Search results for "Integrin alpha3"

showing 4 items of 4 documents

BB0172, a Borrelia burgdorferi Outer Membrane Protein That Binds Integrin Α3Β1

2013

ABSTRACT Lyme disease is a multisystemic disorder caused by Borrelia burgdorferi infection. Upon infection, some B. burgdorferi genes are upregulated, including members of the microbial surface components recognizing adhesive matrix molecule (MSCRAMM) protein family, which facilitate B. burgdorferi adherence to extracellular matrix components of the host. Comparative genome analysis has revealed a new family of B. burgdorferi proteins containing the von Willebrand factor A (vWFA) domain. In the present study, we characterized the expression and membrane association of the vWFA domain-containing protein BB0172 by using in vitro transcription/translation systems in the presence of microsomal …

Models MolecularProtein familyMolecular Sequence DataIntegrinBiologyModels BiologicalMicrobiologyBiotecnologiaMicrobiologyAmino Acid SequenceBorrelia burgdorferiAdhesins BacterialMolecular BiologyIntegrin alpha3beta1Borrelia Burgdorferi InfectionProteïnes de membranaIntegrin alpha3beta1Articlesbiology.organism_classificationCell biologyBacterial adhesinBorrelia burgdorferibiology.proteinMSCRAMMBacterial outer membraneSequence AlignmentBacterial Outer Membrane ProteinsProtein Binding
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ICAM-1 and α3β1 expression by bronchial epithelial cells and theirin vitromodulation by inflammatory and anti-inflammatory mediators

2000

Background: Adhesion molecules are involved in inflammatory and repair processes of the bronchial epithelium. ICAM-1 is mainly involved in inflammatory reactions, whereas integrins, such as α3β1, are mainly involved in repair processes. Methods: Using bronchial biopsies from 10 asthmatics and eight controls, we first evaluated by immunohistochemistry expression of α3β1 and ICAM-1 in intact and damaged epithelium. Then, using the human pulmonary epithelial cell line WI-26 VA, we studied, by flow-cytometry, the modulation of ICAM-1 and α3β1 expression, and, by ELISA, the release of fibronectin by proinflammatory cytokines, such as IL-5, and anti-inflammatory cytokines, such as IL-4, TGF-β, an…

AdultIntegrinsAdolescentBiopsyImmunologyIntegrinIntercellular Adhesion Molecule-1BronchiEnzyme-Linked Immunosorbent AssayInflammationRespiratory MucosaCell LineProinflammatory cytokineTransforming Growth Factor betamedicineHumansImmunology and AllergyAgedInflammationICAM-1Epidermal Growth FactorbiologyCell adhesion moleculeIntegrin alpha3beta1Epithelial CellsMiddle AgedFlow CytometryIntercellular Adhesion Molecule-1Molecular biologyAsthmaEpitheliumFibronectinsFibronectinmedicine.anatomical_structureImmunologybiology.proteinCytokinesInterleukin-4medicine.symptomAllergy
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Transcriptome Analysis of Ullrich Congenital Muscular Dystrophy Fibroblasts Reveals a Disease Extracellular Matrix Signature and Key Molecular Regula…

2015

Background Collagen VI related myopathies encompass a range of phenotypes with involvement of skeletal muscle, skin and other connective tissues. They represent a severe and relatively common form of congenital disease for which there is no treatment. Collagen VI in skeletal muscle and skin is produced by fibroblasts. Aims & Methods In order to gain insight into the consequences of collagen VI mutations and identify key disease pathways we performed global gene expression analysis of dermal fibroblasts from patients with Ullrich Congenital Muscular Dystrophy with and without vitamin C treatment. The expression data were integrated using a range of systems biology tools. Results were validat…

Pathologymedicine.medical_specialtyUllrich congenital muscular dystrophyIntegrin alpha3Integrinlcsh:MedicineDown-RegulationAscorbic AcidBiologyMuscular DystrophiesExtracellular matrixLamininCollagen VImedicineCell AdhesionHumansGene Regulatory NetworksMuscular dystrophylcsh:ScienceWound HealingMultidisciplinarySclerosisGene Expression Profilinglcsh:RFibroblastsmedicine.diseaseMolecular biologyExtracellular MatrixUp-RegulationGene expression profilingMicroRNAsbiology.proteinlcsh:QWound healingResearch ArticleSignal Transduction
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Transcription of α2 Integrin Gene in Osteosarcoma Cells Is Enhanced by Tumor Promoters

1998

Integrin alpha2beta1 is a heterodimeric transmembrane receptor for collagens. In osteogenic cells the expression of alpha2beta1 integrin is induced by both Kirsten sarcoma virus and chemical transformation. The association of alpha2 integrin with transformed cell phenotype was studied further by testing the effects of two tumor promoters, 12-O-tetradecanoylphorbol 13-acetate (TPA) and okadaic acid (OA), on human MG-63 osteosarcoma cells. TPA, an activator of protein kinase C, increased the cell surface expression of alpha2 integrin and the corresponding mRNA levels. Nuclear run-on assays indicated that TPA activated the transcription of alpha2 integrin gene. TPA also slightly increased the …

IntegrinsTime FactorsTranscription GeneticIntegrin alpha3IntegrinIntegrin alpha2CD18Integrin alpha5CD49cCD49bCollagen receptorAntigens CDOkadaic AcidCell AdhesionTumor Cells CulturedHumansCollagenasesRNA MessengerOsteosarcomabiologyActivator (genetics)Integrin beta1Cell BiologyIntegrin alphaVBlotting NorthernFlow CytometryMolecular biologyUp-RegulationIntegrin alpha MCarcinogensbiology.proteinTetradecanoylphorbol AcetateIntegrin beta 6CollagenMatrix Metalloproteinase 1Experimental Cell Research
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