Search results for "PROTEIN KINASE"

showing 10 items of 1188 documents

Existence of muscarinic acetylcholine receptor (mAChR) and fibroblast growth factor receptor (FGFR) heteroreceptor complexes and their enhancement of…

2017

Abstract Background Recently, it was demonstrated that G-protein-coupled receptors (GPCRs) can transactivate tyrosine kinase receptors in absence of their ligands. In this work, driven by the observation that mAChRs and fibroblast growth factor receptors (FGFRs) share signalling pathways and regulation of brain functions, it was decided to explore whether mAChRs activation may transactivate FGFRs and, if so, to characterize the related trophic effects in cultured hippocampal neurons. Methods Oxotremorine-M transactivation of FGFRs and related trophic effects were tested in primary hippocampal neurons. Western blotting and in situ proximity ligation assay (PLA) were used to detect FGFR phosp…

Male0301 basic medicineHippocampusBiochemistryReceptor tyrosine kinaseReceptors G-Protein-CoupledRats Sprague-DawleyTransactivation0302 clinical medicineMuscarinic acetylcholine receptorNeural plasticityNeuronsNeuronal PlasticitybiologyReceptors MuscarinicCell biologyFibroblast growth factor receptorFibroblast Growth Factor 2Signal TransductionProto-oncogene tyrosine-protein kinase Srcmedicine.medical_specialtyNeuriteNeuronal OutgrowthBiophysicsHeteroreceptor03 medical and health sciencesHippocampuInternal medicinemedicineAnimalsReceptor Fibroblast Growth Factor Type 1Rats WistarMolecular BiologyTransactivationAnimalOxotremorineFibroblast growth factor receptor 1Receptor Muscarinic M1NeuronReceptors Fibroblast Growth FactorRatsFGFR1030104 developmental biologyEndocrinologyM1receptorBiophysicHeteroreceptor complexebiology.proteinRat030217 neurology & neurosurgeryBiochimica et Biophysica Acta (BBA) - General Subjects
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Nose-to-brain delivery of insulin enhanced by a nanogel carrier.

2018

Recent evidences suggest that insulin delivery to the brain can be an important pharmacological therapy for some neurodegenerative pathologies, including Alzheimer disease (AD). Due to the presence of the Blood Brain Barrier, a suitable carrier and an appropriate route of administration are required to increase the efficacy and safety of the treatment. Here, poly(N-vinyl pyrrolidone)-based nanogels (NG), synthetized by e-beam irradiation, alone and with covalently attached insulin (NG-In) were characterized for biocompatibility and brain delivery features in a mouse model. Preliminarily, the biodistribution of the "empty" nanocarrier after intraperitoneal (i.p.) injection was investigated b…

Male0301 basic medicineIonizing radiationBiodistributionmedicine.medical_treatmentPharmaceutical SciencePharmacologyBrain delivery; Insulin; Intranasal inoculation; Ionizing radiations; Nanogel; Nanogel biocompatibility and clearanceBlood–brain barrierNanogel biocompatibility and clearance03 medical and health sciencesRoute of administrationNanogel0302 clinical medicinemedicineAnimalsHypoglycemic AgentsInsulinProtein kinase BAdministration IntranasalBrain deliveryDrug CarriersChemistryInsulinBrainPovidoneIntranasal inoculationMice Inbred C57BLNasal Mucosa030104 developmental biologymedicine.anatomical_structureAcrylatesNasal administrationSettore CHIM/07 - Fondamenti Chimici Delle TecnologieNanocarriersGels030217 neurology & neurosurgeryNanogel Ionizing radiationNanogel
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Molecular mechanisms mediating the neuroprotective role of the selective estrogen receptor modulator, bazedoxifene, in acute ischemic stroke: A compa…

2017

As the knowledge on the estrogenic system in the brain grows, the possibilities to modulate it in order to afford further neuroprotection in brain damaging disorders so do it. We have previously demonstrated the ability of the selective estrogen receptor modulator, bazedoxifene (BZA), to reduce experimental ischemic brain damage. The present study has been designed to gain insight into the molecular mechanisms involved in such a neuroprotective action by investigating: 1) stroke-induced apoptotic cell death; 2) expression of estrogen receptors (ER) ERα, ERβ and the G-protein coupled estrogen receptor (GPER); and 3) modulation of MAPK/ ERK1/2 and PI3K/Akt signaling pathways. For comparison, …

Male0301 basic medicineMAPK/ERK pathwayIndolesSignaling pathwaysEndocrinology Diabetes and MetabolismClinical BiochemistryEstrogen receptorApoptosisEstrogen receptorsSecond Messenger SystemsBiochemistryBrain IschemiaReceptors G-Protein-Coupled0302 clinical medicineEndocrinologyPhosphatidylinositol PhosphatesCerebral CortexNeuronsEstradiolNeuroprotectionStrokeNeuroprotective AgentsSelective estrogen receptor modulatorReperfusion InjuryMolecular MedicineSelective estrogen receptor modulatorsGPERmedicine.medical_specialtyMAP Kinase Signaling Systemmedicine.drug_classAcute ischemic strokeNerve Tissue ProteinsBazedoxifeneBiologyNeuroprotection03 medical and health sciencesInternal medicinemedicineAnimalsEstrogen Receptor betaRats WistarMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayEstrogen Receptor alphaEstrogensCell BiologyEstrogen030104 developmental biologyEndocrinologyEstrogen030217 neurology & neurosurgeryThe Journal of Steroid Biochemistry and Molecular Biology
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Overall survival in patients with BRAF-mutant melanoma receiving encorafenib plus binimetinib versus vemurafenib or encorafenib (COLUMBUS): a multice…

2018

Summary Background Encorafenib plus binimetinib and encorafenib alone improved progression-free survival compared with vemurafenib in patients with BRAF V600 -mutant melanoma in the COLUMBUS trial. Here, we report the results of the secondary endpoint of overall survival. Methods COLUMBUS was a two-part, randomised, open-label, phase 3 study done at 162 hospitals in 28 countries. Eligible patients were aged at least 18 years with histologically confirmed, locally advanced, unresectable, or metastatic cutaneous melanoma, or unknown primary melanoma, BRAF V600E or BRAF V600K mutation, an Eastern Cooperative Oncology Group (ECOG) performance status of 0 or 1, and were treatment naive or had pr…

Male0301 basic medicineOncologySkin NeoplasmsTime FactorsMedizinPhases of clinical researchGene mutationchemistry.chemical_compound0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsVemurafenibMelanomaAged 80 and overTrametinibSulfonamides10177 Dermatology ClinicBinimetinibMiddle AgedProgression-Free SurvivalPhenotypeOncologyTolerability030220 oncology & carcinogenesisDisease ProgressionFemale2730 Oncologymedicine.drugAdultProto-Oncogene Proteins B-rafmedicine.medical_specialty610 Medicine & healthYoung Adult03 medical and health sciencesInternal medicineBiomarkers TumormedicineHumansGenetic Predisposition to DiseaseProgression-free survivalProtein Kinase InhibitorsAgedPerformance statusbusiness.industry030104 developmental biologyVemurafenibchemistryMutationBenzimidazolesCarbamatesbusinessThe Lancet Oncology
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Clinical Implications of Discordant Early Molecular Responses in CML Patients Treated with Imatinib

2019

A reduction in BCR-ABL1/ABL1IS transcript levels to &lt

Male0301 basic medicineOncologyTreatment outcomeFusion Proteins bcr-ablAntineoplastic Agentlcsh:ChemistryBcr abl10302 clinical medicinehemic and lymphatic diseasesimatinib mesylateBCR-ABL1; European Leukemia Net; chronic myeloid leukemia; early molecular response; imatinib mesylatelcsh:QH301-705.5<i>BCR-ABL1</i>SpectroscopyAged 80 and overGeneral MedicineMiddle AgedComputer Science ApplicationsTreatment Outcome030220 oncology & carcinogenesisFemaleHumanmedicine.drugAdultmedicine.medical_specialtyProtein Kinase InhibitorAntineoplastic AgentsArticleCatalysisEuropean Leukemia NetInorganic Chemistry03 medical and health scienceschronic myeloid leukemiaLeukemia Myelogenous Chronic BCR-ABL PositiveInternal medicineBiomarkers TumormedicineHumansIn patientRNA MessengerPhysical and Theoretical ChemistryProtein Kinase InhibitorsMolecular BiologyAgedbusiness.industryOrganic ChemistryImatinibBCR-ABL1030104 developmental biologyImatinib mesylatelcsh:Biology (General)lcsh:QD1-999early molecular responsebusiness
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The comparison of outcomes from tyrosine kinase inhibitor monotherapy in second- or third-line for advanced non-small-cell lung cancer patients with …

2016

// Giuseppe Bronte 1, * , Tindara Franchina 2, * , Massimiliano Alu 3, * , Giovanni Sortino 1 , Claudia Celesia 1 , Francesco Passiglia 1 , Giuseppina Savio 3 , Agata Laudani 3 , Alessandro Russo 2 , Antonio Picone 2 , Sergio Rizzo 1 , Michele De Tursi 4 , Elisabetta Gambale 4 , Viviana Bazan 1 , Clara Natoli 4 , Livio Blasi 3 , Vincenzo Adamo 2 , Antonio Russo 1 1 Department of Surgical, Oncological and Oral Sciences, University of Palermo, Palermo, Italy 2 Medical Oncology Unit-AOOR Papardo-Piemonte, Messina and Department of Human Pathology, University of Messina, Messina, Italy 3 Medical Oncology Unit, A.R.N.A.S. Civico, Palermo, Italy 4 Department of Medical, Oral and Biotechnological …

Male0301 basic medicineOncologymedicine.medical_specialtyLung Neoplasmsmedicine.drug_classEGFRTyrosine kinase inhibitorKaplan-Meier EstimateTyrosine-kinase inhibitorErlotinib Hydrochloride03 medical and health sciences0302 clinical medicineGefitinibCarcinoma Non-Small-Cell LungInternal medicinemedicineHumansChemotherapyErlotinib HydrochlorideLung cancerProtein Kinase InhibitorsChemotherapy EGFR Non-small-cell lung cancer Tyrosine kinase inhibitor OncologyAgedRetrospective StudiesAged 80 and overPerformance statusbusiness.industryChemotherapy; EGFR; Non-small-cell lung cancer; Tyrosine kinase inhibitor; OncologyGefitinibRetrospective cohort studyMiddle Agedmedicine.diseaserespiratory tract diseasesSurgeryErbB ReceptorsClinical trialTreatment Outcome030104 developmental biologyOncology030220 oncology & carcinogenesisMutationQuinazolinesFemaleErlotinibbusinessNon-small-cell lung cancerResearch Papermedicine.drug
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Investigating and re-evaluating the role of glycogen synthase kinase 3 beta kinase as a molecular target for cardioprotection by using novel pharmaco…

2019

Aims Glycogen synthase kinase 3 beta (GSK3β) link with the mitochondrial Permeability Transition Pore (mPTP) in cardioprotection is debated. We investigated the role of GSK3β in ischaemia (I)/reperfusion (R) injury using pharmacological tools. Methods and results Infarct size using the GSK3β inhibitor BIO (6-bromoindirubin-3'-oxime) and several novel analogues (MLS2776-MLS2779) was determined in anaesthetized rabbits and mice. In myocardial tissue GSK3β inhibition and the specificity of the compounds was tested. The mechanism of protection focused on autophagy-related proteins. GSK3β localization was determined in subsarcolemmal (SSM) and interfibrillar mitochondria (IFM) isolated from Lang…

Male0301 basic medicinePhysiologyMyocardial InfarctionAutophagy-Related ProteinsMyocardial Reperfusion Injury030204 cardiovascular system & hematologyMitochondrionPharmacologyMitochondrial Membrane Transport ProteinsMitochondria HeartStructure-Activity Relationship03 medical and health scienceschemistry.chemical_compound0302 clinical medicineReperfusion therapyPhysiology (medical)AnimalsMyocytes CardiacProtein Kinase InhibitorsGSK3BMice Knockoutchemistry.chemical_classificationCardioprotectionReactive oxygen speciesGlycogen Synthase Kinase 3 betaMolecular StructureMitochondrial Permeability Transition PoreChemistryKinaseMPTPIsolated Heart PreparationMice Inbred C57BLDisease Models Animal030104 developmental biologyMitochondrial permeability transition poreFemaleRabbitsCardiology and Cardiovascular MedicineCyclophilin DSignal TransductionCardiovascular Research
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Mir-4674 Regulates Angiogenesis In Tissue Injury By Targeting P38K Signaling In Endothelial Cells

2020

Neoangiogenesis is critical for tissue repair in response to injury such as myocardial ischemia or dermal wound healing. MicroRNAs are small noncoding RNAs and important regulators of angiogenesis under physiological and pathological disease states. Therefore, identification of microRNAs that may restore impaired angiogenesis in response to tissue injury may provide new targets for therapy. Using a microRNA microarray profiling approach, we identified a human-specific microRNA, miR-4674, that was significantly decreased in patients after myocardial tissue injury and had an endothelial cell (EC)-enriched expression pattern. Functionally, overexpression of miR-4674 markedly attenuated EC pro…

Male0301 basic medicineSmall interfering RNAMAP Kinase Signaling SystemPhysiologyAngiogenesisNeovascularization Physiologic030204 cardiovascular system & hematologyBiology03 medical and health sciencesOrgan Culture Techniques0302 clinical medicinemicroRNAHuman Umbilical Vein Endothelial CellsHumansProtein kinase ACell ProliferationTube formationEndothelial CellsIRAK1Cell BiologyCell biologyEndothelial stem cellMicroRNAs030104 developmental biologyFemaleWound healingResearch ArticleSignal Transduction
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The SGLT2 inhibitor empagliflozin improves the primary diabetic complications in ZDF rats

2017

Hyperglycemia associated with inflammation and oxidative stress is a major cause of vascular dysfunction and cardiovascular disease in diabetes. Recent data reports that a selective sodium-glucose co-transporter 2 inhibitor (SGLT2i), empagliflozin (Jardiance®), ameliorates glucotoxicity via excretion of excess glucose in urine (glucosuria) and significantly improves cardiovascular mortality in type 2 diabetes mellitus (T2DM). The overarching hypothesis is that hyperglycemia and glucotoxicity are upstream of all other complications seen in diabetes. The aim of this study was to investigate effects of empagliflozin on glucotoxicity, β-cell function, inflammation, oxidative stress and endothel…

Male0301 basic medicineendocrine system diseasesDiabetic CardiomyopathiesFPS-ZM1 RAGE inhibitorClinical BiochemistryAorta ThoracicRAGE receptor for AGEICAM-1 intercellular adhesion molecule-1ECL enhanced chemiluminescence030204 cardiovascular system & hematologyDPP-4 dipeptidyl peptidase-4medicine.disease_causeTNF-α tumor necrosis factor-αBiochemistryeNOS endothelial •NO synthase (type 3)0302 clinical medicineGlucosidesecSOD extracellular superoxide dismutaseInsulin-Secreting CellsCCL-2 see MCP-1HyperlipidemiaHyperinsulinemiaGTN glyceryl trinitrate (nitroglycerin)IFN-γ interferon-γDHE dihydroethidineEndothelial dysfunctionEndothelial dysfunctionIL-6 interleukin-6lcsh:QH301-705.5HO-1 heme oxygenase-1lcsh:R5-920ICAM-1NG normoglycemiaDiabetesNox catalytic subunit of NADPH oxidaseSGLT2 inhibitorβ-cell contentL-012 8-amino-5-chloro-7-phenylpyrido[34-d]pyridazine-14-(2H3H)dione sodium saltChIP chromatin immunoprecipitationC-Reactive ProteinCRP C-reactive proteinAGE advanced glycation end productsHbA1c glycohemoglobinlcsh:Medicine (General)Research PaperZucker diabetic fatty ratsmedicine.medical_specialtyDMSO dimethylsulfoxideMCP-1 monocyte-chemoattractant-protein-1qRT-PCR quantitative reverse transcription polymerase chain reactionZDF Zucker diabetic fatty (rat)Low-grade inflammation03 medical and health sciencesROS reactive oxygen speciesSodium-Glucose Transporter 2Physiology (medical)Internal medicineDiabetes mellitusPKC protein kinase CEmpagliflozinmedicineAnimalsHypoglycemic AgentsBenzhydryl CompoundsCOX2 cyclooxygenase-2SGLT2i SGLT2 inhibitorSodium-Glucose Transporter 2 InhibitorsGlycated HemoglobinACh acetylcholinebusiness.industryOrganic Chemistrynutritional and metabolic diseasesType 2 Diabetes Mellitusmedicine.diseaseH2K9me2 histone3 lysine9 dimethylationRatsRats ZuckerDHFR dihydrofolate reductaseSGLT2 sodium-glucose co-transporter-2Oxidative StresssGC soluable guanylyl cyclaseGlucose030104 developmental biologyEndocrinologylcsh:Biology (General)ALDH-2 mitochondrial aldehyde dehydrogenaseEndothelium VascularAGE/RAGE signalingHG hyperglycemiabusinessOxidative stressRedox Biology
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Faim2 contributes to neuroprotection by erythropoietin in transient brain ischemia.

2018

Delayed cell death in the penumbra region of acute ischemic stroke occurs through apoptotic mechanisms, making it amenable to therapeutic interventions. Fas/CD95 mediates apoptotic cell death in response to external stimuli. In mature neurons, Fas/CD95 signaling is modulated by Fas-apoptotic inhibitory molecule 2 (Faim2), which reduces cell death in animal models of stroke, meningitis, and Parkinson disease. Erythropoietin (EPO) has been studied as a therapeutic strategy in ischemic stroke. Erythropoietin stimulates the phosphatidylinositol-3 kinase/Akt (PI3K/Akt) pathway, which regulates Faim2 expression. Therefore, up-regulation of Faim2 may contribute to neuroprotection by EPO. Male Faim…

Male0301 basic medicinemetabolism [Apoptosis Regulatory Proteins]FAIM2 protein humanlifeguard protein mouseIschemiaNerve Tissue Proteinspathology [Ischemic Attack Transient]physiology [Neuroprotection]PharmacologyBiochemistryNeuroprotectionmetabolism [Erythropoietin]metabolism [Ischemic Attack Transient]Brain ischemiaMice03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicinemedicineAnimalsHumansddc:610ErythropoietinStrokeProtein kinase BPI3K/AKT/mTOR pathwayAgedpharmacology [Erythropoietin]Mice Knockoutmetabolism [Nerve Tissue Proteins]business.industryPenumbraMembrane ProteinsMiddle Agedmedicine.diseaseNeuroprotection030104 developmental biologyIschemic Attack TransientErythropoietinphysiopathology [Ischemic Attack Transient]FemaleDose-dependency ; Erythropoietin ; Fas-apoptotic Inhibitory Molecule 2 ; Ischemia-reperfusion ; Neuroprotection ; StrokeApoptosis Regulatory Proteinsbusinessmetabolism [Membrane Proteins]030217 neurology & neurosurgerymedicine.drug
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