Search results for "histone"

showing 10 items of 522 documents

Brain histamine and behavioral neuroscience

2017

ABSTRACT NON PREVISTO DALLA PUBBLICAZIONE

0301 basic medicineCarboxy-LyasesVideo RecordingEditorial: NeuroscienceBehavioral neuroscienceSettore BIO/09 - Fisiologiabehavioral sequenceHistonesMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAnimalsHumansMedicineMotor NeuronsBehaviorBehavior Animalbusiness.industryNeurosciencesBrainhistaminePhenotype030104 developmental biologyOncologychemistryAnesthesiaBehavior; Behavioral sequence; Histamine; Neuroscience; T-pattern; OncologyT-patternbusinessNeuroscience030217 neurology & neurosurgeryHistamineTourette SyndromeNeuroscienceOncotarget
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Induction of cancer cell stemness by depletion of macrohistone H2A1 in hepatocellular carcinoma.

2017

Hepatocellular carcinomas (HCC) contain a subpopulation of cancer stem cells (CSCs), which exhibit stem cell–like features and are responsible for tumor relapse, metastasis, and chemoresistance. The development of effective treatments for HCC will depend on a molecular-level understanding of the specific pathways driving CSC emergence and stemness. MacroH2A1 is a variant of the histone H2A and an epigenetic regulator of stem-cell function, where it promotes differentiation and, conversely, acts as a barrier to somatic-cell reprogramming. Here, we focused on the role played by the histone variant macroH2A1 as a potential epigenetic factor promoting CSC differentiation. In human HCC section…

0301 basic medicineCarcinoma HepatocellularBiologyMetastasisHistones03 medical and health sciencesCancer stem cellHistone H2AmedicineHumansEpigeneticsPhosphorylationCell ProliferationHepatologyCell growthGene Expression ProfilingLiver NeoplasmsTranscription Factor RelAHep G2 Cellsmedicine.disease030104 developmental biologyHistoneCancer cellCancer researchbiology.proteinNeoplastic Stem CellsReprogrammingHepatology (Baltimore, Md.)
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Extracellular histones activate autophagy and apoptosis via mTOR signaling in human endothelial cells.

2018

Circulating histones have been proposed as targets for therapy in sepsis and hyperinflammatory symptoms. However, the proposed strategies have failed in clinical trials. Although different mechanisms for histone-related cytotoxicity are being explored, those mediated by circulating histones are not fully understood. Extracellular histones induce endothelial cell death, thereby contributing to the pathogenesis of complex diseases such as sepsis and septic shock. Therefore, the comprehension of cellular responses triggered by histones is capital to design effective therapeutic strategies. Here we report how extracellular histones induce autophagy and apoptosis in a dose-dependent manner in cu…

0301 basic medicineCell SurvivalEndothelial cellsFisiologiaApoptosisAMP-Activated Protein KinasesHistones03 medical and health sciencesExtracellularAutophagyHuman Umbilical Vein Endothelial CellsAutophagy-Related Protein-1 HomologHumansMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwaybiologyDose-Response Relationship DrugChemistryTOR Serine-Threonine KinasesAutophagyIntracellular Signaling Peptides and ProteinsAMPKNuclear ProteinsCirculating histonesCell biologyToll-like receptorsEndothelial stem cell030104 developmental biologyHistoneApoptosisbiology.proteinMolecular MedicineProto-Oncogene Proteins c-aktSignal TransductionBiochimica et biophysica acta. Molecular basis of disease
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Epigenetic Regulation of Cardiac Differentiation of Embryonic Stem Cells and Tissues.

2016

International audience; Specific gene transcription is a key biological process that underlies cell fate decision during embryonic development. The biological process is mediated by transcription factors which bind genomic regulatory regions including enhancers and promoters of cardiac constitutive genes. DNA is wrapped around histones that are subjected to chemical modifications. Modifications of histones further lead to repressed, activated or poised gene transcription, thus bringing another level of fine tuning regulation of gene transcription. Embryonic Stem cells (ES cells) recapitulate within embryoid bodies (i.e., cell aggregates) or in 2D culture the early steps of cardiac developme…

0301 basic medicineCellular differentiationGeneral Chemical Engineering[SDV]Life Sciences [q-bio]Human Embryonic Stem Cellscardiac developmentcardiac differentiationEmbryoid bodychromatin immunoprecipitationBiologyGeneral Biochemistry Genetics and Molecular BiologyEpigenesis GeneticHistones03 medical and health sciencesMiceIssue 112AnimalsHumansEpigeneticsEnhancerTranscription factorGeneticsGeneral Immunology and MicrobiologyGeneral NeurosciencePromoterCell DifferentiationHeartgene transcription regulationEmbryonic stem cellES cellsCell biology[SDV] Life Sciences [q-bio]030104 developmental biologyEpigeneticsChromatin immunoprecipitationDevelopmental Biology
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CRISPR-Cas9 screen reveals a MYCN-amplified neuroblastoma dependency on EZH2.

2018

Pharmacologically difficult targets, such as MYC transcription factors, represent a major challenge in cancer therapy. For the childhood cancer neuroblastoma, amplification of the oncogene MYCN is associated with high-risk disease and poor prognosis. Here, we deployed genome-scale CRISPR-Cas9 screening of MYCN-amplified neuroblastoma and found a preferential dependency on genes encoding the polycomb repressive complex 2 (PRC2) components EZH2, EED, and SUZ12. Genetic and pharmacological suppression of EZH2 inhibited neuroblastoma growth in vitro and in vivo. Moreover, compared with neuroblastomas without MYCN amplification, MYCN-amplified neuroblastomas expressed higher levels of EZH2. ChIP…

0301 basic medicineCellular differentiationMedical and Health SciencesNeuroblastomaSUZ12Oncogene MYCNCRISPR-Cas SystemCancerPediatricNeuronsN-Myc Proto-Oncogene ProteinTumorEZH2EpigeneticCell DifferentiationGeneral MedicineUp-RegulationGene Expression Regulation NeoplasticOncology5.1 PharmaceuticalsEpigeneticsDevelopment of treatments and therapeutic interventionsHumanResearch ArticlePediatric Research InitiativePediatric CancerImmunologymacromolecular substancesBiologyN-Myc Proto-Oncogene ProteinCell Line03 medical and health sciencesRare DiseasesNeuroblastomaCell Line TumormedicineGeneticsHumansEnhancer of Zeste Homolog 2 ProteinTranscription factorneoplasmsNeoplasticHuman GenomeNeurosciencesGene AmplificationNeuronmedicine.disease030104 developmental biologyGene Expression RegulationCancer researchHistone deacetylaseCRISPR-Cas SystemsThe Journal of clinical investigation
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A role for Mog1 in H2Bub1 and H3K4me3 regulation affecting RNAPII transcription and mRNA export.

2018

17 páginas, 12 figuras.

0301 basic medicineChromatin ImmunoprecipitationSaccharomyces cerevisiae ProteinsTranscription GeneticSaccharomyces cerevisiaeBiologyyeastEpigenetic RepressionBiochemistryRNA TransportHistones03 medical and health sciencesHistone H30302 clinical medicineTranscription (biology)Gene Expression Regulation FungalGeneticsHistone H2BMonoubiquitinationEpigeneticsRNA MessengerMolecular BiologyGenemRNA exportepigeneticsUbiquitinationMethylationArticlesTATA-Box Binding ProteinYeastCell biology030104 developmental biologyran GTP-Binding ProteinH3K4me3EpigeneticsRNA Polymerase IItranscriptionTranscription030217 neurology & neurosurgeryH2B ubiquitinationEMBO reports
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CENP-A Is Dispensable for Mitotic Centromere Function after Initial Centromere/Kinetochore Assembly

2016

SummaryHuman centromeres are defined by chromatin containing the histone H3 variant CENP-A assembled onto repetitive alphoid DNA sequences. By inducing rapid, complete degradation of endogenous CENP-A, we now demonstrate that once the first steps of centromere assembly have been completed in G1/S, continued CENP-A binding is not required for maintaining kinetochore attachment to centromeres or for centromere function in the next mitosis. Degradation of CENP-A prior to kinetochore assembly is found to block deposition of CENP-C and CENP-N, but not CENP-T, thereby producing defective kinetochores and failure of chromosome segregation. Without the continuing presence of CENP-A, CENP-B binding …

0301 basic medicineChromosomal Proteins Non-HistoneMedical PhysiologyEpigenesis GeneticChromosome segregationModelsChromosome SegregationKinetochoresGeneticsTumormitosiKinetochorekinetochoreCell biologyChromatinChromosomal Proteinsprotein degradationCENP-ACENP-BepigeneticCENP-C1.1 Normal biological development and functioningKinetochore assemblyCentromerechromosome segregationMitosismacromolecular substancesBiologyProtein degradationModels BiologicalGeneral Biochemistry Genetics and Molecular BiologyArticleCell Line03 medical and health sciencesGeneticUnderpinning researchCentromere Protein ACell Line TumorCentromereGeneticsHumansMitosisNon-HistoneBiologicalSettore BIO/18 - Genetica030104 developmental biologyGeneric health relevanceBiochemistry and Cell BiologyauxinCentromere Protein AEpigenesisCell Reports
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Chronic stress leads to epigenetic dysregulation in the neuropeptide-Y and cannabinoid CB1 receptor genes in the mouse cingulate cortex.

2017

Persistent stress triggers a variety of mechanisms, which may ultimately lead to the occurrence of anxiety- and depression-related disorders. Epigenetic modifications represent a mechanism by which chronic stress mediates long-term effects. Here, we analyzed brain tissue from mice exposed to chronic unpredictable stress (CUS), which induced impaired emotional and nociceptive behaviors. As endocannabinoid (eCB) and neuropeptide-Y (Npy) systems modulate emotional processes, we hypothesized that CUS may affect these systems through epigenetic mechanisms. We found reduced Npy expression and Npy type 1 receptor (Npy1r) signaling, and decreased expression of the cannabinoid type 1 receptor (CB1) …

0301 basic medicineCingulate cortexMalemedicine.medical_specialtyCannabinoid receptormedicine.medical_treatmentBiologyGyrus CinguliEpigenesis Genetic03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compoundMice0302 clinical medicineReceptor Cannabinoid CB1Internal medicinemental disordersmedicineAnimalsHumansChronic stressNeuropeptide YPharmacologyHistone deacetylase 2URB597Endocannabinoid systemhumanitiesMice Inbred C57BL030104 developmental biologyEndocrinologychemistryBenzamidesCannabinoidHistone deacetylaseCarbamates030217 neurology & neurosurgeryStress PsychologicalNeuropharmacology
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Histone Post-Translational Modifications and Nucleosome Organisation in Transcriptional Regulation: Some Open Questions

2017

The organisation of chromatin is first discussed to conclude that nucleosomes play both structural and transcription-regulatory roles. The presence of nucleosomes makes difficult the access of transcriptional factors to their target sequences and the action of RNA polymerases. The histone post-translational modifications and nucleosome remodelling are first discussed, from a historical point of view, as mechanisms to remove the obstacles imposed by chromatin structure to transcription. Instead of reviewing the state of the art of the whole field, this review is centred on some open questions. First, some “non-classical” histone modifications, such as short-chain acylations other than acetyl…

0301 basic medicineComputational biologyBiologyChromatin03 medical and health sciences030104 developmental biology0302 clinical medicineHistoneAcetylation030220 oncology & carcinogenesisTranscriptional regulationbiology.proteinHistone codeNucleosomeEpigeneticsTranscription factor
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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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