Search results for "Cyc"

showing 10 items of 11160 documents

The MRN complex is transcriptionally regulated by MYCN during neural cell proliferation to control replication stress

2015

The MRE11/RAD50/NBS1 (MRN) complex is a major sensor of DNA double strand breaks, whose role in controlling faithful DNA replication and preventing replication stress is also emerging. Inactivation of the MRN complex invariably leads to developmental and/or degenerative neuronal defects, the pathogenesis of which still remains poorly understood. In particular, NBS1 gene mutations are associated with microcephaly and strongly impaired cerebellar development, both in humans and in the mouse model. These phenotypes strikingly overlap those induced by inactivation of MYCN, an essential promoter of the expansion of neuronal stem and progenitor cells, suggesting that MYCN and the MRN complex migh…

0301 basic medicineDNA ReplicationTranscription GeneticDNA damageDNA repairDNA-Binding ProteinCell Cycle ProteinsBiology03 medical and health sciencesMRE11 Homologue ProteinCell Cycle ProteinStrand-Break Repair; N-Myc; Dna-Replication; Human Neuroblastoma; Feingold-Syndrome; C-Myc; Mre11-Rad50-Nbs1 Complex; Targeted Disruption; Genomic Instability; Embryonic LethalityHumansProgenitor cellMolecular BiologyneoplasmsCells CulturedNuclear ProteinCell ProliferationGeneticsNeuronsOncogene ProteinsOriginal PaperMRE11 Homologue ProteinN-Myc Proto-Oncogene ProteinCell growthDNA Repair EnzymeDNA replicationOncogene ProteinNuclear ProteinsCell BiologyNeuronCell biologyAcid Anhydride HydrolasesDNA-Binding Proteins030104 developmental biologyDNA Repair EnzymesMRN complexGene Expression RegulationRad50HumanCell Death and Differentiation
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Class I histone deacetylases regulate p53/NF-κB crosstalk in cancer cells

2016

The transcription factors NF-κB and p53 as well as their crosstalk determine the fate of tumor cells upon therapeutic interventions. Replicative stress and cytokines promote signaling cascades that lead to the co-regulation of p53 and NF-κB. Consequently, nuclear p53/NF-κB signaling complexes activate NF-κB-dependent survival genes. The 18 histone deacetylases (HDACs) are epigenetic modulators that fall into four classes (I-IV). Inhibitors of histone deacetylases (HDACi) become increasingly appreciated as anti-cancer agents. Based on their effects on p53 and NF-κB, we addressed whether clinically relevant HDACi affect the NF-κB/p53 crosstalk. The chemotherapeutics hydroxyurea, etoposide, an…

0301 basic medicineDNA damageApoptosisModels BiologicalHistone Deacetylases03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorNeoplasmsHumansHydroxyureaEpigeneticsTranscription factorCellular SenescenceEtoposidebiologyNF-kappa BNF-κBCell Cycle CheckpointsDNA NeoplasmCell BiologyHDAC6Gene Expression Regulation NeoplasticHistone Deacetylase InhibitorsCrosstalk (biology)030104 developmental biologyHistonechemistry030220 oncology & carcinogenesisMutationCancer cellbiology.proteinCancer researchTumor Suppressor Protein p53VidarabineDNA DamageSignal TransductionCellular Signalling
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In Vitro Study of the Cytotoxic, Cytostatic, and Antigenotoxic Profile of Hemidesmus indicus (L.) R.Br. (Apocynaceae) Crude Drug Extract on T Lymphob…

2018

In traditional Indian medicine, the crude drug Hemidesmus indicus root—commonly known as Indian sarsaparilla—is used alone or in poly-herbal preparations for the treatment of a wide range of diseases. The present study focuses on the cancer chemopreventive and therapeutic potential of H. indicus extracts on an acute lymphoblastic leukemia cell line (CCRF-CEM). With this aim in mind, we subjected H. indicus roots to two subsequent extractions (hydro-alcoholic extraction and soxhlet extraction). As DNA damage is an important prerequisite for the induction of mutations/cancer by genotoxic carcinogens, cancer chemoprevention may be achieved by preventing genotoxicity. Through an integrated …

0301 basic medicineDNA damageCell SurvivalHealth Toxicology and MutagenesisPhytochemicalsHemidesmus indicus; cancer cells; apoptosis; cell cycle; genotoxicity; antigenotoxicityantigenotoxicitylcsh:MedicineCancer cellCrude drugPharmacologymedicine.disease_causeToxicologyProtective AgentsPlant RootsArticleNOHemidesmus indicus03 medical and health sciences0302 clinical medicineCell Line TumormedicineHumansCarcinogenHemidesmus indicusHemidesmusbiologyChemistryPlant Extractslcsh:RgenotoxicityapoptosisApoptosiHemidesmus indicuCell cyclePrecursor Cell Lymphoblastic Leukemia-Lymphomabiology.organism_classificationAntineoplastic Agents Phytogenic030104 developmental biologyApoptosis030220 oncology & carcinogenesisCancer cellcancer cellscell cycleGenotoxicity<i>Hemidesmus indicus</i>; cancer cells; apoptosis; cell cycle; genotoxicity; antigenotoxicityDNA DamageToxins
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Alterations in Tau Protein Level and Phosphorylation State in the Brain of the Autistic-Like Rats Induced by Prenatal Exposure to Valproic Acid

2021

Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by deficient social interaction and communication besides repetitive, stereotyped behaviours. A characteristic feature of ASD is altered dendritic spine density and morphology associated with synaptic plasticity disturbances. Since microtubules (MTs) regulate dendritic spine morphology and play an important role in spine development and plasticity the aim of the present study was to investigate the alterations in the content of neuronal α/β-tubulin and Tau protein level as well as phosphorylation state in the valproic acid (VPA)-induced rat model of autism. Our results indicated that maternal exposure to VPA indu…

0301 basic medicineDendritic spineHippocampuslcsh:Chemistry0302 clinical medicinePregnancyTubulinPhosphorylationlcsh:QH301-705.5SpectroscopyValproic AcidbiologyERK1/2Chemistryautism spectrum disorders (ASD)valproic acid (VPA)BrainGeneral MedicineImmunohistochemistryComputer Science Applicationsmedicine.anatomical_structureCerebral cortexMaternal ExposurePrenatal Exposure Delayed EffectsFemaleDisease Susceptibilitymedicine.drugSignal Transductionmedicine.medical_specialtyCDK5Tau proteintau ProteinsCatalysisArticleInorganic Chemistry03 medical and health sciencesInternal medicinemental disordersmedicineAnimalsPhysical and Theoretical ChemistryAutistic DisorderMolecular BiologyCyclin-dependent kinase 5GSK-3βValproic AcidOrganic Chemistryα/β-tubulinRatsEnzyme Activation030104 developmental biologyEndocrinologylcsh:Biology (General)lcsh:QD1-999MAP-TauChromatolysisSynaptic plasticitybiology.proteinAkt/mTOR signalling030217 neurology & neurosurgeryBiomarkersInternational Journal of Molecular Sciences
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Regulation of Dendritic Spine Morphology in Hippocampal Neurons by Copine-6.

2015

Dendritic spines compartmentalize information in the brain, and their morphological characteristics are thought to underly synaptic plasticity. Here we identify copine-6 as a novel modulator of dendritic spine morphology. We found that brain-derived neurotrophic factor (BDNF) - a molecule essential for long-term potentiation of synaptic strength - upregulated and recruited copine-6 to dendritic spines in hippocampal neurons. Overexpression of copine-6 increased mushroom spine number and decreased filopodia number, while copine-6 knockdown had the opposite effect and dramatically increased the number of filopodia, which lacked PSD95. Functionally, manipulation of post-synaptic copine-6 level…

0301 basic medicineDendritic spineVesicular Inhibitory Amino Acid Transport Proteinsdrug effects [Synapses]Tropomyosin receptor kinase BHippocampal formationgenetics [Carrier Proteins]pharmacology [Brain-Derived Neurotrophic Factor]Hippocampusmetabolism [Vesicular Inhibitory Amino Acid Transport Proteins]Mtap2 protein ratMice0302 clinical medicineNeurotrophic factorsdrug effects [Synaptic Vesicles]genetics [Nerve Tissue Proteins]Cells Culturedultrastructure [Neurons]NeuronsChemistryLong-term potentiationSynaptic Potentialsphysiology [Neurons]physiology [Dendritic Spines]Cell biologyultrastructure [Dendritic Spines]metabolism [Receptor trkB]Synaptic VesiclesFilopodiaultrastructure [Synaptosomes]Disks Large Homolog 4 ProteinMicrotubule-Associated ProteinsCognitive NeuroscienceDendritic Spinesmetabolism [Disks Large Homolog 4 Protein]Nerve Tissue Proteinsgenetics [Receptor trkB]03 medical and health sciencesCellular and Molecular NeuroscienceOrgan Culture Techniquesphysiology [Synaptic Vesicles]metabolism [Vesicular Glutamate Transport Protein 1]TrkB protein ratdrug effects [Synaptic Potentials]Synaptic vesicle recyclingAnimalsHumansReceptor trkBddc:610metabolism [Synaptosomes]metabolism [Nerve Tissue Proteins]Viaat protein ratBrain-Derived Neurotrophic Factormetabolism [Microtubule-Associated Proteins]Rats030104 developmental biologygenetics [Synaptic Potentials]nervous systemcytology [Hippocampus]Synaptic plasticityultrastructure [Synapses]SynapsesVesicular Glutamate Transport Protein 1CPNE6 protein ratphysiology [Synapses]Carrier Proteins030217 neurology & neurosurgerymetabolism [Carrier Proteins]SynaptosomesCerebral cortex (New York, N.Y. : 1991)
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DHA induces Jurkat T-cell arrest in G2/M phase of cell cycle and modulates the plasma membrane expression of TRPC3/6 channels.

2021

Abstract We investigated whether docosahexaenoic acid (DHA), a dietary n-3 fatty acid, modulates calcium (Ca2+) signaling and cell cycle progression in human Jurkat T-cells. Our study demonstrates that DHA inhibited Jurkat T-cell cycle progression by blocking their passage from S phase to G2/M phase. In addition, DHA decreased the plasma membrane expression of TRPC3 and TRPC6 calcium channels during T-cell proliferation. Interestingly, this fatty acid increased plasma membrane expression of TRPC6 after 24 h of mitogenic stimulation by phorbol-13-myristate-12-acetate (PMA) and ionomycin. These variations in the membrane expression of TRPC3 and TRPC6 channels were not directly correlated with…

0301 basic medicineDocosahexaenoic AcidsT-Lymphocyteschemistry.chemical_elementCalciumBiochemistryJurkat cellsCalcium in biology03 medical and health scienceschemistry.chemical_compoundJurkat CellsTRPC3TRPC6 Cation ChannelHumansTRPC Cation Channels030102 biochemistry & molecular biologyVoltage-dependent calcium channelIonomycinCell MembraneGeneral MedicineCell cycleCell biologyG2 Phase Cell Cycle Checkpoints030104 developmental biologychemistryGene Expression RegulationDocosahexaenoic acidIonomycinM Phase Cell Cycle CheckpointsTetradecanoylphorbol AcetateBiochimie
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Targeted delivery of Cyclosporine A by polymeric nanocarriers improves the therapy of inflammatory bowel disease in a relevant mouse model

2017

The therapy of inflammatory bowel diseases is still rather inefficient, and about 80% of patients require surgery at some stage. Improving the treatments by more efficient medication is, therefore, an urgent medical need. The objective of this project was to demonstrate targeted delivery of Cyclosporine-A (CYA) to the inflamed areas of the intestinal mucosa after oral administration, enabling improved alleviation of the symptoms and, at the same time, reduced systemic drug absorption and associated adverse effects. As had already been demonstrated in previous studies, nano- to micrometer-sized drug particles will accumulate at inflamed mucosal areas, providing a platform for such purposes. …

0301 basic medicineDrugColonPolymersmedia_common.quotation_subjectAdministration OralBiological AvailabilityPharmaceutical Science02 engineering and technologyPharmacologyInflammatory bowel diseaseMice03 medical and health sciencesDrug Delivery SystemsPolylactic Acid-Polyglycolic Acid CopolymerIntestinal mucosaOral administrationAnimalsMedicineLactic AcidIntestinal MucosaParticle SizeAdverse effectmedia_commonDrug CarriersMice Inbred BALB CCrohn's diseasebusiness.industryGeneral MedicineInflammatory Bowel Diseases021001 nanoscience & nanotechnologymedicine.diseaseBioavailabilityDisease Models Animal030104 developmental biologyCyclosporineNanoparticlesNanocarriers0210 nano-technologybusinessPolyglycolic AcidBiotechnologyEuropean Journal of Pharmaceutics and Biopharmaceutics
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New microRNA Biomarkers for Drug-Induced Steatosis and Their Potential to Predict the Contribution of Drugs to Non-alcoholic Fatty Liver Disease

2017

Background and Aims: Drug-induced steatosis is a major reason for drug failure in clinical trials and post-marketing withdrawal; and therefore, predictive biomarkers are essential. These could be particularly relevant in non-alcoholic fatty liver disease (NAFLD), where most patients show features of the metabolic syndrome and are prescribed with combined chronic therapies, which can contribute to fatty liver. However, specific biomarkers to assess the contribution of drugs to NAFLD are lacking. We aimed to find microRNAs (miRNAs) responsive to steatotic drugs and to investigate if they could become circulating biomarkers for drug induced steatosis. Methods: Human HepG2 cells were treated wi…

0301 basic medicineDrugFarmacologiaMicroarraymedia_common.quotation_subjectBiologyPharmacology03 medical and health scienceshepatosteatosisCyclosporin amedicinePharmacology (medical)predictive biomarkermedia_commonOriginal ResearchPharmacologyFenofibratemicroRNAFatty livernon-alcoholic fatty liver diseasemedicine.diseasePatologiadrug-induced steatosis030104 developmental biologymetabolic syndrome drugDroguesSteatosisMetabolic syndromeTamoxifenmedicine.drugFrontiers in Pharmacology
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Plasmonic Nanosensors for the Determination of Drug Effectiveness on Membrane Receptors.

2016

We demonstrate the potential of the NanoSPR (nanoscale surface plasmon resonance sensors) method as a simple and cheap tool for the quantitative study of membrane protein–protein interactions. We use NanoSPR to determine the effectiveness of two potential drug candidates that inhibit the protein complex formation between FtsA and ZipA at initial stages of bacterial division. As the NanoSPR method relies on individual gold nanorods as sensing elements, there is no need for fluorescent labels or organic cosolvents, and it provides intrinsically high statistics. NanoSPR could become a powerful tool in drug development, drug delivery, and membrane studies.

0301 basic medicineDrugMaterials sciencemedia_common.quotation_subjectNanotechnologyCell Cycle Proteins02 engineering and technology03 medical and health sciencesBacterial ProteinsNanosensorEscherichia coliGeneral Materials ScienceSurface plasmon resonancePlasmonmedia_commonEscherichia coli ProteinsSurface Plasmon Resonance021001 nanoscience & nanotechnologyNanostructuresCytoskeletal Proteins030104 developmental biologyMembraneDrug developmentDrug deliveryFtsA0210 nano-technologyCarrier ProteinsProtein BindingACS applied materialsinterfaces
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Cardiovascular toxicity of abacavir: a clinical controversy in need of a pharmacological explanation.

2017

: There is a long-lasting controversy surrounding an association between abacavir (ABC) and an increased risk of cardiovascular disease in HIV-positive patients. Although differing in their specifics, a number of published cohort studies and clinical trials support such an association, usually relating it to recent exposure to the drug, independently of traditional predisposing factors. However, other clinical trials have failed to reveal such a relation and have pointed to methodological differences to explain discrepancies. Significantly, the controversy has been fueled by the lack of a credible mechanism of action to justify the putative detrimental actions of ABC. There is a myriad of c…

0301 basic medicineDrugVasculitisAnti-HIV Agentsmedia_common.quotation_subjectImmunologyHIV InfectionsDiseasePharmacologyBioinformaticsProinflammatory cytokine03 medical and health sciencesParacrine signallingchemistry.chemical_compound0302 clinical medicineAbacavirImmunology and AllergyMedicineHumans030212 general & internal medicineCyclic guanosine monophosphatemedia_commonbusiness.industryAtherosclerosis030112 virologyDideoxynucleosidesClinical trialInfectious DiseaseschemistryMechanism of actionCardiovascular Diseasesmedicine.symptombusinessmedicine.drugAIDS (London, England)
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