Search results for " YAP"

showing 8 items of 8 documents

Structure and function of the vacuolar Ccc1/VIT1 family of iron transporters and its regulation in fungi

2020

Iron is an essential micronutrient for most living beings since it participates as a redox active cofactor in many biological processes including cellular respiration, lipid biosynthesis, DNA replication and repair, and ribosome biogenesis and recycling. However, when present in excess, iron can participate in Fenton reactions and generate reactive oxygen species that damage cells at the level of proteins, lipids and nucleic acids. Organisms have developed different molecular strategies to protect themselves against the harmful effects of high concentrations of iron. In the case of fungi and plants, detoxification mainly occurs by importing cytosolic iron into the vacuole through the Ccc1/V…

ISC Iron-sulfur lusterCS Consistency scoreCcc1Ribosome biogenesisVacuoleReview ArticleYRE Yap response elementsBiochemistryBiotecnologia0302 clinical medicineStructural BiologyCg Candida glabrata0303 health sciencesMAFFT Multiple Alignment using Fast Fourier TransformNRAMP Natural Resistance-Associated Macrophage ProteinbiologyVIT1ChemistryMBD Metal-binding domainPlantsComputer Science ApplicationsBiochemistry030220 oncology & carcinogenesisCRD Cysteine-rich domainEg Eucalyptus grandisIron detoxificationBiotechnologyCBC CCAAT-binding core complexlcsh:BiotechnologySaccharomyces cerevisiaeVTL Vacuolar iron transporter-likeBiophysicsVIT Vacuolar iron transporterbZIP basic leucine-zipper03 medical and health sciencesFongsLipid biosynthesislcsh:TP248.13-248.65GeneticsFe IronIron transportTranscription factor030304 developmental biologyComputingMethodologies_COMPUTERGRAPHICSBLOSUM BLOcks SUbstitution MatrixTMD Transmembrane domainML Maximum-likelihoodIron regulationDNA replicationFungibiology.organism_classificationYeastYeastMetabolic pathwayH HelixHap Heme activator proteinVacuoleROS Reactive oxygen speciesFerroComputational and Structural Biotechnology Journal
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Molecular mechanisms of sorafenib action in liver cancer cells.

2012

Sorafenib, a multikinase inhibitor, recently received FDA approval for the treatment of advanced hepatocellular carcinoma (HCC). However, as the clinical application of sorafenib evolves, there is increasing interest in defining the mechanisms underlying its anti-tumor activity. Considering that this specific inhibitor could target unexpected molecules depending on the biologic context, a precise understanding of its mechanism of action could be critical to maximize its treatment efficacy, while minimizing adverse effects. Two human HCC cell lines (HepG2 and Huh7), carrying different biological and genetic characteristics, were used in this study to examine the intracellular events leading …

SorafenibDNA ReplicationNiacinamideCarcinoma HepatocellularDNA RepairTranscription GeneticAngiogenesisCell SurvivalPyridinesApoptosisPharmacologyBiologysorafenib HCC mini-chromosome maintenance genes Dickkopf1 Harakiri Acheron/LARP6 YAP1 cell cycle microarray global gene expression analysisCell Line TumormedicineCell AdhesionHumansneoplasmsMolecular BiologyProtein Kinase InhibitorsCell ProliferationYAP1Neovascularization PathologicCell growthGene Expression ProfilingPhenylurea CompoundsBenzenesulfonatesCell CycleLiver NeoplasmsBiological TransportCell BiologyCell cycleSorafenibmedicine.diseasedigestive system diseasesMechanism of actionHepatocellular carcinomaProtein Biosynthesismedicine.symptomMitogen-Activated Protein KinasesLiver cancerDevelopmental Biologymedicine.drugSignal Transduction
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Breast Cancer Organoids Model Patient-Specific Response to Drug Treatment

2020

Tumor organoids are tridimensional cell culture systems that are generated in vitro from surgically resected patients&rsquo

0301 basic medicineCancer ResearchMechanotransductionBreast cancer; Dasatinib; Drug testing; Heterogeneity; Mechanotransduction; Patient‐derived tumor organoids; Statin; YAPPatient‐derived tumor organoidCellDasatinibDrug resistanceSettore MED/08 - Anatomia PatologicaBiologylcsh:RC254-282Article03 medical and health sciencesBreast cancer0302 clinical medicineBreast cancerbreast cancermedicineOrganoidSettore MED/05 - Patologia Clinicadasatinibdrug testingmechanotransductionpatient-derived tumor organoidsGenetic heterogeneitystatinStatinDrug testingBreast cancerDasatinib Drug testing Drug testing Heterogeneity Patient‐derived tumor organoids Statin YAPmedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensIn vitroDasatinib030104 developmental biologymedicine.anatomical_structureOncologyCell culture030220 oncology & carcinogenesisCancer researchPatient‐derived tumor organoidsYAPHeterogeneityheterogeneitymedicine.drugCancers
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Repurposing of Drugs Targeting YAP-TEAD Functions

2018

Drug repurposing is a fast and consolidated approach for the research of new active compounds bypassing the long streamline of the drug discovery process. Several drugs in clinical practice have been reported for modulating the major Hippo pathway’s terminal effectors, namely YAP (Yes1-associated protein), TAZ (transcriptional co-activator with PDZ-binding motif) and TEAD (transcriptional enhanced associate domains), which are directly involved in the regulation of cell growth and tissue homeostasis. Since this pathway is known to have many cross-talking phenomena with cell signaling pathways, many efforts have been made to understand its importance in oncology. Moreover, this could be rele…

0301 basic medicineCell signalingCell signalingCancer ResearchProtein-protein interactionsHippo pathwayDrug repurposingprotein-protein interactionsComputational biologyReviewBiologylcsh:RC254-28203 medical and health sciencesYAP-TEAD disruptioncell signalingRepurposingTissue homeostasisHippo signaling pathwaydrug repurposingEffectorCell growthDrug discoveryYap-tead disruptionlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensDrug repositioning030104 developmental biologyOncologyCell signaling; Drug repurposing; Hippo pathway; Protein-protein interactions; Yap-tead disruption; Oncology; Cancer ResearchCancers
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Missione sacra

2017

Traduzione dal cinese all'italiano

Wang YapingSettore L-OR/21 - Lingue E Letterature Della Cina E Dell'Asia Sud-Orientale
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YAP/TAZ activity in stromal cells prevents ageing by controlling cGAS-STING

2022

Ageing is intimately connected to the induction of cell senescence(1,2), but why this is so remains poorly understood. A key challenge isthe identification of pathways that normally suppress senescence, are lost during ageing and are functionally relevant to oppose ageing(3). Here we connected the structural and functional decline of ageing tissues to attenuated function of the master effectors of cellular mechanosignalling YAP and TAZ. YAP/TAZ activity declines during physiological ageing in stromal cells, and mimicking such decline through genetic inactivation of YAP/TAZ in these cells leads to accelerated ageing. Conversely, sustaining YAP function rejuvenates old cells and opposes the e…

AgingMechanotransductionActin-Related Protein 2; Cellular Senescence; Extracellular Matrix; Healthy Aging; Immunity Innate; Lamin Type B; Mechanotransduction Cellular; Nuclear Envelope; Signal Transduction; Aging; Membrane Proteins; Nucleotidyltransferases; Stromal Cells; Transcriptional Coactivator with PDZ-Binding Motif Proteins; YAP-Signaling ProteinsNuclear EnvelopeSettore MED/08 - Anatomia PatologicaYAP TAZ ageing C-GAS STINGMechanotransduction CellularArticleHealthy AgingInnateCellular SenescenceAdaptor Proteins Signal TransducingMultidisciplinaryLamin Type BImmunityMembrane ProteinsYAP-Signaling ProteinsPhosphoproteinsNucleotidyltransferasesImmunity InnateExtracellular MatrixTranscriptional Coactivator with PDZ-Binding Motif ProteinsActin-Related Protein 2CellularStromal CellsSignal Transduction
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Epigenomic landscape of human colorectal cancer unveils an aberrant core of pan-cancer enhancers orchestrated by YAP/TAZ

2021

Cancer is characterized by pervasive epigenetic alterations with enhancer dysfunction orchestrating the aberrant cancer transcriptional programs and transcriptional dependencies. Here, we epigenetically characterize human colorectal cancer (CRC) using de novo chromatin state discovery on a library of different patient-derived organoids. By exploring this resource, we unveil a tumor-specific deregulated enhancerome that is cancer cell-intrinsic and independent of interpatient heterogeneity. We show that the transcriptional coactivators YAP/TAZ act as key regulators of the conserved CRC gained enhancers. The same YAP/TAZ-bound enhancers display active chromatin profiles across diverse human t…

0301 basic medicineOrganoidEpigenomicsTranscription FactorGeneral Physics and AstronomyColorectal NeoplasmAdaptor Proteins Signal Transducing; Colorectal Neoplasms; Gene Expression Regulation Neoplastic; Histone Code; Humans; Models Genetic; Organoids; RNA-Seq; Single-Cell Analysis; Trans-Activators; Transcription Factors; Tumor Cells Cultured; Enhancer Elements Genetic; Epigenesis GeneticEpigenesis Genetic0302 clinical medicineModelsAdaptor Proteins Signal Transducing Colorectal Neoplasms Gene Expression Regulation NeoplasticHistone Code Humans Models Genetic Organoids RNA-Seq Single-Cell Analysis Trans-Activators Transcription Factors Tumor Cells Cultured Enhancer Elements Genetic Epigenesis GeneticTumor Cells CulturedCancer genomicsHistone codeRNA-SeqEpigenomicsAdaptor Proteins Signal Transducing; Colorectal Neoplasms; Gene Expression Regulation Neoplastic; Histone Code; Humans; Models Genetic; Organoids; RNA-Seq; Single-Cell Analysis; Trans-Activators; Transcription Factors; Transcriptional Coactivator with PDZ-Binding Motif Proteins; Tumor Cells Cultured; YAP-Signaling Proteins; Enhancer Elements Genetic; Epigenesis GeneticMultidisciplinaryCulturedQAdaptor Proteins3. Good healthChromatinTumor CellsGene Expression Regulation NeoplasticHistone CodeOrganoidsSingle-Cell AnalysiEnhancer Elements GeneticTrans-Activator030220 oncology & carcinogenesisSingle-Cell AnalysisColorectal NeoplasmsHumanEnhancer ElementsScienceTumour heterogeneityBiologyGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesGeneticmedicineHumansEpigeneticsEnhancerTranscription factorAdaptor Proteins Signal TransducingNeoplasticModels GeneticSignal TransducingCancerYAP-Signaling ProteinsGeneral Chemistrymedicine.diseaseColorectal cancerdigestive system diseases030104 developmental biologyGene Expression RegulationTranscriptional Coactivator with PDZ-Binding Motif ProteinsCancer cellCancer researchTrans-ActivatorsEpigenesisTranscription Factors
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Reduction of Cardiac Fibrosis by Interference With YAP-Dependent Transactivation

2022

Background: Conversion of cardiac stromal cells into myofibroblasts is typically associated with hypoxia conditions, metabolic insults, and/or inflammation, all of which are predisposing factors to cardiac fibrosis and heart failure. We hypothesized that this conversion could be also mediated by response of these cells to mechanical cues through activation of the Hippo transcriptional pathway. The objective of the present study was to assess the role of cellular/nuclear straining forces acting in myofibroblast differentiation of cardiac stromal cells under the control of YAP (yes-associated protein) transcription factor and to validate this finding using a pharmacological agent that interf…

Transcriptional ActivationPhysiologyfibrosismyofibroblastsVerteporfinheart failureYAP-Signaling ProteinsSettore MED/11 - Malattie dell'Apparato CardiovascolareSettore MED/23 - Chirurgia Cardiacafibrosis; heart failure; myofibroblasts; stromal cell; transcription factorsstromal cellPhosphoproteinscell mechanics; fibrosis; heart failure; myofibroblasts; stromal cell; YAP transcription factor;MiceYAP transcription factorcell mechanicsSettore CHIM/09 - Farmaceutico Tecnologico Applicativotranscription factorsTrans-ActivatorsAnimalsHumansCardiology and Cardiovascular MedicineAdaptor Proteins Signal Transducing
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