Search results for " adhesion"

showing 10 items of 980 documents

Hyaluronan-coated polybenzofulvene brushes as biomimetic materials

2016

Hyaluronic acid (HA) forms pericellular coats in many cell types that are involved in the early stages of cell adhesion by interacting with the CD44 receptor. Based on the largely recognized overexpression of the CD44 receptor in tumor tissues, a polybenzofulvene molecular brush has been enveloped into hyaluronan shells to obtain a tri-component polymer brush (TCPB) composed of intrinsically fluorescent backbones bearing nona(ethylene glycol) arms terminated with low molecular weight HA macromolecules. The nanoaggregates obtained in TCPB water dispersions were characterized on the basis of dimensions, zeta potential, and in vitro cell toxicity. This biomimetic multifunctional material beari…

polymer brushPolymers and PlasticsHyaluronic acidBiomedical EngineeringBioengineering02 engineering and technology010402 general chemistryPolymer brush01 natural sciencesBiochemistrychemistry.chemical_compoundHyaluronic acidPolymer chemistryZeta potentialCell adhesionPolymers and PlasticbiologyCD44polybenzofulveneOrganic Chemistry021001 nanoscience & nanotechnology0104 chemical scienceschemistrySettore CHIM/09 - Farmaceutico Tecnologico ApplicativoDrug deliverybiology.proteinBiophysics0210 nano-technologyEthylene glycolMacromolecule
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PMN membrane fluidity, cytosolic Ca2+ content and beta2-integrin pattern in vascular atherosclerotic disease

2010

polymorphonuclear leukocyte adhesion molecules atherosclerosis
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Activation of NF-kappaB and IL-8 by yersinia enterocolitica invasin protein is conferred by engagement of rac1 and MAP kinase cascades.

2003

International audience; Yersinia enterocolitica triggers activation of the nuclear factor (NF)-kappaB and production of the proinflammatory chemokine interleukin (IL)-8 in intestinal epithelial cells. This activation is due to adhesion of the bacteria via their outer membrane protein invasin to the host cells. Using Clostridium difficile toxins that specifically inactivate small GTPases, and transfection of inhibitory proteins of the Rho-GTPases, we demonstrate that Rac1, but not Cdc42 or Rho, is required for activation of NF-kappaB by invasin. Invasin activated the mitogen activated protein kinases (MAPK) p38 and c-Jun N-terminal protein kinase (JNK) but not extracellular signal regulated …

rac1 GTP-Binding ProteinMAP Kinase Kinase 4MAP Kinase Signaling SystemRNA Stability[SDV]Life Sciences [q-bio]ImmunologyMitogen-activated protein kinase kinasep38 Mitogen-Activated Protein KinasesMicrobiologyBacterial AdhesionMAP2K703 medical and health sciencesBacterial ProteinsVirologyHumansASK1RNA Messengerc-RafAdhesins Bacterialcdc42 GTP-Binding ProteinrhoB GTP-Binding ProteinYersinia enterocolitica030304 developmental biologyMitogen-Activated Protein Kinase Kinases0303 health sciencesbiologyMAP kinase kinase kinase030306 microbiologyInterleukin-8Cyclin-dependent kinase 2JNK Mitogen-Activated Protein KinasesNF-kappa BProtein kinase RMolecular biologyCell biologybiology.proteinCyclin-dependent kinase 9Mitogen-Activated Protein KinasesrhoA GTP-Binding ProteinHeLa CellsSignal Transduction
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Rac1-Regulated Endothelial Radiation Response Stimulates Extravasation and Metastasis That Can Be Blocked by HMG-CoA Reductase Inhibitors

2011

Radiotherapy (RT) plays a key role in cancer treatment. Although the benefit of ionizing radiation (IR) is well established, some findings raise the possibility that irradiation of the primary tumor not only triggers a killing response but also increases the metastatic potential of surviving tumor cells. Here we addressed the question of whether irradiation of normal cells outside of the primary tumor augments metastasis by stimulating the extravasation of circulating tumor cells. We show that IR exposure of human endothelial cells (EC), tumor cells (TC) or both increases TC-EC adhesion in vitro. IR-stimulated TC-EC adhesion was blocked by the HMG-CoA reductase inhibitor lovastatin. Glycyrr…

rac1 GTP-Binding ProteinPathologyCancer TreatmentToxicologyPolymerase Chain ReactionMetastasisMetastasisMiceCirculating tumor cellMolecular Cell BiologyBasic Cancer ResearchNeoplasm MetastasisMice Inbred BALB CMultidisciplinarybiologyChemistryQRTotal body irradiationPrimary tumorExtravasationOncologyMedicineElectrophoresis Polyacrylamide GelLovastatinE-SelectinWhole-Body IrradiationResearch Articlemedicine.drugDrugs and Devicesmedicine.medical_specialtyGenetic ToxicologyScienceBlotting WesternRadiation TherapyCardiovascular PharmacologyE-selectinCell AdhesionmedicineAnimalsHumansLovastatinCell adhesionBiologyDNA PrimersBase SequenceGlycyrrhizic Acidmedicine.diseaseCancer researchbiology.proteinHydroxymethylglutaryl-CoA Reductase InhibitorsExtravasation of Diagnostic and Therapeutic MaterialsPLoS ONE
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HMG-CoA reductase inhibitors (statins) as anticancer drugs (Review)

2005

Apart from their lipid lowering activity, HMG-CoA reductase inhibitors (statins) impair numerous cellular functions associated with metastasis, e.g. gene expression, angiogenesis, cell adhesion, cell motility and invasiveness. Furthermore, statins have impact on apoptotic cell death and modulate cellular susceptibility to cell killing by anticancer drugs and ionizing radiation. Part of the effects provoked by statins are due to the inhibition of the prenylation of low molecular weight GTPases, in particular Ras and Rho, which play key roles in signaling evoked by stimulation of cell surface receptors. C-terminal lipid modification of Ras/Rho GTPases is essential for their correct intracellu…

rho GTP-Binding ProteinsCancer ResearchCell DeathbiologyCell growthGTPaseCell killingOncologyBiochemistryPrenylationras GTPase-Activating ProteinsNeoplasmsRadiation IonizingHMG-CoA reductaseCell AdhesionCancer researchbiology.proteinHumansProtein prenylationHydroxymethylglutaryl-CoA Reductase InhibitorsNeoplasm MetastasisLipid modificationCell adhesionCell ProliferationInternational Journal of Oncology
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Mtlinteracts with members of Egfr signaling and cell adhesion genes in the Drosophila eye

2011

Mtl is a member of the Rho family of small GTPases in Drosophila. It was shown that Mtl is involved in planar cell polarity (PCP) establishment, together with other members of the same family like Cdc42, Rac1, Rac2 and RhoA. However, while Rac1, Rac2 and RhoA function downstream of Dsh in Fz/PCP signaling and upstream of a JNK cassette, Mtl and Cdc42 do not. To determine the functional context of Mtl during PCP establishment in the Drosophila eye, we performed a loss-of-function screen to search for dominant modifiers of a sev>Mtl rough eye phenotype. In addition, genetic interaction assays with candidate genes were also carried out. Our results show that Mtl interacts genetically with memb…

rho GTP-Binding ProteinsGeneticsOmmatidial rotationRHOAbiologyCytoskeleton organizationCell PolarityCDC42Cell biologyErbB ReceptorsPhenotypeInsect ScienceCell polarityCell Adhesionbiology.proteinAnimalsDrosophila ProteinsImmunoglobulin superfamilyDrosophilaCompound Eye ArthropodReceptors Invertebrate PeptideCell adhesionpsychological phenomena and processesDrosophila ProteinSignal TransductionFly
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Lovastatin inhibits Rho-regulated expression of E-selectin by TNFalpha and attenuates tumor cell adhesion.

2003

E-selectin mediated cell-cell adhesion plays an important role in inflammatory processes and extravasation of tumor cells. Tumor necrosis factor-alpha (TNF-alpha) induces E-selectin gene and protein expression in primary human endothelial cells (HUVEC) and in an endothelial cell line (EA.hy-926). As shown by ELISA and FACS analyses, HMG-CoA reductase inhibitors (e.g., lovastatin) impair the TNF-alpha stimulated increase in E-selectin protein expression. Similar results were obtained for E-selectin mRNA expression and promoter activity, indicating that the effect of lovastatin is based on inhibition of gene expression. The effective inhibitory concentration of lovastatin was in a physiologic…

rho GTP-Binding ProteinsRHOATranscription GeneticRHOBAntineoplastic AgentsBiochemistryCell MovementCell Line TumorNeoplasmsGene expressionE-selectinGeneticsmedicineCell AdhesionHumansLovastatinCell adhesionMolecular BiologyCells CulturedbiologyTumor Necrosis Factor-alphaCell biologybiology.proteinCancer researchTumor necrosis factor alphaLovastatinEndothelium VascularSignal transductionE-SelectinBiotechnologymedicine.drugSignal TransductionFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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A DNA‐Encoded FRET Biosensor for Visualizing the Tension across Paxillin in Living Cells upon Shear Stress

2022

Paxillin is a potential participant in the direct intracellular force transmission which is considered as the foundation of cells sensing and responding to extracellular environment. However, the detection of tension across paxillin has not been achieved due to lacking microsized tools. Herein, a paxillin tension sensor (PaxTs) based on Fluorescence Resonance Energy Transfer (FRET) technique was constructed. PaxTs can be expressed and assembled to FA sites spontaneously to visualize the tension across paxillin with FRET efficiency of ~62.4% in living cells. The tension across paxillin was found to decrease upon shear stress, in which the membrane fluidity and contractility of actin acted as…

soluviestintäpaxillinmekaniikkaFRETmacromolecular substancesproteiinitbiological phenomena cell phenomena and immunitybiosensorsfocal adhesionsbiosensoritenvironment and public healthshear stresssolufysiologia
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Regulation of type 1 fimbriae synthesis and biofilm formation by the transcriptional regulator LrhA of Escherichia coli

2005

Type 1 fimbriae ofEscherichia colifacilitate attachment to the host mucosa and promote biofilm formation on abiotic surfaces. The transcriptional regulator LrhA, which is known as a repressor of flagellar, motility and chemotaxis genes, regulates biofilm formation and expression of type 1 fimbriae. Whole-genome expression profiling revealed that inactivation oflrhAresults in an increased expression of structural components of type 1 fimbriae.In vitro, LrhA bound to the promoter regions of the twofimrecombinases (FimB and FimE) that catalyse the inversion of thefimApromoter, and to the invertible element itself. TranslationallacZfusions with these genes and quantification offimEtranscript le…

urinary-tractphase variationFimbrialac operonRepressorsuicide vectorBiologyFlagellummedicine.disease_causeMicrobiologyBacterial AdhesionMicrobiologylysr homologMiceglobal regulatorh-nsEscherichia colimedicineAnimalsHumansgenetic-analysisPromoter Regions GeneticEscherichia coliEscherichia coli InfectionsOligonucleotide Array Sequence AnalysisPhase variationRegulation of gene expressionfim switchEscherichia coli ProteinsGene Expression ProfilingBiofilmGene Expression Regulation Bacterialbiochemical phenomena metabolism and nutritionintegration host factorBiofilmsFimbriae BacterialMutationUrinary Tract Infectionsvirulence determinantsTranscription Factors
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Rational drug discovery : structural studies of protein-ligand complexes

2011

vaskulaarinen adheesioproteiini 1rational drug discoveryrationaalinen lääkeainesuunnitteluVAP-1hydrazinefilamiinitfilaminvascular adhesion protein 1ligandinsitomistaskutmolecular dynamicsligand binding pocketshydratsiinimolekyylidynamiikkaTCPTPCFTR
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