseCadherinsMolecular biologyImmunohistochemistryChromatinGene expression profilingReverse transcription polymerase chain reactionDNA-Binding ProteinsGene Expression Regulation NeoplasticMicroRNAsReal-time polymerase chain reactionmicrorna expressionOncologyGastric Mucosabiology.proteingene expressionFemaleTranscription FactorsResearch PaperOncotarget
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rs629301 CELSR2 polymorphism confers a ten-year equivalent risk of critical stenosis assessed by coronary angiography

2021

Abstract Background and aims Novel genetic determinants associated with coronary artery disease (CAD) have been discovered by genome wide association studies. Variants encompassing the CELSR2- PSRC1-SORT1 gene cluster have been associated with CAD. This study is aimed to investigate the rs629301 polymorphism association with the extent of CAD evaluated by coronary angiography (CAG), and to evaluate its associations with an extensive panel of lipid and lipoprotein measurements in a large Italian cohort of 2429 patients. Methods and results The patients were collected by four Intensive Care Units located in Palermo and Verona (Italy). Clinical Records were filed, blood samples were collected,…

MaleApolipoprotein ETime FactorsApolipoprotein BCoronary StenosiEndocrinology Diabetes and MetabolismMedicine (miscellaneous)Genome-wide association study030204 cardiovascular system & hematologyCoronary AngiographyCoronary artery diseaseSeverity of Illness IndexGastroenterologyCoronary artery disease0302 clinical medicineRisk FactorsGenotypeAge FactorNutrition and DieteticsbiologyGene polymorphismAge FactorsSingle NucleotideLipidMiddle AgedCadherinsPrognosisLipidsApolipoproteinPhenotypeItalyFemalelipids (amino acids peptides and proteins)Cardiology and Cardiovascular Medicinemedicine.medical_specialty030209 endocrinology & metabolismRisk AssessmentPolymorphism Single Nucleotide03 medical and health sciencesPredictive Value of TestsIntensive careInternal medicinemedicineHumansGenetic Predisposition to DiseasePolymorphismGenetic Association StudiesAgedbusiness.industryCoronary StenosisBiomarkerOdds ratiomedicine.diseaseSortilinApolipoproteinsbiology.proteinGene polymorphismbusinessBiomarkersNutrition, Metabolism and Cardiovascular Diseases
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Genome-wide association scan of quantitative traits for attention deficit hyperactivity disorder identifies novel associations and confirms candidate…

2008

Contains fulltext : 70192.pdf (Publisher’s version ) (Closed access) Attention deficit hyperactivity disorder (ADHD) is a complex condition with environmental and genetic etiologies. Up to this point, research has identified genetic associations with candidate genes from known biological pathways. In order to identify novel ADHD susceptibility genes, 600,000 SNPs were genotyped in 958 ADHD proband-parent trios. After applying data cleaning procedures we examined 429,981 autosomal SNPs in 909 family trios. We generated six quantitative phenotypes from 18 ADHD symptoms to be used in genome-wide association analyses. With the PBAT screening algorithm, we identified 2 SNPs, rs6565113 and rs5526…

MaleCandidate geneGenetics and epigenetic pathways of disease [NCMLS 6]2804 Cellular and Molecular NeuroscienceMedizinGenome-wide association studyNeuroinformatics [DCN 3]Genome2738 Psychiatry and Mental Health0302 clinical medicinePerception and Action [DCN 1]Cluster AnalysisGenetics(clinical)Genetics (clinical)Genetics0303 health sciences10058 Department of Child and Adolescent PsychiatryCadherinsPedigreePsychiatry and Mental healthFemaleFunctional Neurogenomics [DCN 2]CDH13AlgorithmsGenetic Markers2716 Genetics (clinical)GenotypeQuantitative Trait Loci610 Medicine & healthSingle-nucleotide polymorphismBiologyQuantitative trait locusPolymorphism Single NucleotideMental health [NCEBP 9]Genetic determinismGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesCellular and Molecular NeuroscienceCognitive neurosciences [UMCN 3.2]medicineADHDAttention deficit hyperactivity disorderHumansGenetic Predisposition to Diseaseddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und JugendaltersGene030304 developmental biologyProbabilityModels GeneticGenome Humancandidate genefamily-based associationmedicine.diseaseIntronsHaplotypesGenetic defects of metabolism [UMCN 5.1]Attention Deficit Disorder with Hyperactivitygenome-wide association030217 neurology & neurosurgeryGenome-Wide Association StudyAmerican Journal of Medical Genetics Part B: Neuropsychiatric Genetics
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Loss of desmoglein 2 suggests essential functions for early embryonic development and proliferation of embryonal stem cells.

2002

Summary Desmoglein 2 (Dsg2) is a Ca 2+ -dependent adhesion molecule of desmosomes and is synthesized in all desmosome-bearing tissues from their earliest appearance onward. To examine the function of Dsg2, its gene was inactivated by homologous recombination in embryonal stem (ES) cells for the generation of knockout mice. DSG2 −/− mice and a considerable number of DSG2 +/− mice died at or shortly after implantation. On the other hand, DSG2 −/− blastocysts developed an apparently normal trophectoderm layer, the first tissue known to produce desmosomes, and hatched properly. Immunofluorescence analyses of these blastocysts showed, however, that the distribution of the desmosomal plaque prote…

MaleHistologyPopulationImmunoblottingFluorescent Antibody TechniqueBiologyPathology and Forensic MedicineAdherens junctionEmbryonic and Fetal DevelopmentMiceDesmosomemedicineInner cell massAnimalseducationbeta CateninMice Knockouteducation.field_of_studyDesmoglein 2CadherinCell growthStem CellsGap JunctionsCell BiologyGeneral MedicineCadherinsEmbryo MammalianEmbryonic stem cellCell biologyCytoskeletal ProteinsMicroscopy Electronmedicine.anatomical_structureBlastocystDesmoplakinsImmunologyTrans-ActivatorsFemaleStem cellDesmogleinsEuropean journal of cell biology
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