Search results for "InAs"

showing 10 items of 4155 documents

An Attachment-Independent Biochemical Timer of the Spindle Assembly Checkpoint.

2017

The spindle assembly checkpoint (SAC) generates a diffusible protein complex that prevents anaphase until all chromosomes are properly attached to spindle microtubules. A key step in SAC initiation is the recruitment of MAD1 to kinetochores, which is generally thought to be governed by the microtubule-kinetochore (MT-KT) attachment status. However, we demonstrate that the recruitment of MAD1 via BUB1, a conserved kinetochore receptor, is not affected by MT-KT interactions in human cells. Instead, BUB1:MAD1 interaction depends on BUB1 phosphorylation, which is controlled by a biochemical timer that integrates counteracting kinase and phosphatase effects on BUB1 into a pulse-generating incohe…

0301 basic medicineMad1KinetochoreBUB1Nuclear ProteinsCell Cycle ProteinsCell BiologySpindle ApparatusBiologyProtein Serine-Threonine KinasesCell biologySpindle apparatus03 medical and health sciencesSpindle checkpoint030104 developmental biology0302 clinical medicineHEK293 CellsHumansTimerKinetochoresMolecular BiologyMitosis030217 neurology & neurosurgeryAnaphaseHeLa CellsMolecular cell
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DNA methylomes reveal biological networks involved in human eye development, functions and associated disorders

2017

This work provides a comprehensive CpG methylation landscape of the different layers of the human eye that unveils the gene networks associated with their biological functions and how these are disrupted in common visual disorders. Herein, we firstly determined the role of CpG methylation in the regulation of ocular tissue-specification and described hypermethylation of retinal transcription factors (i.e., PAX6, RAX, SIX6) in a tissue-dependent manner. Second, we have characterized the DNA methylome of visual disorders linked to internal and external environmental factors. Main conclusions allow certifying that crucial pathways related to Wnt-MAPK signaling pathways or neuroinflammation are…

0301 basic medicineMaleADNlcsh:MedicineUllRetinal NeovascularizationEyeEpigenesis Genetic0302 clinical medicinelcsh:ScienceChildCàncerCancerRegulation of gene expressionMultidisciplinaryRetinoblastomaMelanomaMethylationDNA NeoplasmOphthalmopathiesNeoplasm ProteinsGene Expression Regulation NeoplasticOftalmologiaChild PreschoolDNA methylationFemaleMetilacióOftalmopatiesAdultMAP Kinase Signaling SystemBiologyMethylationArticle03 medical and health sciencesETS1medicineHumansEye ProteinsTranscription factorDiabetic RetinopathyEye Neoplasmslcsh:RDNADNA Methylationmedicine.diseaseeye diseasesOphthalmology030104 developmental biologyImmunology030221 ophthalmology & optometryCancer researchlcsh:QPAX6
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Aging-associated genes and let-7 microRNAs: a contribution to myogenic program dysregulation in oculopharyngeal muscular dystrophy

2019

Oculopharyngeal muscular dystrophy (OPMD) is a late-onset muscle disease caused by an abnormal (GCN) triplet expansion within the polyadenylate-binding protein nuclear 1 gene and consequent mRNA pr...

0301 basic medicineMaleAgingOculopharyngealMuscle DevelopmentBiochemistryMyoblasts0302 clinical medicine80 and overMuscular DystrophyHMGB1 ProteinPAX7 Transcription FactorCell DifferentiationdifferentiationMiddle AgedCell biologymedicine.anatomical_structureFemaleMyogeninMitogen-Activated Protein KinasesBiotechnologyDifferentiation regeneration skeletal muscleAdultBiologyInclusion BodyOculopharyngeal muscular dystrophy03 medical and health sciencesmicroRNAGeneticsmedicineHumansGenetic Predisposition to Diseasedifferentiation; regeneration; skeletal muscle; Adult; Aged; Aged 80 and over; Aging; Antigens Neoplasm; Cell Differentiation; Female; Gene Expression Regulation; HMGB1 Protein; Humans; Male; MicroRNAs; Middle Aged; Mitogen-Activated Protein Kinases; Muscle Development; Muscular Dystrophy Oculopharyngeal; Myoblasts; Myogenin; Myositis Inclusion Body; PAX7 Transcription Factor; Genetic Predisposition to Diseaseskeletal muscleAntigensMolecular BiologyGeneAgedMessenger RNAMyositisRegeneration (biology)Skeletal musclemedicine.diseaseMicroRNAs030104 developmental biologyMuscle diseaseGene Expression RegulationregenerationNeoplasm030217 neurology & neurosurgery
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p38α regulates actin cytoskeleton and cytokinesis in hepatocytes during development and aging.

2017

[Background]: Hepatocyte poliploidization is an age-dependent process, being cytokinesis failure the main mechanism of polyploid hepatocyte formation. Our aim was to study the role of p38α MAPK in the regulation of actin cytoskeleton and cytokinesis in hepatocytes during development and aging. [Methods]: Wild type and p38α liver-specific knock out mice at different ages (after weaning, adults and old) were used. [Results]: We show that p38α MAPK deficiency induces actin disassembly upon aging and also cytokinesis failure leading to enhanced binucleation. Although the steady state levels of cyclin D1 in wild type and p38α knock out old livers remained unaffected, cyclin B1- a marker for G2/M…

0301 basic medicineMaleAgingRHOAPhysiologylcsh:MedicineArp2/3 complexBiochemistryMitogen-Activated Protein Kinase 14Gene Knockout TechniquesMice0302 clinical medicineContractile ProteinsAnimal CellsMedicine and Health SciencesSmall interfering RNAsCell Cycle and Cell DivisionPost-Translational ModificationPhosphorylationlcsh:ScienceCytoskeletonCyclin B1Cells CulturedCellular SenescenceCytoskeletonMice KnockoutMultidisciplinarybiologyChemistryImmunohistochemistry3. Good healthCell biologyNucleic acidsLiverCell Processes030220 oncology & carcinogenesisCellular TypesAnatomyCellular Structures and OrganellesProtein BindingResearch ArticleMitosismacromolecular substancesProtein Serine-Threonine Kinases03 medical and health sciencesHsp27CyclinsGeneticsAnimalsNon-coding RNAActinCytokinesislcsh:RBiology and Life SciencesProteinsCell BiologyActin cytoskeletonActinsGene regulationCytoskeletal Proteins030104 developmental biologybiology.proteinHepatocytesRNAlcsh:QGene expressionProtein MultimerizationPhysiological ProcessesOrganism DevelopmentCytokinesisBiomarkersDevelopmental BiologyPloS one
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NT3/TrkC Pathway Modulates the Expression of UCP-1 and Adipocyte Size in Human and Rodent Adipose Tissue

2021

Neurotrophin-3 (NT3), through activation of its tropomyosin-related kinase receptor C (TrkC), modulates neuronal survival and neural stem cell differentiation. It is widely distributed in peripheral tissues (especially vessels and pancreas) and this ubiquitous pattern suggests a role for NT3, outside the nervous system and related to metabolic functions. The presence of the NT3/TrkC pathway in the adipose tissue (AT) has never been investigated. Present work studies in human and murine adipose tissue (AT) the presence of elements of the NT3/TrkC pathway and its role on lipolysis and adipocyte differentiation. qRT-PCR and immunoblot indicate that NT3 (encoded by NTF3) was present in human re…

0301 basic medicineMaleAgingSympathetic Nervous SystemEndocrinology Diabetes and Metabolismbeta-adrenoceptorsAdipose tissueWhite adipose tissueTropomyosin receptor kinase Clcsh:Diseases of the endocrine glands. Clinical endocrinologychemistry.chemical_compound0302 clinical medicineEndocrinologyAdipocyteBrown adipose tissueUncoupling Protein 1Original ResearchbiologyChemistryCell Differentiationtropomyosin-related kinase receptor CCell biologymedicine.anatomical_structureAdipose Tissueembryonic structuresFemaleSignal Transductionanimal structuresadipocytesLipolysisUCP-1Mice TransgenicNeurotrophin-303 medical and health scienceswhite adipose tissueneurotrophin-3Receptors Adrenergic betamedicineLipolysisAnimalsHumansReceptor trkCRats WistarAgedCell Sizelcsh:RC648-665Body Weightbrown adipose tissue030104 developmental biologybiology.proteinBlood VesselsThermogenesis030217 neurology & neurosurgeryBiomarkersFrontiers in Endocrinology
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Oleoylethanolamide restores alcohol-induced inhibition of neuronal proliferation and microglial activity in striatum

2019

Previous findings demonstrate a homeostatic role for oleoylethanolamide (OEA) signaling in the ethanol-related neuroinflammation and behavior. However, extensive research is still required in order to unveil the effects of OEA on a number of neurobiological functions such as adult neurogenesis, cell survival and resident neuroimmunity that become notably altered by alcohol. Daily consumption of ethanol (10%) for 2 weeks (6.3& #x202F;± 1.1 g/kg/day during last 5 days) caused hypolocomotor activity in rats. This effect appears to rely on central signaling mechanisms given that alcohol increased the OEA levels, the gene expression of OEA-synthesizing enzyme Nape-pld and the number of PPARα-imm…

0301 basic medicineMaleApoptosisOleic AcidsStriatumPPARαOleoylethanolamidechemistry.chemical_compound0302 clinical medicineNeuronseducation.field_of_studyCaspase 3NeurogenesisMicrofilament ProteinsAlanine Transaminasegamma-GlutamyltransferaseHepatobiliary EliminationEthanolaminesMicrogliaAlcoholProto-Oncogene Proteins c-fosLocomotionFOSBSignal Transductionmedicine.medical_specialtyAlcohol DrinkingCell SurvivalPolyunsaturated AlkamidesNeurogenesisPopulationCaspase 3Arachidonic AcidsStriatumAmidohydrolases03 medical and health sciencesCellular and Molecular NeuroscienceInternal medicineGlial Fibrillary Acidic ProteinmedicinePhospholipase DAnimalsPPAR alphaAspartate AminotransferasesProgenitor cellRats WistareducationNeuroinflammationCell ProliferationPharmacologyEthanolCalcium-Binding ProteinsRatsNeostriatum030104 developmental biologyEndocrinologychemistry030217 neurology & neurosurgeryEndocannabinoids
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Somatic copy number alterations are associated with EGFR amplification and shortened survival in patients with primary glioblastoma.

2019

Glioblastoma (GBM) is the most common malignant primary tumor of the central nervous system. With no effective therapy, the prognosis for patients is terrible poor. It is highly heterogeneous and EGFR amplification is its most frequent molecular alteration. In this light, we aimed to examine the genetic heterogeneity of GBM and to correlate it with the clinical characteristics of the patients. For that purpose, we analyzed the status of EGFR and the somatic copy number alterations (CNAs) of a set of tumor suppressor genes and oncogenes. Thus, we found GBMs with high level of EGFR amplification, low level and with no EGFR amplification. Highly amplified tumors showed histological features of…

0301 basic medicineMaleCancer ResearchBiopsyL-amp GB EGFR-low amplified glioblastomamedicine.disease_causewt wildtypeMYBPC3 myosin-binding protein C0302 clinical medicineHIC1 hypermethylated in cancer 1Gene duplicationIn Situ Hybridization FluorescenceIDH2 isocitrate dehydrogenase 2MutationRB-pat RB signaling pathwayEGFRvIII epidermal growth factor receptor variant number IIIPAH phenylalanine hydroxylaseGBM glioblastoma IDH-wildtype (glioblastoma multiforme primary glioblastoma).ANOVA ANalysis Of VArianceN-amp GB EGFR-no amplified glioblastomaMiddle AgedCDKN2A cyclin-dependent kinase inhibitor 2Alcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisPrimary tumorImmunohistochemistryH-amp GB EGFR-high amplified glioblastomaErbB ReceptorsTKR-pat tyrosine-kinase receptors signaling pathway030220 oncology & carcinogenesisDisease ProgressionCDK6 cyclin-dependent kinase 6CDH1 Cadherin 1FemaleCREM cAMP response element modulatorIHC immunohistochemistryAdultOriginal articleDNA Copy Number VariationsCDKN1B cyclin-dependent kinase inhibitor 1BBiologyRARB retinoic acid receptor betaCNS central nervous systemlcsh:RC254-282IDH1 isocitrate dehydrogenase 1BCL2 B-cell cll/ lymphoma 2CNAs copy number algerationsWHO World Health Organization03 medical and health sciencesYoung Adultp53-pat p53 signaling pathwaymedicineBiomarkers TumorTMA tissue microarrayPTENHumansProtein kinase BPI3K/AKT/mTOR pathwaySurvival analysisAgedGenetic heterogeneityGene AmplificationGFAP glial fibrillary acidic proteinMLPA multiplex ligation-dependent probe amplificationmedicine.diseaseFISH fluorescence in situ hibridizationSurvival AnalysisCDKN2B cyclin-dependent kinase inhibitor 2BPTEN phosphatase and tensin homologEGFR epidermal growth factor receptorCNV-load load of copy number variations030104 developmental biologyMutationPARK2 parkinCancer researchbiology.proteinTCGA The Cancer Genome AtlasLARGE1 acetylglucosaminyltransferase-like protein 1GlioblastomaCHD7 Chromodomain Helicase DNA Binding Protein 7DAPI 4′6-diamidino-2-phenylindoleNeoplasia (New York, N.Y.)
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BRG1/SMARCA4 is essential for neuroblastoma cell viability through modulation of cell death and survival pathways.

2016

Neuroblastoma (NB) is a neoplasm of the sympathetic nervous system, and is the most common solid tumor of infancy. NBs are very heterogeneous, with a clinical course ranging from spontaneous regression to resistance to all current forms of treatment. High-risk patients need intense chemotherapy, and only 30-40% will be cured. Relapsed or metastatic tumors acquire multi-drug resistance, raising the need for alternative treatments. Owing to the diverse mechanisms that are responsible of NB chemoresistance, we aimed to target epigenetic factors that control multiple pathways to bypass therapy resistance. We found that the SWI/SNF-related, matrix-associated, actin-dependent regulator of chromat…

0301 basic medicineMaleCancer ResearchCombination therapyCell SurvivalBiologyMolecular oncologyTranscriptome03 medical and health sciencesNeuroblastomaPhosphatidylinositol 3-Kinases0302 clinical medicineGrowth factor receptorNeuroblastomaCell Line TumorGeneticsmedicineHumansMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayCell ProliferationCell DeathDNA HelicasesNuclear ProteinsCell cyclemedicine.diseaseGene Expression Regulation Neoplastic030104 developmental biologyProto-Oncogene Proteins c-bcl-2030220 oncology & carcinogenesisImmunologyCancer researchFemaleTranscriptomeSignal TransductionTranscription FactorsOncogene
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The prognostic value of the myeloid-mediated immunosuppression marker Arginase-1 in classic Hodgkin lymphoma

2016

// Alessandra Romano 1 , Nunziatina Laura Parrinello 1 , Calogero Vetro 1 , Daniele Tibullo 1 , Cesarina Giallongo 1 , Piera La Cava 1 , Annalisa Chiarenza 1 , Giovanna Motta 1 , Anastasia L. Caruso 1 , Loredana Villari 2 , Claudio Tripodo 3 , Sebastiano Cosentino 4 , Massimo Ippolito 4 , Ugo Consoli 5 , Andrea Gallamini 6 , Stefano Pileri 7 , Francesco Di Raimondo 1 1 Division of Hematology, AOU “Policlinico - Vittorio Emanuele”, University of Catania, Catania, Italy 2 Division of Pathology, AOU “Policlinico - Vittorio Emanuele”, Catania, Italy 3 Tumor Immunology Unit, Department of Health Science, University of Palermo, Palermo, Italy 4 Nuclear Medicine Center, Azienda Ospedaliera Cannizz…

0301 basic medicineMaleCancer ResearchMyeloidNeutrophilsmedicine.medical_treatmentArginase-1Treatment outcomeKaplan-Meier EstimateGastroenterology0302 clinical medicineHematologyHealthy subjectsImmunosuppressionHematologyMiddle AgedPrognosisHodgkin DiseaseTreatment Outcomemedicine.anatomical_structureOncology030220 oncology & carcinogenesisFemaleArginase-1; Hodgkin Lymphoma; PET-2Tumor immunologyResearch PaperAdultmedicine.medical_specialtyPrognostic variableAdolescentAntineoplastic AgentsPET-2Sensitivity and SpecificityDisease-Free SurvivalYoung Adult03 medical and health sciencesInternal medicineBiomarkers TumormedicineHumansProgression-free survivalAgedArginasebusiness.industryMyeloid-Derived Suppressor Cells030104 developmental biologyPotential biomarkersImmunologyHodgkin lymphomabusinessHodgkin lymphoma030215 immunologyOncotarget
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Imatinib spares cKit-expressing prostate neuroendocrine tumors, whereas kills seminal vesicle epithelial-stromal tumors by targeting PDGFR-β

2017

Abstract Prostate cancer is a leading cause of cancer-related death in males worldwide. Indeed, advanced and metastatic disease characterized by androgen resistance and often associated with neuroendocrine (NE) differentiation remains incurable. Using the spontaneous prostate cancer TRAMP model, we have shown that mast cells (MCs) support in vivo the growth of prostate adenocarcinoma, whereas their genetic or pharmacologic targeting favors prostate NE cancer arousal. Aiming at simultaneously targeting prostate NE tumor cells and MCs, both expressing the cKit tyrosine kinase receptor, we have tested the therapeutic effect of imatinib in TRAMP mice. Imatinib-treated TRAMP mice experience a pa…

0301 basic medicineMaleCancer ResearchReceptor tyrosine kinaseAntineoplastic AgentProstate cancerMice0302 clinical medicineProstatebiologySeminal VesiclesImmunohistochemistryGene Expression Regulation NeoplasticNeuroendocrine TumorsProto-Oncogene Proteins c-kitmedicine.anatomical_structureOncology030220 oncology & carcinogenesisImatinib MesylateFemaleNeuroendocrine Tumormedicine.drugTrampHumanSignal TransductionPCA3medicine.medical_specialtyStromal cellXenograft Model Antitumor AssayProtein Kinase InhibitorAntineoplastic AgentsMice TransgenicReceptor Platelet-Derived Growth Factor beta03 medical and health sciencesInternal medicineSeminal VesiclemedicineAnimalsHumansProtein Kinase InhibitorsAnimalProstatic NeoplasmsImatinibBiomarkermedicine.diseaseXenograft Model Antitumor AssaysDisease Models Animal030104 developmental biologyEndocrinologyImatinib mesylateProstatic Neoplasmbiology.proteinCancer researchBiomarkers
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