Search results for "I3"

showing 10 items of 278 documents

Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascade inhibitors: How mutations can result in therapy resistance and how to overcome resistance

2012

// James A. McCubrey 1 , Linda S. Steelman 1 , William H. Chappell 1 , Stephen L. Abrams 1 , Richard A. Franklin 1 , Giuseppe Montalto 2 , Melchiorre Cervello 3 , Massimo Libra 4 , Saverio Candido 4 , Grazia Malaponte 4 , Maria C. Mazzarino 4 , Paolo Fagone 4 , Ferdinando Nicoletti 4 , Jorg Basecke 5 , Sanja Mijatovic 6 , Danijela Maksimovic-Ivanic 6 , Michele Milella 7 , Agostino Tafuri 8 , Francesca Chiarini 9 , Camilla Evangelisti 9 , Lucio Cocco 10 , Alberto M. Martelli 9,10 1 Department of Microbiology and Immunology, Brody School of Medicine at East Carolina University, Greenville, NC, USA 2 Department of Internal Medicine and Specialties, University of Palermo, Palermo, Italy 3 Consi…

MAPK/ERK pathwaymedicine.medical_treatmentPI3KTargeted therapyTargeted therapyPhosphatidylinositol 3-Kinases0302 clinical medicineNeoplasmsTreatment resistanceExtracellular Signal-Regulated MAP KinasesPhosphoinositide-3 Kinase InhibitorsGenetics0303 health sciencesbiologyCancer stem cellsTOR Serine-Threonine KinasesMAP Kinase Kinase KinasesDiscovery and development of mTOR inhibitorshumanities3. Good healthOncology030220 oncology & carcinogenesismTORSignal TransductionProto-Oncogene Proteins B-rafReviewsAntineoplastic Agents03 medical and health sciencesCell Line TumormedicineHumansPTENProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biologybusiness.industryAkt; Cancer stem cells; mTOR; PI3K; Raf; Targeted therapy; Therapy resistanceAktPTEN PhosphohydrolaseTherapy resistanceRafProtein phosphatase 2Targeted Therapy Therapy Resistance Cancer Stem Cells Raf Akt PI3K mTORDrug Resistance NeoplasmMutationras ProteinsCancer researchbiology.proteinbusinessProto-Oncogene Proteins c-akt
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Synergistic Growth Inhibitory Activity of Combined Mek/Mtor Pathway Blockade in Pten-Null Cancers

2014

ABSTRACT Aim: We have recently shown that induction of PTEN expression plays an integral role in MEK inhibitors' antitumor activity. Here we hypothesize that PTEN status critically influences the functional outcome of combined MEK and PI3K/mTOR inhibition. Methods: Single and combined MEK (trametinib, T) and mTOR (everolimus, E) blockade were assessed in a panel of cancer cell lines and in patient-derived lung and colon cancer stem cells (L- or C-CSC). Pharmacologic interactions were analyzed by conservative isobologram analysis. PTEN role was assessed by shRNA-mediated silencing or overexpression by stable transfection. Treatment-induced changes in the phosphoproteome were analyzed by anti…

MEK/MTORMAPK/ERK pathwayTrametinibPhosphoinositide 3-kinasebiologyKinaseRPTORHematologyOncologySettore MED/04 - PATOLOGIA GENERALEbiology.proteinCancer researchPTENProtein kinase BPI3K/AKT/mTOR pathwayAnnals of Oncology
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Monolayer-to-mesoscale modulation of the optical properties in 2D CrI3 mapped by hyperspectral microscopy

2023

Magnetic 2D materials hold promise to change the miniaturization paradigm of unidirectional photonic components. However, the integration of these materials in devices hinges on the accurate determination of the optical properties down to the monolayer limit, which is still missing. By using hyperspectral wide-field imaging at room temperature, we reveal a nonmonotonic thickness dependence of the complex optical dielectric function in the archetypal magnetic 2D material CrI3 extending across different length scales: onsetting at the mesoscale, peaking at the nanoscale, and decreasing again down to the single layer. These results portray a modification of the electronic properties of the mat…

Magnetic 2D materialsCrI3Condensed Matter - Mesoscale and Nanoscale PhysicsOptical propertiesMesoscaleHyperspectral microscopyMesoscale and Nanoscale Physics (cond-mat.mes-hall)MonolayerFOS: Physical sciences
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Muscle follistatin gene delivery increases muscle protein synthesis independent of periodical physical inactivity and fasting

2020

Blocking of myostatin and activins effectively counteracts muscle atrophy. However, the potential interaction with physical inactivity and fasting in the regulation of muscle protein synthesis is poorly understood. We used blockade of myostatin and activins by recombinant adeno-associated virus (rAAV)-mediated follistatin (FS288) overexpression in mouse tibialis anterior muscle. To investigate the effects on muscle protein synthesis, muscles were collected 7 days after rAAV-injection in the nighttime or in the daytime representing high and low levels of activity and feeding, respectively, or after overnight fasting, refeeding, or ad libitum feeding. Muscle protein synthesis was increased by…

Male0301 basic medicineFollistatinMuscle Proteinsphysical activitylihaksetMyostatinBiochemistryMice0302 clinical medicineTibialis anterior musclemedia_common2. Zero hungerbiologyChemistryactivinsFastingDependovirusMuscle atrophyCircadian RhythmMuscular Atrophymyostatinmedicine.symptomfyysinen aktiivisuusBiotechnologymedicine.medical_specialtyfastingmedia_common.quotation_subjectMechanistic Target of Rapamycin Complex 1Gene delivery03 medical and health sciencesPhysical Conditioning AnimalInternal medicineGeneticsmedicineAnimalsMolecular BiologypaastoPI3K/AKT/mTOR pathwaysolufysiologiaSarcolemmaJNK Mitogen-Activated Protein Kinasesmechanistic target of rapamycin proteinAppetiteGenetic TherapyMice Inbred C57BL030104 developmental biologyEndocrinologybiology.protein1182 Biochemistry cell and molecular biology3111 BiomedicineproteiinitEnergy Metabolismlihassurkastumasairaudet030217 neurology & neurosurgeryFollistatin
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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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A phase 2 randomized, double-blind, placebo-controlled, proof-of-concept study of oral seletalisib in primary Sjögren’s syndrome

2020

Abstract Objectives This phase 2 proof-of-concept study (NCT02610543) assessed efficacy, safety and effects on salivary gland inflammation of seletalisib, a potent and selective PI3Kδ inhibitor, in patients with moderate-to-severe primary Sjögren’s syndrome (PSS). Methods Adults with PSS were randomized 1:1 to seletalisib 45 mg/day or placebo, in addition to current PSS therapy. Primary end points were safety and tolerability and change from baseline in EULAR Sjögren’s Syndrome Disease Activity Index (ESSDAI) score at week 12. Secondary end points included change from baseline at week 12 in EULAR Sjögren’s Syndrome Patient Reported Index (ESSPRI) score and histological features in salivary …

Male0301 basic medicineSalivamedicine.medical_specialtyPyridinesprimary Sjögren’s syndromeAdministration Oralprimary Sjogren's syndromePlaceboProof of Concept StudyGastroenterologySalivary Glandshistologyseletalisib03 medical and health sciences0302 clinical medicineDouble-Blind MethodRheumatologyInternal medicineproof-of-conceptmedicineHumansPharmacology (medical)Adverse effect030203 arthritis & rheumatologySalivary glandbiologySurrogate endpointbusiness.industryMiddle Agedmedicine.diseaseSialadenitisphosphatidylinositol 3-kinase delta (PI3K delta)primary Sjögren's syndrome3. Good healthSjogren's Syndrome030104 developmental biologymedicine.anatomical_structureTolerabilityImmunoglobulin MAntirheumatic Agentsphosphatidylinositol 3-kinase delta (PI3Kδ)Quinolinesbiology.protein[SDV.IMM]Life Sciences [q-bio]/ImmunologyFemalebusiness
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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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Pterostilbene Prevents Early Diabetic Retinopathy Alterations in a Rabbit Experimental Model

2019

Oxidative stress generated by diabetes plays a key role in the development of diabetic retinopathy (DR), a common diabetic complication. DR remains asymptomatic until it reaches advanced stages, which complicate its treatment. Although it is known that good metabolic control is essential for preventing DR, knowledge of the disease is incomplete and an effective treatment with no side effects is lacking. Pterostilbene (Pter), a natural stilbene with good antioxidant activity, has proved to beneficially affect different pathologies, including diabetes. Therefore, our study aimed to analyse the protective and/or therapeutic capacity of Pter against oxidant damage by characterising early retina…

Male0301 basic medicinepterostilbenePterostilbeneretinal damageNF-E2-Related Factor 2lcsh:TX341-641Pharmacologymedicine.disease_causeAntioxidantsArticlePhosphatidylinositol 3-Kinases03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDiabetes mellitusStilbenesmedicineAnimalsoxidative stressProtein kinase BPI3K/AKT/mTOR pathwayType 1 diabetesGlycogen Synthase Kinase 3 betaNutrition and Dieteticsbusiness.industryDiabetic retinopathymedicine.diseaseEnzyme ActivationDisease Models Animaldiabetic retinopathypolyphenol030104 developmental biologychemistryHyperglycemia030220 oncology & carcinogenesisMetabolic control analysisRabbitsbusinesslcsh:Nutrition. Foods and food supplyProto-Oncogene Proteins c-aktOxidative stressSignal TransductionFood ScienceNutrients
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The K63 deubiquitinase CYLD modulates autism-like behaviors and hippocampal plasticity by regulating autophagy and mTOR signaling.

2021

Nondegradative ubiquitin chains attached to specific targets via Lysine 63 (K63) residues have emerged to play a fundamental role in synaptic function. The K63-specific deubiquitinase CYLD has been widely studied in immune cells and lately also in neurons. To better understand if CYLD plays a role in brain and synapse homeostasis, we analyzed the behavioral profile of CYLD-deficient mice. We found that the loss of CYLD results in major autism-like phenotypes including impaired social communication, increased repetitive behavior, and cognitive dysfunction. Furthermore, the absence of CYLD leads to a reduction in hippocampal network excitability, long-term potentiation, and pyramidal neuron s…

MaleAutism Spectrum DisorderNerve Tissue ProteinsHippocampal formationHippocampusDeubiquitinating enzymeSynapseMiceUbiquitinAutophagyAnimalsAutistic DisorderMechanistic target of rapamycinPI3K/AKT/mTOR pathwayNeuronsMultidisciplinarybiologyUbiquitinLysineTOR Serine-Threonine KinasesAutophagyMicrofilament ProteinsUbiquitinationLong-term potentiationBiological SciencesDeubiquitinating Enzyme CYLDMice Inbred C57BLSynapsesbiology.proteinFemaleNeuroscienceSignal TransductionProceedings of the National Academy of Sciences of the United States of America
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TGF-β Signaling Pathways in Different Compartments of the Lower Airways of Patients With Stable COPD

2017

Background: The expression and localization of transforming growth factor-β (TGF-β) pathway proteins in different compartments of the lower airways of patients with stable COPD is unclear. We aimed to determine TGF-β pathway protein expression in patients with stable COPD. Methods: The expression and localization of TGF-β pathway components was measured in the bronchial mucosa and peripheral lungs of patients with stable COPD (n = 44), control smokers with normal lung function (n = 24), and control nonsmoking subjects (n = 11) using immunohistochemical analysis. Results: TGF-β1, TGF-β3, and connective tissue growth factor expression were significantly decreased in the bronchiolar epithelium…

MaleCCN2 connective tissue growth factorSmad Proteinsairway inflammationCritical Care and Intensive Care MedicineTRAP-1 transforming growth factor-β receptor-associated binding proteinPulmonary Disease Chronic ObstructiveLAP latency-associated peptideSMAD small mother against decapentaplegicBAMBI CTGF SMAD TGF-B airway inflammation autoimmunityLungTGF transforming growth factorLLC large latent complexBAMBI CTGF SMAD TGF-β Airway Inflammation AutoimmunityautoimmunityMiddle Agedrespiratory systemLTBP latent transforming growth factor-β binding proteinImmunohistochemistryTGIF 5′-TG-3′-interacting factorECM extracellular matrixTGFBI transforming growth factor-β-induced proteinFemaleCardiology and Cardiovascular MedicinePI3K phosphoinositide 3-kinaseSignal TransductionTGF-βPulmonary and Respiratory MedicineTGF-βR TGF-β receptorSocio-culturaleBronchiRespiratory MucosaArticleTGF-BTransforming Growth Factor beta1Transforming Growth Factor beta3Macrophages AlveolarHumansAgedBAMBI; CTGF; SMAD; TGF-β; airway inflammation; autoimmunityBAMBIMembrane ProteinsCTGFBMP bone morphogenetic proteinBAMBI; CTG; SMAD; TGF-β; airway inflammation; autoimmunityCTGBAMBI bone morphogenetic proteins and activin membrane-bound inhibitorrespiratory tract diseasesairway inflammation; autoimmunity; BAMBI; CTGF; SMAD; TGF-β; Pulmonary and Respiratory Medicine; Critical Care and Intensive Care Medicine; Cardiology and Cardiovascular MedicineCase-Control StudiesBiomarkersMAPK mitogen-activated protein kinaseSMAD
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