Search results for " catenin"

showing 10 items of 57 documents

Cleavage of desmoglein 3 can explain its depletion from keratinocytes in pemphigus vulgaris.

2008

We have previously demonstrated that serum of patients with pemphigus vulgaris induces reduction of desmoglein 3 (Dsg3) half-life in keratinocytes (FEBS Lett 2006: 580: 3276). This phenomenon seems to occur as a consequence of the progressive depletion of Dsg3 from desmosomes. Here we reported that reduction of full-length Dsg3 may be due to its progressive cleavage, leading to the formation of two fragmentation products with apparent molecular masses of about 60 kDa (fragment 1) and 70 kDa (fragment 2), as revealed by Western blotting. Unexpectedly, analysis of fragmentation pattern suggested cleavage to occur intracellularly. Consistently, fragment 1 was shed and localized within the cyto…

KeratinocytesPathologymedicine.medical_specialtyBlotting WesternPlakoglobinDermatologyBiologyCleavage (embryo)BiochemistryCell LinemedicineHumanseducationMolecular Biologyeducation.field_of_studyDesmoglein 3Desmoglein 1Pemphigus vulgarisBlood Proteinsmedicine.diseaseMolecular biologyBlotPemphigusmedicine.anatomical_structureDesmoplakinsDesmoglein 1Desmoglein 3gamma CateninKeratinocytePemphigusExperimental dermatology
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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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Multifaceted roles of GSK-3 and Wnt/beta-catenin in hematopoiesis and leukemogenesis: opportunities for therapeutic intervention

2013

Glycogen synthase kinase-3 (GSK-3) is well documented to participate in a complex array of critical cellular processes. It was initially identified in rat skeletal muscle as a serine/threonine kinase that phosphorylated and inactivated glycogen synthase. This versatile protein is involved in numerous signaling pathways that influence metabolism, embryogenesis, differentiation, migration, cell cycle progression and survival. Recently, GSK-3 has been implicated in leukemia stem cell pathophysiology and may be an appropriate target for its eradication. In this review, we will discuss the roles that GSK-3 plays in hematopoiesis and leukemogenesis as how this pivotal kinase can interact with mul…

MAPK/ERK pathwayCancer ResearchBeta-catenintherapy resistanceCarcinogenesisWnt ProteinReviewmacromolecular substancesAkt; GSK-3; leukemia stem cells; targeted therapy; therapy resistance; Wnt/b-cateninWNTGlycogen Synthase Kinase 3GSK-3PTENAnimalsHumansHematopoiesiProtein kinase BCarcinogenesiPI3K/AKT/mTOR pathwaybeta CateninWnt/β-cateninGSK-3LeukemiabiologyAnimalKinaseAktleukemia stem cellWnt signaling pathwayHematologyleukemia stem cellstargeted therapy3. Good healthHematopoiesisWnt ProteinsAnesthesiology and Pain MedicineOncologyCancer researchbiology.proteinWnt/b-cateninHuman
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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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M2 Macrophages Activate WNT Signaling Pathway in Epithelial Cells: Relevance in Ulcerative Colitis

2013

Macrophages, which exhibit great plasticity, are important components of the inflamed tissue and constitute an essential element of regenerative responses. Epithelial Wnt signalling is involved in mechanisms of proliferation and differentiation and expression of Wnt ligands by macrophages has been reported. We aim to determine whether the macrophage phenotype determines the expression of Wnt ligands, the influence of the macrophage phenotype in epithelial activation of Wnt signalling and the relevance of this pathway in ulcerative colitis. Human monocyte-derived macrophages and U937-derived macrophages were polarized towards M1 or M2 phenotypes and the expression of Wnt1 and Wnt3a was analy…

MaleFarmacologiaBeta-cateninMedicinaCellular differentiationlcsh:MedicineWnt1 ProteinProto-Oncogene Proteins c-mycAntigens CDWnt3A ProteinHumanslcsh:ScienceWnt Signaling Pathwaybeta CateninMultidisciplinarybiologyU937 cellMacrophageslcsh:RWnt signaling pathwayLGR5Cell DifferentiationLRP5U937 CellsWnt3A ProteinEnterocytesAparell digestiu Malaltiesbiology.proteinCancer researchColitis UlcerativeFemalelcsh:QEnterocyte differentiationCaco-2 CellsResearch ArticlePLoS ONE
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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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β-Catenin in dendritic cells exerts opposite functions in cross-priming and maintenance of CD8+ T cells through regulation of IL-10

2015

Recent studies have demonstrated that β-catenin in DCs serves as a key mediator in promoting both CD4(+) and CD8(+) T-cell tolerance, although how β-catenin exerts its functions remains incompletely understood. Here we report that activation of β-catenin in DCs inhibits cross-priming of CD8(+) T cells by up-regulating mTOR-dependent IL-10, suggesting blocking β-catenin/mTOR/IL-10 signaling as a viable approach to augment CD8(+) T-cell immunity. However, vaccination of DC-β-catenin(-/-) (CD11c-specific deletion of β-catenin) mice surprisingly failed to protect them against tumor challenge. Further studies revealed that DC-β-catenin(-/-) mice were deficient in generating CD8(+) T-cell immunit…

Mice KnockoutImmunity CellularMultidisciplinaryTOR Serine-Threonine KinasesPriming (immunology)Dendritic CellsBiologyBiological SciencesCD8-Positive T-LymphocytesCancer VaccinesCell biologyInterleukin-10Interleukin 10MiceMediatorImmunityCateninNeoplasmsImmunologyCytotoxic T cellAnimalsPI3K/AKT/mTOR pathwayCD8beta Catenin
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Expression profile of components of the β-catenin destruction complex in oral dysplasia and oral cancer

2021

Background Oral cancer represents the sixth most common cancer in the world and is associated with 40-50% survival at 5 years. Within oral malignancies, oral squamous cell carcinoma (OSCC) is commonly preceded by potentially malignant lesions, which, according to histopathological criteria, are referred to as oral dysplasia and their diagnosis are associated with higher rates of malignant transformation towards cancer. We recently reported that aberrant activation of the Wnt/β‑catenin pathway is due to overexpression of Wnt ligands in oral dysplasia. However, the expression of other regulators of this pathway, namely components of the β-catenin destruction complex has not been explored in o…

Mild DysplasiaAdenomatous polyposis coliMalignant transformationmalignantOral Cancer and Potentially malignant disordersHumansMedicineWnt Signaling PathwayGeneral DentistryGSK3Bbeta CateninUNESCO:CIENCIAS MÉDICASOral DysplasiaAxin Signaling ComplexGlycogen Synthase Kinase 3 betabiologySquamous Cell Carcinoma of Head and Neckbusiness.industryResearchWnt signaling pathwayCancerfloor of the mouthmedicine.diseasestomatognathic diseasesOtorhinolaryngologyCateninCarcinoma Squamous Cellbiology.proteinCancer researchMouth NeoplasmsepidemiologySurgerybenignbusinessMedicina Oral Patología Oral y Cirugia Bucal
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Nemo regulates cell dynamics and represses the expression of miple, a midkine/pleiotrophin cytokine, during ommatidial rotation

2013

AbstractOmmatidial rotation is one of the most important events for correct patterning of the Drosophila eye. Although several signaling pathways are involved in this process, few genes have been shown to specifically affect it. One of them is nemo (nmo), which encodes a MAP-like protein kinase that regulates the rate of rotation throughout the entire process, and serves as a link between core planar cell polarity (PCP) factors and the E-cadherin–β-catenin complex. To determine more precisely the role of nmo in ommatidial rotation, live-imaging analyses in nmo mutant and wild-type early pupal eye discs were performed. We demonstrate that ommatidial rotation is not a continuous process, and …

Ommatidial rotationRotationCellMutantEyePleiotrophinModels BiologicalArticleImaging Three-DimensionalmedicineAnimalsDrosophila ProteinsMipleProtein kinase AMolecular BiologyGenetic Association Studiesbeta CateninBody PatterningMidkineLive-imagingbiologyGene Expression ProfilingMidkineGene Expression Regulation DevelopmentalCell BiologyCadherinsPhenotypeMolecular biologyCell biologyDrosophila melanogasterPhenotypemedicine.anatomical_structureImaginal DiscsNemoMutationbiology.proteinCytokinesDrosophila eyeFemaleGene expressionMitogen-Activated Protein KinasesSignal transductionOmmatidial rotationDevelopmental BiologyDevelopmental Biology
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New molecular targets for the treatment of osteoarthritis.

2009

Osteoarthritis (OA) is a chronic degenerative joint disorder characterized by destruction of the articular cartilage, subchondral bone alterations and synovitis. Current treatments are focused on symptomatic relief but they lack efficacy to control the progression of this disease which is a leading cause of disability. Therefore, the development of effective disease-modifying drugs is urgently needed. Different initiatives are in progress to define the molecular mechanisms involved in the initiation and progression of OA. These studies support the therapeutic potential of pathways relevant in joint metabolism such as Wnt/beta-catenin, discoidin domain receptor 2 or proteinase-activated rece…

OsteoarthritisBioinformaticsBiochemistryModels BiologicalSynovitismicroRNAOsteoarthritismedicineAnimalsHumansbeta CateninPharmacologybusiness.industryCartilageADAMTSWnt signaling pathwayGenetic Therapymedicine.diseaseSymptomatic reliefWnt ProteinsMicroRNAsmedicine.anatomical_structureFrzbImmunologyCytokinesIntercellular Signaling Peptides and ProteinsbusinessBiochemical pharmacology
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