Search results for "Extracellular signal"

showing 10 items of 55 documents

Carboxyamidotriazole-Orotate Inhibits the Growth of Imatinib-Resistant Chronic Myeloid Leukaemia Cells and Modulates Exosomes-Stimulated Angiogenesis

2012

The Bcr/Abl kinase has been targeted for the treatment of chronic myelogenous leukaemia (CML) by imatinib mesylate. While imatinib has been extremely effective for chronic phase CML, blast crisis CML are often resistant. New therapeutic options are therefore needed for this fatal disease. Although more common in solid tumors, increased microvessel density was also reported in chronic myelogenous leukaemia and was associated with a significant increase of angiogenic factors, suggesting that vascularity in hematologic malignancies is a controlled process and may play a role in the leukaemogenic process thus representing an alternative therapeutic target. Carboxyamidotriazole-orotate (CTO) is …

MaleResearch ValidityPhysiologyAngiogenesisTumor PhysiologyFusion Proteins bcr-ablCancer Treatmentlcsh:MedicinePharmacologyExosomesCardiovascular PhysiologyBiochemistryPiperazinesHematologic Cancers and Related DisordersMicechemistry.chemical_compoundCell Movementhemic and lymphatic diseasesMolecular Cell BiologyBasic Cancer ResearchMedicine and Health SciencesPhosphorylationPost-Translational ModificationExtracellular Signal-Regulated MAP Kinaseslcsh:ScienceChronic Myelogenous LeukemiaMultidisciplinaryABLNeovascularization PathologicGene Expression Regulation LeukemicChemistryHematologyResearch AssessmentOncologyBenzamidesImatinib MesylateMedicineOncology AgentsAntiangiogenesis Therapymedicine.drugResearch ArticleChronic Myeloid LeukemiaAntineoplastic AgentsResearch and Analysis MethodsCell GrowthCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositiveLeukemiasCell AdhesionHuman Umbilical Vein Endothelial CellsmedicineAnimalsHumansRNA MessengerPhosphotyrosineBiologyCell ProliferationOrotic AcidTumor microenvironmentCarboxyamidotriazoleInterleukin-8lcsh:RBiology and Life SciencesProteinsCancers and NeoplasmsImatinibTriazolesmedicine.diseaseXenograft Model Antitumor AssaysRetractionExosomePyrimidinesImatinib mesylateDrug Resistance NeoplasmCarboxyamidotriazole Orotatelcsh:QAngiogenesisCell Adhesion MoleculesProto-Oncogene Proteins c-aktDevelopmental BiologyChronic myelogenous leukemiaPLoS ONE
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Morphological, molecular and hormonal adaptations to early morning versus afternoon resistance training

2018

It has been clearly established that maximal force and power is lower in the morning compared to noon or afternoon hours. This morning neuromuscular deficit can be diminished by regularly training in the morning hours. However, there is limited and contradictory information upon hypertrophic adaptations to time-of-day-specific resistance training. Moreover, no cellular or molecular mechanisms related to muscle hypertrophy adaptation have been studied with this respect. Therefore, the present study examined effects of the time-of-day-specific resistance training on muscle hypertrophy, phosphorylation of selected proteins, hormonal concentrations and neuromuscular performance. Twenty five pre…

MaleTime FactorsHydrocortisonePhysiologyMuscle ProteinsPhysiologylihaksetNoonp38 Mitogen-Activated Protein KinasesQuadriceps MuscleMuscle hypertrophy0302 clinical medicinePeptide Elongation Factor 2harjoitteluTestosteronePhosphorylationExtracellular Signal-Regulated MAP Kinasesta315vuorokausirytmiMorningRibosomal Protein S6resistanssiRibosomal Protein S6 Kinases 70-kDafood and beveragescell signallingAdaptation PhysiologicalMagnetic Resonance ImagingCircadian Rhythmmedicine.anatomical_structurevoimaharjoitteluhypertrophyAdultYoung Adult03 medical and health sciencesIsometric ContractionPhysiology (medical)medicineHumansMuscle Strengthdiurnalskeletal musclebusiness.industryfungiResistance trainingSkeletal muscle030229 sport sciencesresistance trainingbusinessBiomarkers030217 neurology & neurosurgeryHormoneChronobiology International
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Engineered microenvironments for synergistic VEGF - Integrin signalling during vascularization

2017

We have engineered polymer-based microenvironments that promote vasculogenesis both in vitro and in vivo through synergistic integrin-growth factor receptor signalling. Poly(ethyl acrylate) (PEA) triggers spontaneous organization of fibronectin (FN) into nanonetworks which provide availability of critical binding domains. Importantly, the growth factor binding (FNIII12-14) and integrin binding (FNIII9-10) regions are simultaneously available on FN fibrils assembled on PEA. This material platform promotes synergistic integrin/VEGF signalling which is highly effective for vascularization events in vitro with low concentrations of VEGF. VEGF specifically binds to FN fibrils on PEA compared to …

MaleVascular Endothelial Growth Factor AIntegrinsBiophysicsNeovascularization PhysiologicBioengineeringpoly(ethyl acrylate)ArticleBiomaterialsHuman Umbilical Vein Endothelial CellsImage Processing Computer-AssistedAnimalsHumansPhosphorylationExtracellular Signal-Regulated MAP KinasesFibronectinTissue EngineeringPhospholipase C gammaProtein assemblyVascularizationVEGFFibronectinsMice Inbred C57BLCellular MicroenvironmentMechanics of MaterialsFocal Adhesion Protein-Tyrosine KinasesFISICA APLICADAMutationCeramics and CompositesINGENIERIA ELECTRICAGrowth factorsProtein BindingSignal Transduction
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Muscle protein synthesis, mTORC1/MAPK/Hippo signaling, and capillary density are altered by blocking of myostatin and activins

2012

Loss of muscle mass and function occurs in various diseases. Myostatin blocking can attenuate muscle loss, but downstream signaling is not well known. Therefore, to elucidate associated signaling pathways, we used the soluble activin receptor IIb (sActRIIB-Fc) to block myostatin and activins in mice. Within 2 wk, the treatment rapidly increased muscle size as expected but decreased capillary density per area. sActRIIB-Fc increased muscle protein synthesis 1–2 days after the treatment correlating with enhanced mTORC1 signaling (phosphorylated rpS6 and S6K1, r = 0.8). Concurrently, increased REDD1 and eIF2Bε protein contents and phosphorylation of 4E-BP1 and AMPK was observed. In contrast, pr…

Malemedicine.medical_specialtyPhysiologyEndocrinology Diabetes and MetabolismMuscle ProteinsCell CountP70-S6 Kinase 1MyostatinMechanistic Target of Rapamycin Complex 1Protein Serine-Threonine KinasesBiologyMice03 medical and health sciences0302 clinical medicinePhysiology (medical)Internal medicinemedicineAnimalsHippo Signaling PathwayExtracellular Signal-Regulated MAP KinasesMuscle Skeletalta315030304 developmental biology0303 health sciencesHippo signaling pathwayMyogenesisTOR Serine-Threonine KinasesSkeletal muscleActivin receptorMyostatinActivinsCapillariesMice Inbred C57BLmedicine.anatomical_structureEndocrinologyHippo signalingMultiprotein ComplexesProtein Biosynthesisbiology.proteinIntercellular Signaling Peptides and ProteinsPhosphorylation030217 neurology & neurosurgerySignal TransductionAmerican Journal of Physiology-Endocrinology and Metabolism
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Extended gate electrode arrays for extracellular signal recordings

2000

Abstract We have fabricated arrays of planar gold electrodes arranged in a matrix of 8×8 with active areas ranging from 6 to 30 μm in diameter. An electronic amplification circuitry based on commercial junction field-effect transistors was used where the gold sensor fields act as extended gate electrodes (EGE) of the transistors, which leads to a new approach for long-term extracellular recording systems in vitro. The high input resistance of the amplification circuitry allows the use of small planar bare gold electrodes without further modification which therefore extends the frequency range of the measuring set-up down to the DC-level. The performance of our recording system has been test…

Materials sciencebusiness.industryTransistorMetals and AlloysAnalytical chemistryRangingCondensed Matter PhysicsCapacitanceSurfaces Coatings and FilmsElectronic Optical and Magnetic Materialslaw.inventionMatrix (chemical analysis)PlanarExtracellular signalSensor arraylawElectrodeMaterials ChemistryOptoelectronicsElectrical and Electronic EngineeringbusinessInstrumentationSensors and Actuators B: Chemical
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Redox signaling in acute pancreatitis

2015

Acute pancreatitis is an inflammatory process of the pancreatic gland that eventually may lead to a severe systemic inflammatory response. A key event in pancreatic damage is the intracellular activation of NF-κB and zymogens, involving also calcium, cathepsins, pH disorders, autophagy, and cell death, particularly necrosis. This review focuses on the new role of redox signaling in acute pancreatitis. Oxidative stress and redox status are involved in the onset of acute pancreatitis and also in the development of the systemic inflammatory response, being glutathione depletion, xanthine oxidase activation, and thiol oxidation in proteins critical features of the disease in the pancreas. On th…

NecrosisGSH reduced glutathioneSTAT3 signal transducer and activator of transcription 3ERK extracellular signal-regulated kinasesClinical BiochemistryCCK cholecystokininTRAFs TNF receptor associated factorsReview ArticleIκB kinasePharmacologymedicine.disease_causeBiochemistrySHP small heterodimer partnerSTIM1 stromal interaction molecule 1chemistry.chemical_compoundHATs histone acetyltransferasesMedicineASK1GCL glutamate cysteine ligaseTNF-α tumor necrosis factor alphaIKK IκB kinaseNOS nitric oxide synthaseAcute inflammationHIF hypoxia inducible factorlcsh:QH301-705.5NF-κB nuclear factor kappa BDAMPs damage-associated molecular pattern moleculeslcsh:R5-920biologyGSSG oxidized glutathioneNF-kappa BNLRs nucleotide-binding oligomerization domain (NOD) like receptorsTRADD tumor necrosis factor receptor type 1-associated DEATH domain proteinTRPC3 transient receptor potential channel 3VEGF vascular endothelial growth factorGlutathioneTNFR tumor necrosis factor receptorHMGB1 high-mobility group Box 1 proteinIP3R inositol 145-trisphosphate receptor type 3VCAM-1 Vascular Cell adhesion protein 1Acute DiseaseJNK c-Jun N-terminal kinaseAcute pancreatitisTLRs toll-like receptorsmedicine.symptomlcsh:Medicine (General)Oxidation-ReductionAP-1 activator protein-1Signal TransductionmRNA messenger ribonucleic acidHMGB1ASC apoptosis-associated speck-like protein containing a carboxy-terminal CARDRNS reactive nitrogen speciesPTPs protein tyrosine phosphatasesROS reactive oxygen speciesNADH nicotinamide adenine dinucleotidepHe extracellular pHFAEE fatty acid ethyl estersAP acute pancreatitisHumansXanthine oxidaseCBP CREB-binding proteinRyR endoplasmic reticulum membrane ryanodine receptorsMDA malondialdehydeNO nitric oxideXO xanthine oxidaseASK1 apoptosis signal-regulating kinase-1business.industryOrganic ChemistryAutophagyNADPH nicotinamide adenine dinucleotide phosphateHDACs histone deacetylasesmedicine.diseaseCARS compensatory anti-inflammatory response syndromeXDH xanthine dehydrogenaseIL interleukinIκB inhibitor of kappa BAcute pancreatitisETC Electron transport chainPancreatitisMKPs MAPK phosphatasesSAP severe acute pancreatitischemistrylcsh:Biology (General)DTT dithiothreitolOxidative stressNAC N-acetyl cysteineImmunologybiology.proteinCalciumLysosomesReactive Oxygen SpeciesbusinessMAPK mitogen-activated protein kinaseOxidative stressERCP endoscopic retrograde cholangiopancreatographyRedox Biology
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Role of mitochondria in parvovirus pathology.

2014

Proper functioning of the mitochondria is crucial for the survival of the cell. Viruses are able to interfere with mitochondrial functions as they infect the host cell. Parvoviruses are known to induce apoptosis in infected cells, but the role of the mitochondria in parvovirus induced cytopathy is only partially known. Here we demonstrate with confocal and electron microscopy that canine parvovirus (CPV) associated with the mitochondrial outer membrane from the onset of infection. During viral entry a transient depolarization of the mitochondrial transmembrane potential and increase in ROS level was detected. Subsequently, mitochondrial homeostasis was normalized shortly, as detected by rep…

PathologyvirusesCelllcsh:MedicineMitochondrionSignal transductionERK signaling cascadeMolecular cell biologyInner mitochondrial membraneExtracellular Signal-Regulated MAP Kinaseslcsh:SciencepatologiaCellular Stress ResponsesMembrane Potential MitochondrialMultidisciplinarybiologyCell DeathCanine parvovirusapoptosisSignaling cascadesCellular StructuresCell biologyMitochondriaHost-Pathogen Interactionmedicine.anatomical_structureMitochondrial MembranesResearch Articlemedicine.medical_specialtyViral EntryParvovirus CanineMAP Kinase Signaling SystemmitokondriotMicrobiologyCell LineParvoviridae InfectionsDogsViral entryVirologymedicineAnimalsBiologysoluviestintäParvovirusta1183parvoviruslcsh:Rta1182biology.organism_classificationMolecular biologyEnzyme ActivationViral replicationSubcellular OrganellesApoptosisCatsCalciumlcsh:QReactive Oxygen SpeciesViral Transmission and InfectionPLoS ONE
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Effects of polyphenols and lipids from Pennisetum glaucum grains on T-cell activation: modulation of Ca2+ and ERK1/ERK2 signaling

2015

International audience; BACKGROUND: Pearl millet (PM), i.e., Pennisetum glaucum, is widely grown in Africa and known for its anti-oxidant and anti-hyperlipidemic properties.METHODS: The P. glaucum grains were obtained from the region of Ouled Aïssa (South of Algeria). We assessed the effects of phenolic compounds and lipids, extracted from seeds of P. glaucum, on rat lymphocyte proliferation, activated by phorbol 12-myristate 13-acetate and ionomycin. In order to explore signaling pathway, triggered by these compounds, we assessed interleukin-2 (IL-2) mRNA expression and extracellular signal-regulated kinase-1/2 (ERK1/ERK2) phosphorylation. Finally, we determined increases in free intracell…

PennisetumT-LymphocytesLymphocyte proliferationLymphocyte ActivationAntioxidantsPearl milletchemistry.chemical_compoundExtracellularAnimalsGallic acidExtracellular Signal-Regulated MAP KinasesCell ProliferationHypolipidemic AgentsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologybiologyPlant ExtractsT-cellsPolyphenolsGeneral Medicinebiology.organism_classificationLipidsRatschemistryBiochemistryComplementary and alternative medicinePolyphenolIonomycinSeedsPhorbolPhosphorylationCalciumEdible GrainPennisetum[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologySignal TransductionResearch Article
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Urokinase activates macrophage PON2 gene transcription via the PI3K/ROS/MEK/SREBP-2 signalling cascade mediated by the PDGFR-β

2009

Aims We have recently shown that urokinase plasminogen activator (uPA) increases oxidative stress (OS), cholesterol biosynthesis, and paraoxonase 2 (PON2) expression in macrophages via binding to its receptor, the uPAR. Since PON2 is regulated by both OS and cholesterol content, we hypothesized that uPA elicits a cascade of signal transduction events shared by NADPH oxidase and cholesterol biosynthesis that culminates in PON2 gene expression. Here, we investigated the signalling pathway that leads to the expression of PON2 in macrophages in response to uPA. Methods and results The increase in macrophage PON2 mRNA levels in response to uPA was shown to depend on PON2 gene promoter activation…

Transcription GeneticPhysiologyReceptor Platelet-Derived Growth Factor betaPhosphatidylinositol 3-KinasesPhysiology (medical)Gene expressionHumansExtracellular Signal-Regulated MAP KinasesTranscription factorCells CulturedMitogen-Activated Protein Kinase KinasesRegulation of gene expressionNADPH oxidasebiologyAryldialkylphosphataseKinaseMacrophagesNADPH OxidasesUrokinase-Type Plasminogen ActivatorCell biologySterol regulatory element-binding proteinUrokinase receptorGene Expression RegulationBiochemistryTissue Plasminogen Activatorbiology.proteinSignal transductionReactive Oxygen SpeciesCardiology and Cardiovascular MedicineSignal TransductionSterol Regulatory Element Binding Protein 2Cardiovascular Research
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Reactive oxygen species activation of MAPK pathway results in VEGF upregulation as an undesired irradiation response

2013

Background Radioresistance limits the effectiveness of radiotherapy in head and neck squamous cell carcinoma. We previously demonstrated post-radiogenic mitogen-activated protein kinase (MAPK) pathway activation and vascular endothelial growth factor (VEGF) release resulting in reduced tumor cell response. Here, we examined the association of this mechanism with the induction of reactive oxygen species (ROS) under irradiation (IR). Methods Intracellular ROS after IR were measured. We modeled radiation-induced ROS by exposure of two SCC lines to H2O2 and evaluated the impact of irradiation and ROS on ERK phosphorylation by Western blot, immunohistochemistry, and ELISA. Results We found eleva…

Vascular Endothelial Growth Factor AMAPK/ERK pathwayCancer ResearchPathologymedicine.medical_specialtyMAP Kinase Signaling SystemBlotting WesternEnzyme-Linked Immunosorbent AssayBiologyRadiation TolerancePathology and Forensic Medicinechemistry.chemical_compoundDownregulation and upregulationCell Line TumorNitrilesButadienesmedicineHumansEnzyme InhibitorsExtracellular Signal-Regulated MAP KinasesProtein kinase Achemistry.chemical_classificationReactive oxygen speciesHydrogen PeroxideImmunohistochemistryCytoprotectionUp-RegulationVascular endothelial growth factorVascular endothelial growth factor AOtorhinolaryngologychemistryCytoprotectionCarcinoma Squamous CellCancer researchPeriodonticsElectrophoresis Polyacrylamide GelOral SurgeryReactive Oxygen SpeciesIntracellularJournal of Oral Pathology & Medicine
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