Search results for "Cell adhesion"

showing 10 items of 812 documents

Author response: The fibronectin synergy site re-enforces cell adhesion and mediates a crosstalk between integrin classes

2016

FibronectinCrosstalk (biology)biologyChemistryIntegrinbiology.proteinCell adhesionCell biology
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Modified Silk with Cell-Adhesive and Non-Thrombogenic Properties as a Tissue Engineering Substrate

2016

IntroductionReplacement of damaged tissue is nowadays an aim of tissue engineering. This technique involves the use of porous or fibrous structures – the so-called scaffolds – that support the colonization with the desired cell type and which are degraded after fulfilling their temporary supporting function. Basic requirements for the prevailing materials used in this field are nontoxicity, low immunogenicity and cell-adhesiveness. Furthermore blood-contacting devices should exhibit low thrombogenicity.The biopolymer silk, mainly consisiting of the protein silk fibroin, matches some of these criteria but bare silk does not facilitate cellular adhesion and growth and unfortunately the materi…

FibronectinSILKMaterials scienceTissue engineeringbiologyBiophysicsbiology.proteinThrombogenicityBiomaterialFibroinAdhesionCell adhesionBiomedical engineeringQatar Foundation Annual Research Conference Proceedings Volume 2016 Issue 1
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Integrins α5β1, αvβ1, and αvβ6 Collaborate in Squamous Carcinoma Cell Spreading and Migration on Fibronectin

2000

Abstract The expression of αvβ6 fibronectin/tenascin receptor integrin is induced in malignant transformation of oral epithelium. In this study, we demonstrate the contribution of αvβ6 as well as other fibronectin receptor integrins in squamous cell carcinoma (SCC) cell adhesion and migration. Of 11 SCC cell lines isolated from the head and neck area, 8 (73%) expressed αvβ6 integrin on the cell surface. Three cell lines were chosen for further functional experiments: 1 with relatively high, 1 with moderate, and 1 with minimal surface expression of αvβ6 integrin. In addition to αvβ6, all 3 cell lines expressed α5β1 and αvβ1 fibronectin receptor integrins. Function-blocking experiments with i…

Fibronectinstomatognathic diseasesbiologyCell adhesion moleculeIntegrinbiology.proteinCell migrationCell BiologyCell adhesionReceptorCollagen receptorCell biologySquamous carcinomaExperimental Cell Research
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Non-syndromic Mitral Valve Dysplasia Mutation Changes the Force Resilience and Interaction of Human Filamin A

2018

International audience; Filamin A (FLNa), expressed in endocardial endothelia during fetal valve morphogenesis, is key in cardiac development. Missense mutations in FLNa cause non-syndromic mitral valve dysplasia (FLNA-MVD). Here, we aimed to reveal the currently unknown underlying molecular mechanism behind FLNA-MVD caused by the FLNa P637Q mutation. The solved crystal structure of the FLNa3-5 P637Q revealed that this mutation causes only minor structural changes close to mutation site. These changes were observed to significantly affect FLNa's ability to transmit cellular force and to interact with its binding partner. The performed steered molecular dynamics simulations showed that signi…

Filamins[SDV]Life Sciences [q-bio]Protein Tyrosine Phosphatase Non-Receptor Type 12Heart Valve DiseasesMutation MissenseMorphogenesisProtein tyrosine phosphataseMolecular Dynamics SimulationBiologyFilaminta3111ArticleFLNA-MVD03 medical and health sciencessteered molecular dynamics simulationsStructural Biologymechanical forcesmedicineHumansMitral valve prolapseMissense mutationFLNAmolekyylidynamiikkasydäntauditCell adhesionMolecular Biology030304 developmental biologyX-ray crystallography0303 health sciencesBinding Sites030302 biochemistry & molecular biologyta1182filamiinitprotein tyrosine phosphatase 12medicine.disease3. Good healthCell biologyFilamin AMutation (genetic algorithm)cardiovascular systemMitral Valveproteiinitmitral valve prolapseröntgenkristallografiaProtein Binding
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β1-Integrin Cytoplasmic Subdomains Involved in Dominant Negative Function

1998

The beta1-integrin cytoplasmic domain consists of a membrane proximal subdomain common to the four known isoforms ("common" region) and a distal subdomain specific for each isoform ("variable" region). To investigate in detail the role of these subdomains in integrin-dependent cellular functions, we used beta1A and beta1B isoforms as well as four mutants lacking the entire cytoplasmic domain (beta1TR), the variable region (beta1COM), or the common region (beta1 deltaCOM-B and beta1 deltaCOM-A). By expressing these constructs in Chinese hamster ovary and beta1 integrin-deficient GD25 cells (Wennerberg et al., J Cell Biol 132, 227-238, 1996), we show that beta1B, beta1COM, beta1 deltaCOM-B, a…

Gene isoformTalinCytoplasmProtein ConformationIntegrinMolecular Sequence DataCHO CellsIntegrin alpha5Platelet Membrane GlycoproteinsArticleFocal adhesionchemistry.chemical_compoundMiceAntigens CDCricetinaeCell AdhesionAnimalsActininAmino Acid SequencePhosphorylationCell adhesionMolecular BiologyBinding SitesbiologyCell adhesion moleculeChinese hamster ovary cellIntegrin beta1Integrin beta3Tyrosine phosphorylationCell BiologyIntegrin alphaVProtein-Tyrosine KinasesRecombinant ProteinsCell biologyFibronectinsFibronectinchemistryFocal Adhesion Kinase 1Focal Adhesion Protein-Tyrosine KinasesMutationbiology.proteinCell Adhesion MoleculesSignal Transduction
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Targeting Aberrant Ncam (neural cell adhesion molecule; CD56) Expression in Acute Myeloid Leukemia

2015

Abstract Background Acute myeloid leukemia (AML) is a heterogeneous disease of the hematopoietic progenitor cell driven by the subsequent acquisition of genetic alterations. Approximately 20% of AML patients show strong expression of CD56 (neural cell adhesion molecule; NCAM). Expression of NCAM is associated with poor overall survival; however, the functional role of aberrant NCAM expression has not been investigated to date. The goal of this study is to examine the biological role of NCAM in AML and to explore whether NCAM represents a potential therapeutic target. Results In order to evaluate the clinical significance of elevated NCAM expression in AML, we screened a panel of human cell …

Gene knockdownChemistryCell growthImmunologyCellMyeloid leukemiaCell BiologyHematologymedicine.diseaseBiochemistryLeukemiamedicine.anatomical_structurenervous systemCell cultureCancer researchmedicineNeural cell adhesion moleculeK562 cellsBlood
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Specific phosphorylation of proteins in pore complex-laminae from the sponge Geodia cydonium by the homologous aggregation factor and phorbol ester. …

1987

We have recently shown that the aggregation factor (AF) from the sponge Geodia cydonium stimulates DNA synthesis in quiescent, dissociated cells from the same organism; this event was correlated with the release of the two second messengers: inositol trisphosphate and diacylglycerol. Here we describe that after binding of the AF to the plasma membrane-bound aggregation receptor, a rapid and drastic increase in the incorporation of 32Pi into a series of proteins in the pore complex-lamina fraction occurs. Addition of the tumor promoter, 12-O-tetradecanoylphorbol-13-acetate, to quiescent cells resulted in a similar stimulation of phosphorylation of nuclear proteins. Among them we have selecte…

General Immunology and MicrobiologyDNA synthesisGeneral NeuroscienceProteinsInositol trisphosphateDNA topoisomerase II activityBiologyGeneral Biochemistry Genetics and Molecular BiologyCell aggregationPoriferachemistry.chemical_compoundDNA Topoisomerases Type IIBiochemistrychemistrySecond messenger systemPhosphorylationAnimalsSignal transductionPhosphorylationMolecular BiologyCell Adhesion MoleculesProtein kinase CProtein Kinase CResearch ArticleCell Aggregation
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Cohen syndrome is associated with major glycosylation defects

2014

International audience; Cohen syndrome (CS) is a rare autosomal recessive disorder with multisytemic clinical features due to mutations in the VPS13B gene, which has recently been described encoding a mandatory membrane protein involved in Golgi integrity. As the Golgi complex is the place where glycosylation of newly synthesized proteins occurs, we hypothesized that VPS13B deficiency, responsible of Golgi apparatus disturbance, could lead to glycosylation defects and/or mysfunction of this organelle, and thus be a cause of the main clinical manifestations of CS. The glycosylation status of CS serum proteins showed a very unusual pattern of glycosylation characterized by a significant accum…

GlycanGlycosylationGlycosylationEndosomeDevelopmental Disabilities[SDV]Life Sciences [q-bio]Vesicular Transport ProteinsGolgi ApparatusFingers03 medical and health scienceschemistry.chemical_compoundsymbols.namesake0302 clinical medicineAntigens CDIntellectual DisabilityMyopiaGeneticsHumansObesityMolecular BiologyGenetics (clinical)030304 developmental biology0303 health sciencesbiology[ SDV ] Life Sciences [q-bio]Retinal DegenerationTransferrinGeneral MedicineFibroblastsBrefeldin AGolgi apparatusIntercellular Adhesion Molecule-1Cell biologyVPS13BchemistryMembrane proteinBiochemistryMicrocephalysymbolsO-linked glycosylationbiology.proteinMuscle HypotoniaElectrophoresis Polyacrylamide GelRNA InterferenceCell Adhesion Molecules030217 neurology & neurosurgery
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Establishment of a quantitative RT-pCR for detection of vascular cell adhesion molecule-1 transcripts in endothelial cells after stimulation with adv…

1998

Advanced glycation endproducts (AGE) are supposed to increase endothelial expression of adhesion molecules like vascular cell adhesion molecule-1 (VCAM-1) by inducing an intracellular stress with subsequent activation of nuclear transcription factor NF-kappa-B. Quantitative analysis of VCAM-1-transcription has not been demonstrated concerning this topic. Thus, the aim of this study was to establish quantitative reverse transcription polymerase chain reaction (RT-PCR) assays using a spacer gene in order to measure the amounts of specific mRNA for VCAM-1 in human umbilical vein endothelial cells (HUVEC) which were stimulated with AGE-albumin (AGE-BSA). A recombinant RNA-standard was synthesiz…

Glycation End Products AdvancedCell adhesion moleculeReverse Transcriptase Polymerase Chain ReactionCellEndothelial CellsReproducibility of ResultsVascular Cell Adhesion Molecule-1Serum Albumin BovineGeneral MedicineCell cycleBiologyUmbilical veinCell biologyReverse transcription polymerase chain reactionReal-time polymerase chain reactionmedicine.anatomical_structureGeneticsmedicineHumansEndothelium VascularRNA MessengerCell adhesionIntracellularCells CulturedInternational journal of molecular medicine
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The influence of advanced glycation endproducts (AGE) on the expression of human endothelial adhesion molecules.

1998

Advanced glycation endproducts (AGEs) possibly play a dominant role in the pathogenesis of macrovascular disease in diabetes. Recent studies could demonstrate that glycated albumin (AGE-BSA) was able to stimulate vascular cell adhesion molecule-1 (VCAM.1) on endothelial cells. The aim of this study was to find out if AGE-BSA was not only able to enhance the expression of vascular cell adhesion molecule-1, but also of intercellular adhesion molecule-1 (ICAM-1) and E-Selectin on human endothelial cells. Stimulation of endothelial cells with AGE-BSA for six hours predominantly increased the expression of VCAM-1, but ICAM-1 and E-Selectin were also upregulated as shown by immunoilluminometric a…

Glycation End Products AdvancedTranscription GeneticEndocrinology Diabetes and MetabolismIntercellular Adhesion Molecule-1Gene ExpressionVascular Cell Adhesion Molecule-1BiologyPolymerase Chain ReactionEndocrinologyGlycationAlbuminsE-selectinInternal MedicinemedicineHumansCell adhesionMacrovascular diseaseDose-Response Relationship DrugCell adhesion moleculeGeneral MedicineAdhesionmedicine.diseaseIntercellular Adhesion Molecule-1ImmunohistochemistryEndothelial stem cellImmunologyLuminescent Measurementsbiology.proteinCancer researchEndothelium VascularE-SelectinExperimental and clinical endocrinologydiabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
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