Search results for "Intracellular"

showing 10 items of 821 documents

Acute cytotoxicity and apoptotic effects after l-Pam exposure in different cocultures of the proximal and distal respiratory system.

2009

Abstract Sulphur and nitrogen mustard are strong alkylating agents which can cause after inhalation acute lung injury in the larynx, trachea and large bronchi and can lead to alveolar edema. In our study we tested the N-Lost l -Phenylalanine Mustard ( l -Pam). Therefore we seeded the alveolar type II cell line NCI H441 on the upper membrane of a Transwell filter plate and the endothelial cell line ISO-Has-1 on the lower side of the membrane for the alveolar model and combined the human bronchial explant-outgrowth cells and fibroblasts in the bronchial model and exposed both models with various concentrations of l -Pam. Treatment with l -Pam led to a concentration-dependent decrease of the t…

ProteomeIntracellular SpaceBioengineeringApoptosisBronchiBiologyLung injuryApplied Microbiology and BiotechnologyCell Linechemistry.chemical_compoundMicroscopy Electron TransmissionmedicineElectric ImpedanceToxicity Tests AcuteHumansRespiratory systemMelphalanOrganellesAnalysis of VarianceLungCytotoxinsEndothelial CellsGeneral Medicinerespiratory systemMolecular biologyWI-38Nitrogen mustardCoculture TechniquesEndothelial stem cellPulmonary Alveolimedicine.anatomical_structurechemistryApoptosisImmunologyVacuolesIntracellularBiotechnologyJournal of biotechnology
researchProduct

Osteogenic commitment and differentiation of human mesenchymal stem cells by low‐intensity pulsed ultrasound stimulation

2018

Low-intensity pulsed ultrasound (LIPUS) as an adjuvant therapy in in vitro and in vivo bone engineering has proven to be extremely useful. The present study aimed at investigating the effect of 30 mW/cm(2) LIPUS stimulation on commercially available human mesenchymal stem cells (hMSCs) cultured in basal or osteogenic medium at different experimental time points (7d, 14d, 21d). The hypothesis was that LIPUS would improve the osteogenic differentiation of hMSC and guarantying the maintenance of osteogenic committed fraction, as demonstrated by cell vitality and proteomic analysis. LIPUS stimulation (a) regulated the balance between osteoblast commitment and differentiation by specific network…

Proteomics0301 basic medicineTime FactorsUltrasonic WaveTranscription FactorPhysiologyCellular differentiationClinical BiochemistryLow-intensity pulsed ultrasoundOsteogenesisProtein Interaction MapsStem Cell Nichemesenchymal stem cellCells CulturedProtein metabolic processproteomic analysiMesenchymal Stromal CellReverse Transcriptase Polymerase Chain ReactionOsteogenesiIntracellular Signaling Peptides and ProteinsCell DifferentiationOsteoblastproteomic analysisFlow CytometryCell biologyRUNX2Phenotypemedicine.anatomical_structureUltrasonic Wavesosteoblast differentiationosteogenic commitmentProtein Interaction MapHumanSignal TransductionHomeobox protein NANOGlow-intensity pulsed ultrasoundTime FactorCell SurvivalEnzyme-Linked Immunosorbent AssayBiology03 medical and health sciencesSOX2medicineHumansCell LineageMesenchymal stem cellProteomicMesenchymal Stem CellsCell Biology030104 developmental biologyGene Expression RegulationIntracellular Signaling Peptides and ProteinImmunologyTranscription FactorsJournal of Cellular Physiology
researchProduct

Integrative genomic and proteomic analyses identify targets for Lkb1 deficient metastatic lung tumors

2010

SummaryIn mice, Lkb1 deletion and activation of KrasG12D results in lung tumors with a high penetrance of lymph node and distant metastases. We analyzed these primary and metastatic de novo lung cancers with integrated genomic and proteomic profiles, and have identified gene and phosphoprotein signatures associated with Lkb1 loss and progression to invasive and metastatic lung tumors. These studies revealed that SRC is activated in Lkb1-deficient primary and metastatic lung tumors, and that the combined inhibition of SRC, PI3K, and MEK1/2 resulted in synergistic tumor regression. These studies demonstrate that integrated genomic and proteomic analyses can be used to identify signaling pathw…

ProteomicsCancer ResearchLung NeoplasmsMAP Kinase Kinase 2MAP Kinase Kinase 1CELLCYCLEAMP-Activated Protein Kinasesmedicine.disease_causeMice0302 clinical medicineAMP-Activated Protein Kinase KinasesCell MovementCarcinoma Non-Small-Cell LungEnzyme InhibitorsNeoplasm MetastasisPhosphorylationLymph nodePhosphoinositide-3 Kinase Inhibitors0303 health sciencesTOR Serine-Threonine KinasesIntracellular Signaling Peptides and ProteinsGenomicsCell cycleProtein-Tyrosine KinasesPenetrance3. Good healthUp-RegulationGene Expression Regulation Neoplasticmedicine.anatomical_structuresrc-Family KinasesOncologySIGNALING030220 oncology & carcinogenesisDrug Therapy CombinationFemaleRNA InterferenceKRASSignal TransductionMice NudeBiologyProtein Serine-Threonine KinasesArticleProto-Oncogene Proteins p21(ras)03 medical and health sciencesCell Line TumorProto-Oncogene ProteinsmedicineCell AdhesionAnimalsHumansEpithelial–mesenchymal transitionProtein Kinase Inhibitors030304 developmental biologyFocal AdhesionsGene Expression ProfilingCell BiologyXenograft Model Antitumor AssaysMice Mutant StrainsGene expression profilingFocal Adhesion Protein-Tyrosine KinasesCancer cellCell TransdifferentiationCancer researchras ProteinsCarcinogenesis
researchProduct

Mass Spectrometry and Imaging Analysis of Nanoparticle-Containing Vesicles Provide a Mechanistic Insight into Cellular Trafficking

2014

Rational design of nanocarriers for drug delivery approaches requires an unbiased knowledge of uptake mechanisms and intracellular trafficking pathways. Here we dissected these processes using a quantitative proteomics approach. We isolated intracellular vesicles containing superparamagnetic iron oxide polystyrene nanoparticles and analyzed their protein composition by label-free quantitative mass spectrometry. The proteomic snapshot of organelle marker proteins revealed that an atypical macropinocytic-like mechanism mediated the entry of nanoparticles. We show that the entry mechanism is controlled by actin reorganization, atypical macropinocytic signaling, and ADP-ribosylation factor 1. A…

ProteomicsEndosomeVesicleQuantitative proteomicsGeneral EngineeringGeneral Physics and AstronomyBiological TransportBiologyProteomicsEndocytosisMass SpectrometryCell biologylaw.inventionMicroscopy Electron TransmissionConfocal microscopylawOrganelleNanoparticlesGeneral Materials ScienceNanocarriersIntracellularACS Nano
researchProduct

Increased oxidative stress and impaired antioxidant response in Lafora disease.

2014

15 páginas, 10 figuras

ProteomicsGenetically modified mouseAntioxidantmedicine.medical_treatmentNeuroscience (miscellaneous)Proteomic analysisMice TransgenicBiologymedicine.disease_causeBiochemistryAntioxidantsLafora diseaseMiceCellular and Molecular NeuroscienceLaforinPhysiology (medical)AutophagymedicineAnimalsHumansLafora diseaseMice Knockoutchemistry.chemical_classificationReactive oxygen speciesAutophagymedicine.diseaseMalinCell biologyNeurologychemistryBiochemistryOxidative stressMutationAntioxidant enzymesReactive Oxygen SpeciesLaforinOxidative stressIntracellularFree radical biologymedicine
researchProduct

B-Raf Acts via the ROCKII/LIMK/Cofilin Pathway To Maintain Actin Stress Fibers in Fibroblasts

2004

Members of the Raf family of serine/threonine protein kinases have been well studied in a variety of organisms ranging from Drosophila to humans. Three raf homologues (raf-1, B-raf, and A-raf) exist in mammals, while a single prototypic homologue exists in lower organisms. A wealth of genetic and biochemical data have indicated that Raf family members are signaling kinases that are integral components of the conserved Ras/Raf/MEK/ERK signaling cascade. Following activation by Ras-dependent mechanisms, Raf protein kinases act as mitogen-activated protein (MAP) kinase kinase kinases, which phosphorylate and activate the type 1/2 MAP kinase kinases, also known as MEK1/2. These dual-specificity…

Proto-Oncogene Proteins B-rafMAPK/ERK pathwaymacromolecular substancesProtein Serine-Threonine KinasesTransfectionCell LineProto-Oncogene Proteins B-rafLim kinaseMiceCell MovementStress FibersAnimalsHumansPhosphorylationKinase activityCell Growth and DevelopmentMolecular BiologyRho-associated protein kinaseCytoskeletonrho-Associated KinasesbiologyKinaseMicrofilament ProteinsIntracellular Signaling Peptides and ProteinsLim KinasesCell BiologyFibroblastsMolecular biologyActinsCell biologyProto-Oncogene Proteins c-rafActin Depolymerizing FactorsMitogen-activated protein kinasebiology.proteinProto-Oncogene Proteins c-rafMitogen-Activated Protein KinasesProtein KinasesSignal TransductionMolecular and Cellular Biology
researchProduct

Theileria parasites secrete a prolyl isomerase to maintain host leukocyte transformation

2015

Infectious agents develop intricate mechanisms to interact with host cell pathways and hijack their genetic and epigenetic machinery to change host cell phenotypic states. Among the Apicomplexa phylum of obligate intracellular parasites, which cause veterinary and human diseases, Theileria is the only genus that transforms its mammalian host cells. Theileria infection of bovine leukocytes induces proliferative and invasive phenotypes associated with activated signalling pathways, notably JNK and AP-1 (ref. 2). The transformed phenotypes are reversed by treatment with the theilericidal drug buparvaquone. We used comparative genomics to identify a homologue of the peptidyl-prolyl isomerase PI…

Proto-Oncogene Proteins c-jun[SDV]Life Sciences [q-bio]Drug ResistanceparasitesBiologyArticleCell LineHost-Parasite InteractionsmiR-155TheileriaTheileriaLeukocytesProlyl isomeraseAnimalsHumanscancerSecretionNIMA-Interacting Peptidylprolyl IsomeraseZebrafishComputingMilieux_MISCELLANEOUSPeptidylprolyl isomeraseSKP Cullin F-Box Protein LigasesMultidisciplinaryProtein StabilityGeneral CommentaryIntracellular parasiteUbiquitinationPeptidylprolyl Isomerasebiology.organism_classificationXenograft Model Antitumor AssaysMolecular biology3. Good healthCell biologyUbiquitin ligaseNIMA-Interacting Peptidylprolyl IsomeraseTranscription Factor AP-1Cell Transformation NeoplasticSchistosoma haematobiumPIN1biology.proteinMedicineCattleNaphthoquinonesSignal Transduction
researchProduct

The role of mucin 1 in respiratory diseases

2020

Recent evidence has demonstrated that mucin 1 (MUC1) is involved in many pathological processes that occur in the lung. MUC1 is a transmembrane protein mainly expressed by epithelial and hematopoietic cells. It has a receptor-like structure, which can sense the external environment and activate intracellular signal transduction pathways through its cytoplasmic domain. The extracellular domain of MUC1 can be released to the external environment, thus acting as a decoy barrier to mucosal pathogens, as well as serving as a serum biomarker for the diagnosis and prognosis of several respiratory diseases such as lung cancer and interstitial lung diseases. Furthermore, bioactivated MUC1-cytoplasmi…

Pulmonary and Respiratory MedicineAnti-Inflammatory Agents03 medical and health sciencesPulmonary Disease Chronic Obstructive0302 clinical medicinePulmonary fibrosismedicineAnimalsHumansRespiratory systemLung cancerMUC1lcsh:RC705-779Lungbusiness.industryMucinMucin-1lcsh:Diseases of the respiratory systemmedicine.diseaseAsthmaIntracellular signal transductionBiomarkermedicine.anatomical_structure030228 respiratory system030220 oncology & carcinogenesisCancer researchbusinessSignal Transduction
researchProduct

Aclidinium inhibits cigarette smoke-induced lung fibroblast-to-myofibroblast transition.

2012

Cigarette smoking contributes to lung remodelling in chronic obstructive pulmonary disease (COPD). As part of this remodelling, peribronchiolar fibrosis is observed in the small airways of COPD patients and contributes to airway obstruction. Fibroblast-to-myofibroblast transition is a key step in peribronchiolar fibrosis formation. This in vitro study examined the effect of cigarette smoke on bronchial fibroblast-to-myofibroblast transition, and whether aclidinium bromide inhibits this process. Human bronchial fibroblasts were incubated with aclidinium bromide (10 −9 –10 −7 M) and exposed to cigarette smoke extract. Collagen type I and α-smooth muscle actin (α-SMA) expression were measured …

Pulmonary and Respiratory MedicineTime FactorsBronchiPharmacologyCholinergic AntagonistsCollagen Type Ichemistry.chemical_compoundAclidinium bromideFibrosisSmokemedicineExtracellularCyclic AMPHumansRNA Small InterferingFibroblastMyofibroblastsLungCells CulturedInflammationbusiness.industrySmokingFibroblastsmedicine.diseaseFluoresceinsAcetylcholinesteraseFibrosisActinsrespiratory tract diseasesmedicine.anatomical_structurechemistryGene Expression RegulationMicroscopy FluorescencebusinessReactive Oxygen SpeciesMyofibroblastAcetylcholineIntracellularmedicine.drugTropanesThe European respiratory journal
researchProduct

Rho protein inactivation induced apoptosis of cultured human endothelial cells.

2002

Small GTP-binding Rho GTPases regulate important signaling pathways in endothelial cells, but little is known about their role in endothelial cell apoptosis. Clostridial cytotoxins specifically inactivate GTPases by glucosylation [ Clostridium difficile toxin B-10463 (TcdB-10463), C. difficile toxin B-1470 (TcdB-1470)] or ADP ribosylation ( C. botulinum C3 toxin). Exposure of human umbilical cord vein endothelial cells (HUVEC) to TcdB-10463, which inhibits RhoA/Rac1/Cdc42, or to C3 toxin, which inhibits RhoA, -B, -C, resulted in apoptosis, whereas inactivation of Rac1/Cdc42 with TcdB-1470 was without effect, suggesting that Rho inhibition was responsible for endothelial apoptosis. Disruptio…

Pulmonary and Respiratory Medicinerac1 GTP-Binding Proteinrho GTP-Binding ProteinsProgrammed cell deathUmbilical VeinsEndotheliumPhysiologyBacterial ToxinsCASP8 and FADD-Like Apoptosis Regulating ProteinApoptosisBcl-2-associated X proteinBacterial ProteinsPhysiology (medical)Proto-Oncogene ProteinsmedicineCyclic AMPIn Situ Nick-End LabelingHumanscdc42 GTP-Binding ProteinCells Culturedbcl-2-Associated X ProteinAdenosine Diphosphate RibosebiologyCaspase 3Intracellular Signaling Peptides and ProteinsCell BiologyCaspase 9Cell biologyNeoplasm ProteinsEndothelial stem cellmedicine.anatomical_structureCdc42 GTP-Binding ProteinProto-Oncogene Proteins c-bcl-2Cell cultureApoptosisCaspasesbiology.proteinMyeloid Cell Leukemia Sequence 1 ProteinEndothelium VascularSignal transductionCarrier ProteinsrhoA GTP-Binding ProteinBH3 Interacting Domain Death Agonist ProteinSignal TransductionAmerican journal of physiology. Lung cellular and molecular physiology
researchProduct