Search results for "HDAC"

showing 10 items of 72 documents

Evolutionary diversification of type-2 HDAC structure, function and regulation in Nicotiana tabacum

2018

Ministère de l'Education Nationale et de la Recherche ; Conseil Régional de Bourgogne (PARI AGRALE8) ; Association pour la Recherche sur les Nicotianacées ; Conseil Régional de Bourgogne; International audience; Type-2 HDACs (HD2s) are plant-specific histone deacetylases that play diverse roles during development and in responses to biotic and abiotic stresses. In this study we characterized the six tobacco genes encoding HD2s that mainly differ by the presence or the absence of a typical zinc finger in their C-terminal part. Of particular interest, these HD2 genes exhibit a highly conserved intron/exon structure. We then further investigated the phylogenetic relationships among the HD2 gen…

0106 biological sciences0301 basic medicineNicotiana tabacumPlant Science01 natural sciencesEvolution MolecularType-2 HDAC (HD2)03 medical and health sciencesPhylogeneticsZinc fingerTobaccoGeneticsArabidopsis thalianaGene family[SDV.BV]Life Sciences [q-bio]/Vegetal BiologyAmino Acid SequenceGenePhylogenySolanaceaePlant ProteinsZinc fingerGeneticsbiologyModels GeneticIntronZinc FingersGeneral MedicineSalt Tolerancebiology.organism_classificationSalt stress responseComplementation030104 developmental biologyHistone DeACetylase (HDAC)Agronomy and Crop ScienceSequence Alignment010606 plant biology & botany
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Plant Responses to Abiotic Stress Regulated by Histone Deacetylases

2017

In eukaryotic cells, histone acetylation and deacetylation play an important role in the regulation of gene expression. Histone acetylation levels are modulated by histone acetyltransferases (HATs) and histone deacetylases (HDACs). Recent studies indicate that HDACs play essential roles in the regulation of gene expression in plant response to environmental stress. In this review, we discussed the recent advance regarding the plant HDACs and their functions in the regulation of abiotic stress responses. The role of HDACs in autophagy was also discussed.

0106 biological sciences0301 basic medicineautophagyabiotic stressHistone acetylation and deacetylationMini ReviewPlant Sciencelcsh:Plant culture01 natural sciencesEnvironmental stress03 medical and health scienceschemistry.chemical_compoundhistone deacetylationlcsh:SB1-1110Histone AcetyltransferasesRegulation of gene expressionprotein complexesbiologyAbiotic stressAutophagyHDACsCell biology030104 developmental biologyHistonechemistryAcetylationbiology.protein010606 plant biology & botanyFrontiers in Plant Science
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Type 2 histone deacetylases play a major role in the control of elicitor-induced cell death in tobacco

2011

article addendum : Bourque S, Dutartre A, Hammoudi V, Blanc S, Dahan J, Jeandroz S, Pichereaux C, Rossignol M, Wendehenne D., 2011. Type-2 histone deacetylases as new regulators of elicitorinduced cell death in plants. New Phytologist, 192 (1), 127–139. DOI: 10.1111/j.1469-8137.2011.03788.x; International audience; The cell death which characterizes the onset of the Hypersensitive Response (HR) is a very important weapon evolved by plants to block pathogen development. By the use of numerous plant/avirulent pathogen or plant/elicitor models, we have now obtained detailed signalling pathways allowing, after pathogen or elicitor perception, the control of the expression of specific sets of ge…

0106 biological sciencesHypersensitive responseProgrammed cell death[SDV]Life Sciences [q-bio]Histone Deacetylase 2Plant ScienceModels Biological01 natural sciences03 medical and health sciencesGene Expression Regulation PlantHDACPlant CellsTobaccoNuclear proteinPlant Proteinsacetylation030304 developmental biology0303 health scienceselicitorbiologyphosphorylationHistone deacetylase 2nucleusfood and beveragesprotein kinaseAddendumElicitorCell biologycell deathHistonebiology.proteinHistone deacetylaseSignal transductionSignal Transduction010606 plant biology & botanyPlant Signaling & Behavior
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Mutant p53 induces Golgi tubulo-vesiculation driving a prometastatic secretome

2020

TP53 missense mutations leading to the expression of mutant p53 oncoproteins are frequent driver events during tumorigenesis. p53 mutants promote tumor growth, metastasis and chemoresistance by affecting fundamental cellular pathways and functions. Here, we demonstrate that p53 mutants modify structure and function of the Golgi apparatus, culminating in the increased release of a pro-malignant secretome by tumor cells and primary fibroblasts from patients with Li-Fraumeni cancer predisposition syndrome. Mechanistically, interacting with the hypoxia responsive factor HIF1α, mutant p53 induces the expression of miR-30d, which in turn causes tubulo-vesiculation of the Golgi apparatus, leading …

0301 basic medicineBiopsyGeneral Physics and AstronomyGolgi ApparatusAnimals Biopsy Breast Neoplasms Cell Line Tumor Cell Transformation Neoplastic Female Fibroblasts Gene Expression Regulation Neoplastic Golgi Apparatus Humans Hypoxia-Inducible Factor 1 alpha Subunit Li-Fraumeni Syndrome Mice MicroRNAs Microtubules Mutation Primary Cell Culture Secretory Vesicles Signal TransductionSkin Tumor Microenvironment Tumor Suppressor Protein p53 Xenograft Model Antitumor Assays02 engineering and technologymedicine.disease_causeCell TransformationMicrotubulesSettore BIO/09 - FisiologiaMetastasisLi-Fraumeni SyndromeMiceTumor MicroenvironmentGolgisecretory machinerySuper-resolution microscopyAnimals; Biopsy; Breast Neoplasms; Cell Line Tumor; Cell Transformation Neoplastic; Female; Fibroblasts; Gene Expression Regulation Neoplastic; Golgi Apparatus; Humans; Hypoxia-Inducible Factor 1 alpha Subunit; Li-Fraumeni Syndrome; Mice; MicroRNAs; Microtubules; Mutation; Primary Cell Culture; Secretory Vesicles; Signal Transduction; Skin; Tumor Microenvironment; Tumor Suppressor Protein p53; Xenograft Model Antitumor Assayslcsh:ScienceSkinMultidisciplinaryTumorChemistrymutant p53QCell migrationMicroRNASecretomics021001 nanoscience & nanotechnologyCell biologyGene Expression Regulation NeoplasticCell Transformation NeoplasticsymbolsFibroblastmiR-30dFemaleHypoxia-Inducible Factor 10210 nano-technologyBreast NeoplasmHumanSignal TransductionCancer microenvironmentStromal cellSecretory VesicleSciencePrimary Cell CultureBreast NeoplasmsMicrotubuleGolgi ApparatuSettore MED/08 - Anatomia Patologicaalpha SubunitGeneral Biochemistry Genetics and Molecular BiologyArticleCell Line03 medical and health sciencessymbols.namesakeCell Line TumormedicineAnimalsHumansSettore MED/05 - Patologia ClinicaSecretionTumor microenvironmentNeoplasticAnimalSecretory VesiclesGeneral ChemistryOncogenesGolgi apparatusHDAC6FibroblastsMicroreviewHypoxia-Inducible Factor 1 alpha SubunitmicroenvironmentXenograft Model Antitumor AssaysMicroRNAs030104 developmental biologyGene Expression RegulationMutationlcsh:QTumor Suppressor Protein p53Carcinogenesis
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HDAC1 and HDAC2 integrate the expression of p53 mutants in pancreatic cancer.

2015

Mutation of p53 is a frequent genetic lesion in pancreatic cancer being an unmet clinical challenge. Mutants of p53 have lost the tumour-suppressive functions of wild type p53. In addition, p53 mutants exert tumour-promoting functions, qualifying them as important therapeutic targets. Here, we show that the class I histone deacetylases HDAC1 and HDAC2 contribute to maintain the expression of p53 mutants in human and genetically defined murine pancreatic cancer cells. Our data reveal that the inhibition of these HDACs with small molecule HDAC inhibitors (HDACi), as well as the specific genetic elimination of HDAC1 and HDAC2, reduce the expression of mutant p53 mRNA and protein levels. We fur…

0301 basic medicineCancer ResearchProteasome Endopeptidase ComplexMutantHistone Deacetylase 2Histone Deacetylase 1Biologymedicine.disease_causeMolecular oncologyProto-Oncogene Proteins c-myc03 medical and health sciencesMicePancreatic cancerGeneticsmedicineAnimalsHumansRNA MessengerPromoter Regions GeneticMolecular BiologyRegulation of gene expressionMice KnockoutMutationWild typeCancerProto-Oncogene Proteins c-mdm2medicine.diseaseGenes p53HDAC13. Good healthGene Expression Regulation NeoplasticHistone Deacetylase InhibitorsPancreatic NeoplasmsDisease Models Animal030104 developmental biologyMutationCancer researchOncogene
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Relevance of the natural HDAC inhibitor sulforaphane as a chemopreventive agent in urologic tumors.

2018

Due to an increased understanding of molecular biology and the genomics of cancer, new and potent agents have been approved by the Food and Drug Administration (FDA) to fight this disease. However, all of these drugs cause severe side effects and resistance inevitably develops, re-activating tumor growth and dissemination. For this reason, patients turn to natural compounds as alternative or complementary treatment options, since it has been found that natural plant products may block, inhibit, or reverse cancer development. The present review focusses on the role of the natural compound sulforaphane (SFN) as an anti-tumor agent in urologic cancer. SFN is a natural compound found in crucife…

0301 basic medicineCancer ResearchUrologic NeoplasmsApoptosisDisease03 medical and health scienceschemistry.chemical_compound0302 clinical medicineIn vivoIsothiocyanatesCell Line TumorHDAC inhibitorMedicineAnticarcinogenic AgentsHumansEpigeneticsMode of actionBiological ProductsMolecular Structurebusiness.industryCruciferous vegetablesCancermedicine.diseaseHistone Deacetylase Inhibitors030104 developmental biologyOncologychemistry030220 oncology & carcinogenesisSulfoxidesBrassicaceaeCancer researchbusinessSulforaphaneCancer letters
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Epigenetic Regulation of TRAIL Signaling: Implication for Cancer Therapy

2019

International audience; One of the main characteristics of carcinogenesis relies on genetic alterations in DNA and epigenetic changes in histone and non-histone proteins. At the chromatin level, gene expression is tightly controlled by DNA methyl transferases, histone acetyltransferases (HATs), histone deacetylases (HDACs), and acetyl-binding proteins. In particular, the expression level and function of several tumor suppressor genes, or oncogenes such as c-Myc, p53 or TRAIL, have been found to be regulated by acetylation. For example, HATs are a group of enzymes, which are responsible for the acetylation of histone proteins, resulting in chromatin relaxation and transcriptional activation,…

0301 basic medicineCancer Researchtumor necrosis factor (TNF)TRAILReviewmedicine.disease_causelcsh:RC254-282Chromatin remodelingchromatin remodeling03 medical and health sciences0302 clinical medicinemedicinetumor necrosis factor (TNF).[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular Biologycancer[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyEpigeneticsHistone Acetyltransferasesbiologyhistone deacetylase (HDAC)lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens3. Good healthChromatin030104 developmental biologyHistonehistone deacetylase inhibitors (HDACIs)OncologyAcetylation030220 oncology & carcinogenesissilencingCancer researchbiology.proteinHistone deacetylasemethylationCarcinogenesisCancers
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The HDAC6 Inhibitor tubacin induces release of CD133+ extracellular vesicles from cancer cells

2017

Tumor-derived extracellular vesicles (EVs) are emerging as an important mode of intercellular communication, capable of transferring biologically active molecules that facilitate the malignant growth and metastatic process. CD133 (Prominin-1), a stem cell marker implicated in tumor initiation, differentiation and resistance to anti-cancer therapy, is reportedly associated with EVs in various types of cancer. However, little is known about the factors that regulate the release of these CD133+ EVs. Here, we report that the HDAC6 inhibitor tubacin promoted the extracellular release of CD133+ EVs from human FEMX-I metastatic melanoma and Caco-2 colorectal carcinoma cells, with a concomitant dow…

0301 basic medicineCellBiologyBiochemistry03 medical and health sciencesDownregulation and upregulationSettore BIO/13 - Biologia ApplicataExtracellularmedicineLIPIDMolecular BiologyCancerCD 133TubacinCell BiologyHDAC6MicrovesiclesCell biologyExosome030104 developmental biologymedicine.anatomical_structureTrichostatin ACancer cellCancer researchextracellular vesicleIntracellularDeacetylase activitymedicine.drug
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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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Dual inhibitors of histone deacetylases and other cancer-related targets: A pharmacological perspective.

2020

International audience; Epigenetic enzymes histone deacetylases (HDACs) are clinically validated anticancer drug targets which have been studied intensively in the past few decades. Although several drugs have been approved in this field, they are still limited to a subset of hematological malignancies (in particular T-cell lymphomas), with therapeutic potential not fully realized and the drug-resistance occurred after a certain period of use. To maximize the therapeutic potential of these classes of anticancer drugs, and to extend their application to solid tumors, numerous combination therapies containing an HDACi and an anticancer agent from other mechanisms are currently ongoing in clin…

0301 basic medicineDual targeting[SDV]Life Sciences [q-bio]Cancer therapyKinasesAntineoplastic AgentsBioinformaticsBiochemistryAnticancer drugsSynergistic effectsHistone Deacetylases03 medical and health sciences0302 clinical medicineDrug Delivery SystemsNeoplasmsReceptorsmedicineAnimalsHumansEpigeneticsPharmacologybiologybusiness.industryCancerDUAL (cognitive architecture)medicine.diseaseAnticancer drug3. Good healthEnzymesClinical trial[SDV] Life Sciences [q-bio]Histone Deacetylase Inhibitors030104 developmental biologyHistone030220 oncology & carcinogenesisbiology.proteinHistone deacetylases (HDACs)EpigeneticsDual inhibitorbusinessBiochemical pharmacology
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