Search results for "binding proteins"

showing 10 items of 911 documents

Acute telomerase components depletion triggers oxidative stress as an early event previous to telomeric shortening

2018

Loss of function of dyskerin (DKC1), NOP10 and TIN2 are responsible for different inheritance patterns of Dyskeratosis congenita (DC; ORPHA1775). They are key components of telomerase (DKC1 and NOP10) and shelterin (TIN2), and play an important role in telomere homeostasis. They participate in several fundamental cellular processes by contributing to Dyskeratosis congenita through mechanisms that are not fully understood. Presence of oxidative stress was postulated to result from telomerase ablation. However, the resulting disturbed redox status can promote telomere attrition by generating a vicious circle, which promotes cellular senescence. This fact prompted us to study if acute loss of …

0301 basic medicineAgingTelomeraseTelomere-Binding ProteinsClinical BiochemistryCell Cycle ProteinsBiologymedicine.disease_causeBiochemistryDyskeratosis CongenitaDyskerin03 medical and health sciencesTelomere HomeostasisRibonucleoproteins Small NucleolarmedicineHumanslcsh:QH301-705.5TelomeraseCellular SenescenceTelomere ShorteningRibonucleoproteinlcsh:R5-920TelomeropathiesOrganic ChemistryNuclear ProteinsShelterinmedicine.diseaseMolecular biologyTelomereCell biologyOxidative Stress030104 developmental biologylcsh:Biology (General)DNA damageRNA InterferenceAntioxidantlcsh:Medicine (General)Oxidative stressDyskeratosis congenitaResearch PaperHeLa CellsRedox Biology
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Palmitoylation is a post-translational modification of Alix regulating the membrane organization of exosome-like small extracellular vesicles.

2018

Abstract Background Virtually all cell types have the capacity to secrete nanometer-sized extracellular vesicles, which have emerged in recent years as potent signal transducers and cell-cell communicators. The multifunctional protein Alix is a bona fide exosomal regulator and skeletal muscle cells can release Alix-positive nano-sized extracellular vesicles, offering a new paradigm for understanding how myofibers communicate within skeletal muscle and with other organs. S-palmitoylation is a reversible lipid post-translational modification, involved in different biological processes, such as the trafficking of membrane proteins, achievement of stable protein conformations, and stabilization…

0301 basic medicineAlix (also known as PDCD6IP)Protein ConformationLipoylationLipid BilayersBiophysicsSkeletal muscle cellsCell Cycle ProteinsExosomesBiochemistryExosomeTetraspanin 29Cell Line03 medical and health sciencesExtracellular VesiclesPalmitoylationTetraspaninExtracellularHumansLipid bilayerMuscle SkeletalMolecular BiologyCells CulturedEndosomal Sorting Complexes Required for TransportChemistryVesicleCalcium-Binding ProteinsCell MembraneExtracellular vesicleTetraspaninSettore FIS/07 - Fisica Applicata(Beni Culturali Ambientali Biol.e Medicin)Cell biologyExosomeProtein Transport030104 developmental biologyS-palmitoylationMembrane proteinextracellular vesicles (EVs)Skeletal muscle cellProtein Processing Post-TranslationalProtein BindingSignal TransductionBiochimica et biophysica acta. General subjects
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Expression of Alpha-Enolase (ENO1), Myc Promoter-Binding Protein-1 (MBP-1) and Matrix Metalloproteinases (MMP-2 and MMP-9) Reflect the Nature and Agg…

2019

Breast cancer is a complex and heterogeneous disease: Several molecular alterations cause cell proliferation and the acquisition of an invasive phenotype. Extracellular matrix (ECM) is considered essential for sustaining tumor growth and matrix metalloproteinases (MMPs) have been identified as drivers of many aspects of the tumor phenotype. Mounting evidence indicates that both &alpha

0301 basic medicineAlpha-enolaseENO1Kaplan-Meier EstimateMatrix metalloproteinasemedicine.disease_causeMetastasisExtracellular matrixlcsh:Chemistry0302 clinical medicineSettore BIO/06 - Anatomia Comparata E Citologialcsh:QH301-705.5SpectroscopybiologyMMP-2General MedicineComputer Science ApplicationsDNA-Binding ProteinsGene Expression Regulation NeoplasticMatrix Metalloproteinase 9030220 oncology & carcinogenesisDisease ProgressionMatrix Metalloproteinase 2FemaleMMP-9Breast NeoplasmsCatalysisArticleInorganic Chemistry03 medical and health sciencesBreast cancerbreast cancerCell Line TumormedicineBiomarkers TumorHumansPhysical and Theoretical ChemistryMBP-1Molecular BiologyCell ProliferationTumor Suppressor ProteinsOrganic ChemistryCancermedicine.diseaseSettore BIO/18 - Genetica030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Phosphopyruvate HydrataseCancer cellbiology.proteinCancer researchCarcinogenesisInternational Journal of Molecular Sciences
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Numerous Fasciola plasminogen-binding proteins may underlie blood-brain barrier leakage and explain neurological disorder complexity and heterogeneit…

2019

15 páginas, 5 figuras y 1 tabla

0301 basic medicineAntifibrinolyticContact systemmedicine.drug_classmedicine.medical_treatment030231 tropical medicineBradykininInflammationNeurological disorderFibrinolysis systemProteomic and mass spectrometry analysesBlood–brain barrierFasciola excretome/secretomeProinflammatory cytokine03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBlood-brain barrier leakageFibrinolysismedicineIndicators and preventionAcute and chronic phasesPlasminogen-binding proteinsFasciolabiologyHuman fascioliasis030108 mycology & parasitologymedicine.diseasebiology.organism_classificationInfectious Diseasesmedicine.anatomical_structurechemistryImmunologyAnimal Science and ZoologyParasitologymedicine.symptomNeurological disordersResearch Article
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PPAR gamma agonist leriglitazone improves frataxin-loss impairments in cellular and animal models of Friedreich Ataxia

2020

Friedreich ataxia (FRDA), the most common autosomal recessive ataxia, is characterized by degeneration of the large sensory neurons and spinocerebellar tracts, cardiomyopathy, and increased incidence in diabetes. The underlying pathophysiological mechanism of FRDA, driven by a significantly decreased expression of frataxin (FXN), involves increased oxidative stress, reduced activity of enzymes containing iron‑sulfur clus-ters (ISC), defective energy production, calcium dyshomeostasis, and impaired mitochondrial biogenesis, leading to mitochondrial dysfunction. The peroxisome proliferator-activated receptor gamma (PPARγ) is a ligand-activated transcriptional factor playing a key role in mito…

0301 basic medicineAtaxiaCell SurvivalCaspase 3PPAR agonistlcsh:RC321-57103 medical and health sciencesMice0302 clinical medicineIron-Binding ProteinsmedicineNeuritesAnimalsHumansMyocytes CardiacNeurodegenerationDorsal root ganglia neuronslcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMembrane Potential MitochondrialNeuronsCardiomyocytesbiologyChemistryFrataxinNeurodegenerationCalpainLipid DropletsPeroxisomemedicine.diseaseCell biologyMitochondriaRatsPPAR gamma030104 developmental biologyNeurologyMitochondrial biogenesisFriedreich AtaxiaFrataxinbiology.proteinThiazolidinedionesmedicine.symptomMitochondrial function030217 neurology & neurosurgery
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On-demand autophagic network adaptations upon limited lipid availability

2020

The de novo synthesis of autophagic vesicles is strongly dependent on sufficient lipid supply. Recently, the RAB GTPase RAB18 was shown to affect autophagy by mediating fatty acid release from lipid droplets, which are lipid sources for autophagosome formation. The stable loss of RAB18 interfered with fatty acid release from the lipid reservoirs and provoked autophagy network adaptations aiming to maintain autophagic activity under lipid limiting conditions.

0301 basic medicineAutophagy-Related ProteinsGTPaseBiologyModels Biological03 medical and health sciencesLipid dropletAutophagyHumansMolecular Biologychemistry.chemical_classification030102 biochemistry & molecular biologyVesicleAutophagyFatty acidLipid DropletsCell BiologyAdaptation PhysiologicalLipidsCell biologyDe novo synthesis030104 developmental biologychemistryrab GTP-Binding Proteinslipids (amino acids peptides and proteins)RabCommentary and ViewsRAB18Autophagy
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Progranulin overexpression in sensory neurons attenuates neuropathic pain in mice: Role of autophagy

2016

Peripheral or central nerve injury is a frequent cause of chronic pain and the mechanisms are not fully understood. Using newly generated transgenic mice we show that progranulin overexpression in sensory neurons attenuates neuropathic pain after sciatic nerve injury and accelerates nerve healing. A yeast-2-hybrid screen revealed putative interactions of progranulin with autophagy-related proteins, ATG12 and ATG4b. This was supported by colocalization and proteomic studies showing regulations of ATG13 and ATG4b and other members of the autophagy network, lysosomal proteins and proteins involved in endocytosis. The association of progranulin with the autophagic pathway was functionally confi…

0301 basic medicineAutophagy-Related ProteinsMiceProgranulinsGanglia SpinalDorsal root gangliaGranulinsPain MeasurementCD11b AntigenMicrofilament ProteinsChronic painSciatic nerve injuryCysteine Endopeptidasesmedicine.anatomical_structureNociceptionNeurologyNeuropathic painIntercellular Signaling Peptides and Proteinsmedicine.symptomMicrotubule-Associated ProteinsNerve injuryProgranulinSensory Receptor CellsGreen Fluorescent ProteinsPainMice Transgeniclcsh:RC321-571ATG1203 medical and health sciencesLysosomal-Associated Membrane Protein 1mental disordersmedicineAutophagyAnimalslcsh:Neurosciences. Biological psychiatry. NeuropsychiatryActivating Transcription Factor 3Sensory neuronbusiness.industryAutophagyCalcium-Binding ProteinsNerve injurymedicine.diseaseSensory neuronMice Inbred C57BLDisease Models Animal030104 developmental biologyGene OntologyNeuralgiabusinessApoptosis Regulatory ProteinsNeuroscienceNeurobiology of Disease
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Virus-encoded microRNA contributes to the molecular profile of EBV-positive Burkitt lymphomas

2015

Burkitt lymphoma (BL) is an aggressive neoplasm characterized by consistent morphology and phenotype, typical clinical behavior and distinctive molecular profile. The latter is mostly driven by the MYC over-expression associated with the characteristic translocation (8;14) (q24; q32) or with variant lesions. Additional genetic events can contribute to Burkitt Lymphoma pathobiology and retain clinical significance. A pathogenetic role for Epstein-Barr virus infection in Burkitt lymphomagenesis has been suggested; however, the exact function of the virus is largely unknown. In this study, we investigated the molecular profiles (genes and microRNAs) of Epstein-Barr virus-positive and -negative…

0301 basic medicineBART6; Burkitt lymphoma; EBV; miRNA; pathogenesisEpstein-Barr Virus InfectionsHerpesvirus 4 HumanpathogenesiRNA-binding proteinRNA-Binding ProteinEpstein-Barr Virus Infectionhemic and lymphatic diseasesCluster AnalysisViralOligonucleotide Array Sequence AnalysisGeneticsBART6; Burkitt lymphoma; EBV; miRNA; pathogenesis; Burkitt Lymphoma; Cluster Analysis; Cytoskeletal Proteins; Epstein-Barr Virus Infections; Gene Expression Profiling; Gene Expression Regulation Neoplastic; Gene Expression Regulation Viral; Herpesvirus 4 Human; Host-Pathogen Interactions; Humans; Immunohistochemistry; MicroRNAs; Neoplasm Proteins; Oligonucleotide Array Sequence Analysis; Phospholipase C delta; RNA Viral; RNA-Binding Proteins; Reverse Transcriptase Polymerase Chain Reaction; ras Proteins; OncologyReverse Transcriptase Polymerase Chain ReactionpathogenesisMicrofilament ProteinsIntracellular Signaling Peptides and ProteinsBurkitt lymphomaRNA-Binding ProteinsMicroRNAPhenotypeImmunohistochemistryNeoplasm ProteinsHost-Pathogen InteractionGene Expression Regulation NeoplasticOncologyHost-Pathogen InteractionsRNA ViralHumanResearch PaperGene Expression Regulation ViralBART6BiologySettore MED/08 - Anatomia PatologicaVirusNeoplasm Protein03 medical and health sciencesEBVmicroRNACytoskeletal ProteinmedicineHumansEpstein–Barr virus infectionGenemiRNANeoplasticCluster AnalysiOligonucleotide Array Sequence AnalysiGene Expression ProfilingHerpesvirus 4ras Proteinmedicine.diseaseLymphomaGene expression profilingCytoskeletal ProteinsMicroRNAs030104 developmental biologyGene Expression Regulationras ProteinsRNABART6; EBV; burkitt lymphoma; miRNA; pathogenesisPhospholipase C deltaOncotarget
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Dynamics and predicted drug response of a gene network linking dedifferentiation with β-catenin dysfunction in hepatocellular carcinoma

2019

Background & Aims Alterations of individual genes variably affect the development of hepatocellular carcinoma (HCC). Thus, we aimed to characterize the function of tumor-promoting genes in the context of gene regulatory networks (GRNs). Methods Using data from The Cancer Genome Atlas, from the LIRI-JP (Liver Cancer – RIKEN, JP project), and from our transcriptomic, transfection and mouse transgenic experiments, we identify a GRN which functionally links LIN28B-dependent dedifferentiation with dysfunction of β-catenin (CTNNB1). We further generated and validated a quantitative mathematical model of the GRN using human cell lines and in vivo expression data. Results We found that LIN28B and C…

0301 basic medicineBeta-cateninCarcinoma HepatocellularHepatocellular carcinomaLIN28BCellGene regulatory networkPrincipal component analysisMice TransgenicBiologyTransfectionTranscriptomeCohort Studies03 medical and health sciencesMice0302 clinical medicineMathematical modelmicroRNAmedicineAnimalsHumansGene Regulatory NetworksCTNNB1Genebeta CateninHepatologySequence Analysis RNALiver NeoplasmsGene regulatory networkRNA-Binding ProteinsHGF/MET pathwayMicroRNAHep G2 CellsHCCSModels TheoreticalPrognosisPersonalized medicinedigestive system diseases030104 developmental biologymedicine.anatomical_structureCancer researchSMARCA4biology.protein030211 gastroenterology & hepatologyTranscriptome
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Extracellular Vesicles Shed by Melanoma Cells Contain a Modified Form of H1.0 Linker Histone and H1.0 mRNA-binding Proteins

2016

Extracellular vesicles (EVs) are shed in the extracellular environment by both prokaryotes and eukaryotes. Although produced from both normal and cancer cells, malignant cells release a much higher amount of EVs, which also contain tumor-specific proteins and RNAs. We previously found that G26/24 oligodendroglioma cells shed EVs that contain the pro-apoptotic factors FasL and TRAIL1-2. Interestingly, G26/24 release, via EVs, extracellular matrix remodelling proteases3, and H1° histone protein4, and mRNA. To shed further light on the role of EVs in discarding proteins and mRNAs otherwise able to counteract proliferative signals, we studied a melanoma cell line (A375). We found that also thes…

0301 basic medicineCancer ResearchCellular differentiationBlotting WesternFluorescent Antibody TechniqueMYEF2ApoptosisRNA-binding proteinexosomesmembrane vesiclesReal-Time Polymerase Chain ReactionChromatography AffinityHistones03 medical and health sciencesH1.0 linker histone; RNA-binding proteins (RBPs); extracellular vesicles (EVs) membrane vesicles (MVs); exosomes; MYEF2Settore BIO/10 - BiochimicaTumor Cells CulturedHumansexosomeSecretionRNA MessengerSettore BIO/06 - Anatomia Comparata E Citologiamelanoma cell line (A375) myelin expression factor-2 (MYEF2)MelanomaTranscription factorCell ProliferationH1.0 linker histonebiologyReverse Transcriptase Polymerase Chain ReactionEXTRACELLULAR VESICLESRNA-Binding ProteinsRNACell DifferentiationArticlesCell biologyBlotCell Transformation Neoplastic030104 developmental biologyHistoneOncologySpectrometry Mass Matrix-Assisted Laser Desorption-IonizationCancer cellbiology.proteinRNA-binding proteins (RBPs)extracellular vesicles (EVs) membrane vesicles (MVs)
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