Search results for "I3"

showing 10 items of 278 documents

Longitudinal CSF proteome profiling in mice to uncover the acute and sustained mechanisms of action of rapid acting antidepressant (2R,6R)-hydroxynor…

2021

Delayed onset of antidepressant action is a shortcoming in depression treatment. Ketamine and its metabolite (2R,6R)-hydroxynorketamine (HNK) have emerged as promising rapid-acting antidepressants. However, their mechanism of action remains unknown. In this study, we first described the anxious and depression-prone inbred mouse strain, DBA/2J, as an animal model to assess the antidepressant-like effects of ketamine and HNK in vivo. To decode the molecular mechanisms mediating HNK's rapid antidepressant effects, a longitudinal cerebrospinal fluid (CSF) proteome profiling of its acute and sustained effects was conducted using an unbiased, hypothesis-free mass spectrometry-based proteomics app…

ProteomicsNeurophysiology and neuropsychologyanimal structuresHydroxynorketaminePhysiologyGlucocorticoid receptor signalingAntidepressantCSFNeurosciences. Biological psychiatry. NeuropsychiatryBiologyPharmacologyProteomicsBiochemistryCellular and Molecular NeuroscienceEndocrinologyGlucocorticoid receptorNeurotrophic factorsmedicineOriginal Research ArticleKetamine ; CSF ; Antidepressant ; (2R6R)-Hydroxynorketamine ; Glucocorticoid receptor signaling ; ProteomicsRC346-429Molecular BiologyPI3K/AKT/mTOR pathwayEndocrine and Autonomic SystemsQP351-495Mechanism of action(2R6R)-Hydroxynorketamineembryonic structuresAntidepressantKetamineNeurology. Diseases of the nervous systemmedicine.symptomSignal transductionRC321-571Neurobiology of Stress
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ErbB-3 activation by NRG-1β sustains growth and promotes vemurafenib resistance in BRAF-V600E colon cancer stem cells (CSCs)

2015

Approximately 5-10% of metastatic colorectal cancers harbor a BRAF-V600E mutation, which is correlated with resistance to EGFR-targeted therapies and worse clinical outcome. Vice versa, targeted inhibition of BRAF-V600E with the selective inhibitor PLX 4032 (Vemurafenib) is severely limited due to feedback re-activation of EGFR in these tumors. Mounting evidence indicates that upregulation of the ErbB-3 signaling axis may occur in response to several targeted therapeutics, including Vemurafenib, and NRG-1β-dependent re-activation of the PI3K/AKT survival pathway has been associated with therapy resistance. Here we show that colon CSCs express, next to EGFR and ErbB-2, also significant amoun…

Proto-Oncogene Proteins B-rafMAPK/ERK pathwayIndolesReceptor ErbB-3Colorectal cancerNeuregulin-1colon cancer stem cellsMice NudeAntineoplastic AgentsMiceErbBErbB-3medicineAnimalsHumansNeuregulin 1VemurafenibClonogenic assayskin and connective tissue diseasesProtein kinase BneoplasmsPI3K/AKT/mTOR pathwayCell ProliferationOligonucleotide Array Sequence AnalysisNRG-1βSulfonamidesbiologyReverse Transcriptase Polymerase Chain Reactionbusiness.industryFlow Cytometrymedicine.diseaseImmunohistochemistryXenograft Model Antitumor AssaysVemurafenibOncologyDrug Resistance NeoplasmColonic NeoplasmsImmunologyNeoplastic Stem CellsCancer researchbiology.proteinbusinessPriority Research Papermedicine.drug
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Novel Cancer Chemotherapy Hits by Molecular Topology: Dual Akt and Beta-Catenin Inhibitors

2015

Background and purposeColorectal and prostate cancers are two of the most common types and cause of a high rate of deaths worldwide. Therefore, any strategy to stop or at least slacken the development and progression of malignant cells is an important therapeutic choice. The aim of the present work is the identification of novel cancer chemotherapy agents. Nowadays, many different drug discovery approaches are available, but this paper focuses on Molecular Topology, which has already demonstrated its extraordinary efficacy in this field, particularly in the identification of new hit and lead compounds against cancer. This methodology uses the graph theoretical formalism to numerically chara…

Quantitative structure–activity relationshipCell SurvivalColorectal cancerScienceQuantitative Structure-Activity RelationshipAntineoplastic AgentsComputational biologyBiologyBioinformaticsProstate cancerCell Line TumorNeoplasmsDrug DiscoverymedicineHumansProtein Kinase InhibitorsProtein kinase Bbeta CateninPI3K/AKT/mTOR pathwayBiological ProductsMultidisciplinaryMolecular StructureDrug discoveryTOR Serine-Threonine KinasesQRBiological activitymedicine.diseaseMedicineTOR Serine-Threonine KinasesProto-Oncogene Proteins c-aktSignal TransductionResearch ArticlePLOS ONE
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EBV-Induced Gene 3 Transcription Is Induced by TLR Signaling in Primary Dendritic Cells via NF-κB Activation

2005

Abstract The EBV-induced gene 3 (EBI3) is expressed in dendritic cells (DCs) and part of the cytokine IL-27 that controls Th cell development. However, its regulated expression in DCs is poorly understood. In the present study we demonstrate that EBI3 is expressed in splenic CD8−, CD8+, and plasmacytoid DC subsets and is induced upon TLR signaling. Cloning and functional analysis of the EBI3 promoter using in vivo footprinting and mutagenesis showed that stimulation via TLR2, TLR4, and TLR9 transactivated the promoter in primary DCs via NF-κB and Ets binding sites at −90 and −73 bp upstream of the transcriptional start site, respectively. Furthermore, we observed that NF-κB p50/p65 and PU.1…

RNA Capsmedicine.medical_treatmentDNA Mutational AnalysisMolecular Sequence DataImmunologyAntigen-Presenting CellsReceptors Cell SurfaceBiologyCell LineMinor Histocompatibility AntigensJurkat CellsMiceCell Line TumorGene expressionmedicineAnimalsHumansImmunology and AllergyReceptors CytokinePromoter Regions GeneticGlycoproteinsMice KnockoutMembrane GlycoproteinsInnate immune systemBase SequenceToll-Like ReceptorsHEK 293 cellsNF-kappa BTLR9hemic and immune systemsEBI3Dendritic CellsMolecular biologyToll-Like Receptor 2Up-RegulationMice Inbred C57BLToll-Like Receptor 4Protein SubunitsTLR2CytokineGene Expression RegulationToll-Like Receptor 9NIH 3T3 CellsTLR4Protein BindingSignal TransductionThe Journal of Immunology
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A chemical and electrochemical multivalent memory made from FeNi3-graphene nanocomposites

2014

FeNi3-graphene nanocomposites present in acetonitrile solutions a redox couple with an electrochemical hysteresis of 2.4 V between the oxidation and the reduction maxima. In view of the high energy required for the reverse transitions, they are here proposed as chemical multilevel memories: permanent, after drying, or erasable in electrolytes, respectively. Keywords: FeNi3-graphene nanocomposites, Voltammetry, Coulovoltammetry, Redox couple, Redox hysteresis

Redox hysteresisHigh energyMaterials scienceInorganic chemistryRedox coupleFeNi3-graphene nanocompositesElectrolyteElectrochemistryRedoxlcsh:ChemistryHysteresischemistry.chemical_compoundlcsh:Industrial electrochemistrylcsh:QD1-999Graphene nanocompositeschemistryChemical engineeringCoulovoltammetryElectrochemistryVoltammetryAcetonitrileVoltammetrylcsh:TP250-261Electrochemistry Communications
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PO-350 MiRNAs and their relation to biological pathways in left- and right-sided colorectal cancer

2018

Introduction MicroRNAs (miRNAs) are involved in the regulation of gene expression in colorectal cancer (CRC), which has specific biological pathways that are predominant in either left- or right-sided CRC. However, it is unclear how miRNAs are associated with biological pathways in these two forms of CRC. Our hypothesis is that a comprehensive understanding of the fundamental biological signalling pathways in the two sides of CRC may aid in developing a decisive step towards precision medicine. We aim to clarify specific biological pathway differences of differentially expressed miRNAs between left- and right-sided CRC. Material and methods We extracted total RNA from 24 of left- and right-…

Regulation of gene expressionCancer ResearchSmall RNAColorectal cancerWnt signaling pathwayComputational biologyBiologyPrecision medicinemedicine.diseasedigestive system diseasesBiological pathwayOncologymicroRNAmedicinePI3K/AKT/mTOR pathwayESMO Open
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Mboat7 down-regulation by hyper-insulinemia induces fat accumulation in hepatocytes.

2020

Background: Naturally occurring variation in Membrane-bound O-acyltransferase domain-containing 7 (MBOAT7), encoding for an enzyme involved in phosphatidylinositol acyl-chain remodelling, has been associated with fatty liver and hepatic disorders. Here, we examined the relationship between hepatic Mboat7 down-regulation and fat accumulation. Methods: Hepatic MBOAT7 expression was surveyed in 119 obese individuals and in experimental models. MBOAT7 was acutely silenced by antisense oligonucleotides in C57Bl/6 mice, and by CRISPR/Cas9 in HepG2 hepatocytes. Findings: In obese individuals, hepatic MBOAT7 mRNA decreased from normal liver to steatohepatitis, independently of diabetes, inflammatio…

Research paperTGFβ Transforming Growth Factor BetaIntracellular SpaceCRISPR Clustered Regularly Interspaced Short Palindromic RepeatshHEPS Human HepatocytesMice0302 clinical medicineLPIAT1DAG Diacylglyceroli.p. Intraperitonealmedia_commonFatty AcidsGeneral Medicine3. Good health030220 oncology & carcinogenesisHOMA-IR homeostasis Model Assessment of Insulin ResistanceMPO morpholinolcsh:Medicine (General)medicine.medical_specialtyPE Phosphatidyl-EthanolamineNashGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesTNFα tumor Necrosis Factor AlphaLDL Low Density LipoproteinsHyperinsulinismNAFLDSD Standard Dietmedia_common.cataloged_instanceHumansCPT1 Carnitine Palmitoyltransferase IPhosphatidylinositolGene SilencingEuropean unionVLDL Very Low Density Lipoproteinlcsh:RhHSC Human Hepatic Stellate Cellsmedicine.diseaseLipid MetabolismOA Oleic AcidCI Confidence IntervalMboat7 Membrane bound O-acyltransferase domain containing 7MCD methionine choline deficient diet030104 developmental biologyEndocrinologychemistryCDP Cytidine-DiphosphateFOXO1 Forkhead Box protein O1NAFLD nonalcoholic fatty liver diseaseSteatohepatitisBMI Body Mass IndexCL CardiolipinAcyltransferases0301 basic medicineAlcoholic liver diseaseCXCL10 C-X-C Motif Chemokine 10lcsh:Medicinechemistry.chemical_compoundNon-alcoholic Fatty Liver DiseaseIFG Impaired Fasting GlucoseAPOB Apolipoprotein BNonalcoholic fatty liver diseasePIP Phosphatidyl-Inositol-PhosphateSteatohepatitisqRT-PCR quantitative Real Time Polymerase Chain ReactionMice Knockoutlcsh:R5-920ORO Oil Red O StainingPI PhosphatidylinositolFatty liverTM6SF2 Transmembrane 6 Superfamily Member 2PhospholipidTAG TriglyceridesNASH Nonalcoholic SteatohepatitisLipogenesisLPA Lyso-Phosphatidic AcidPhosphatidylinositolSignal TransductionPS Phosphatidyl-SerinePA Palmitic AcidALD alcoholic liver diseasePC Phosphatidylcholinei.v. IntravenousFATP1 Fatty Acid Transport Protein 1Models BiologicalInternal medicinemedicineAnimalsNonalcoholic fatty liver diseasePPARα Peroxisome Proliferator-Activated Receptor alphaObesityG3P Glyceraldehyde-3-PhosphateSREBP1c Sterol Regulatory Element-Binding Protein 1HDL High Density Lipoproteinsbusiness.industryPI3K Phosphatidylinositol 3 KinaseMembrane ProteinsNHEJ Non-Homologues End JoiningPNPLA3 Patatin-like Phospholipase Domain-containing-3MTTP Microsomal Triglyceride Transfer ProteinLPIAT1 Lysophosphatidylinositol Acyltransferase 1TMC4 Transmembrane Channel-Like 4Disease Models AnimalGene Expression RegulationHepatocytesFOXA2 Forkhead Box A2mTOR mammalian target of RapamycinSteatosisInsulin ResistancebusinessPG Phosphatidyl-GlycerolFABP1 Fatty Acid-Binding Protein 1 FAS Fatty Acid SynthaseT2DM Type 2 Diabetes MellitusEBioMedicine
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Pathogenesis and molecular mechanisms of anderson–fabry disease and possible new molecular addressed therapeutic strategies

2021

Anderson–Fabry disease (AFD) is a rare disease with an incidenceof approximately 1:117,000 male births. Lysosomal accumulation of globotriaosylceramide (Gb3) is the element characterizing Fabry disease due to a hereditary deficiency α-galactosidase A (GLA) enzyme. The accumulation of Gb3 causes lysosomal dysfunction that compromises cell signaling pathways. Deposition of sphingolipids occurs in the autonomic nervous system, dorsal root ganglia, kidney epithelial cells, vascular system cells, and myocardial cells, resulting in organ failure. This manuscript will review the molecular pathogenetic pathways involved in Anderson–Fabry disease and in its organ damage. Some studies reported that i…

ReviewConstriction Pathologicendothelial dysfunctionPathogenesisMicechemistry.chemical_compoundKCa3.1 activitypodocyturiaProtein IsoformsEndothelial dysfunctionBiology (General)SpectroscopyglobotriaosylceramideGlobosidesMicrogliabiologyTOR Serine-Threonine KinasesTrihexosylceramidesmiR-26a-5pGeneral MedicineMitochondriaComputer Science ApplicationsCell biologymiR-152-5pChemistrymedicine.anatomical_structureCerebrovascular CirculationAnderson–Fabry disease Endothelial dysfunction Globotriaosylceramide KCa3.1 activity MiR-1307-5p MiR-152-5p MiR-21-5p MiR-26a-5p Podocyturia Valvular dysfunctionmiR-21-5pSignal TransductionQH301-705.5GlobotriaosylceramideCatalysisInorganic ChemistryAutophagymedicineAnimalsHumansEnzyme Replacement TherapyPhysical and Theoretical ChemistryMolecular BiologyMechanistic target of rapamycinQD1-999PI3K/AKT/mTOR pathwaySphingolipidsAnderson–Fabry diseasebusiness.industryMicrocirculationOrganic ChemistryEndothelial Cellsmedicine.diseaseFabry diseaseSphingolipidMicroRNAschemistrymiR-1307-5palpha-Galactosidasebiology.proteinFabry DiseaseGlycolipidsvalvular dysfunctionLysosomesbusiness
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Suppressor of cytokine signaling 3 sensitizes anaplastic thyroid cancer to standard chemotherapy

2009

We previously showed that cancer cells from papillary, follicular, and anaplastic thyroid carcinomas produce interleukin-4 and interleukin-10, which counteract the cytotoxic activity of conventional chemotherapy through the up-regulation of antiapoptotic molecules. Here, we identify Janus kinase/signal transducers and activators of transcription (STAT) and phosphatidyl inositol 3-kinase (PI3K)/AKT as the down-stream pathways through which these cytokines confer resistance to cell death in thyroid cancer. We found that the absence of suppressors of cytokine signaling (SOCS) molecules allows the propagation of the survival signaling. Exogenous expression of SOCS1, SOCS3, and SOCS5 in the high…

STAT3 Transcription FactorCancer ResearchCancer Research; OncologyDown-RegulationMice NudeSuppressor of Cytokine Signaling Proteinsthyroidcancer spheres cytokines apoptosis chemoterapyMicePhosphatidylinositol 3-KinasesSuppressor of Cytokine Signaling 1 ProteinMedicineAnimalsHumansSOCS3Thyroid NeoplasmsAnaplastic thyroid cancerPhosphorylationThyroid cancerPI3K/AKT/mTOR pathwayAgedSettore MED/04 - Patologia GeneraleJanus kinase 1business.industrySuppressor of cytokine signaling 1Settore BIO/16 - Anatomia UmanaGene Transfer TechniquesCancerJanus Kinase 1Middle Agedmedicine.diseaseXenograft Model Antitumor AssaysSettore MED/18 - Chirurgia GeneraleOncologyDrug Resistance NeoplasmSuppressor of Cytokine Signaling 3 ProteinImmunologyCancer researchFemalebusinessJanus kinaseSTAT6 Transcription FactorProto-Oncogene Proteins c-akt
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Effect of LIF-withdrawal on acetylcholine synthesis in the embryonic stem cell line CGR8 is not mediated by STAT3, PI3Ks or cAMP/PKA pathways.

2015

Acetylcholine (ACh) acts as a local cellular signaling molecule and is widely expressed in nature, including mammalian cells and embryonic stem cells. The murine embryonic stem cell line CGR8 synthesizes and releases substantial amounts of ACh. Particularly during early differentiation - a period associated with multiple alterations in geno-/phenotype functions - synthesis and release of ACh are increased by 10-fold. In murine stem cells second messengers of the STAT-3, PI3K and cAMP/PKA pathways are involved in maintaining self-renewal and pluripotency. The present experiments were designed to test whether blockers of these signaling pathways enhance ACh cell content in the presence of LIF…

STAT3 Transcription FactorCell signalingCurcuminMorpholinesImmunologyBiologyLeukemia Inhibitory FactorGene Expression Regulation Enzymologicchemistry.chemical_compoundMicePhosphatidylinositol 3-KinasesCyclic AMPImmunology and AllergyAnimalsLY294002PI3K/AKT/mTOR pathwayEmbryonic Stem CellsPharmacologySulfonamidesForskolinColforsinIsoquinolinesEmbryonic stem cellCyclic AMP-Dependent Protein KinasesAcetylcholineCell biologychemistryChromonesSecond messenger systemSignal transductionStem cellSignal TransductionInternational immunopharmacology
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