Search results for "Transcription"

showing 10 items of 2278 documents

Synergistic targeting of FLT3 mutations in AML via combined menin-MLL and FLT3 inhibition

2020

Abstract The interaction of menin (MEN1) and MLL (MLL1, KMT2A) is a dependency and provides a potential opportunity for treatment of NPM1-mutant (NPM1mut) and MLL-rearranged (MLL-r) leukemias. Concomitant activating driver mutations in the gene encoding the tyrosine kinase FLT3 occur in both leukemias and are particularly common in the NPM1mut subtype. In this study, transcriptional profiling after pharmacological inhibition of the menin-MLL complex revealed specific changes in gene expression, with downregulation of the MEIS1 transcription factor and its transcriptional target gene FLT3 being the most pronounced. Combining menin-MLL inhibition with specific small-molecule kinase inhibitors…

NPM1Transcription GeneticImmunologyApoptosisBiochemistryMiceRandom AllocationMice Inbred NODCell Line TumorProto-Oncogene Proteinshemic and lymphatic diseasesAntineoplastic Combined Chemotherapy ProtocolsGene expressionmedicineAnimalsHumansMEN1PhosphorylationMyeloid Ecotropic Viral Integration Site 1 ProteinProtein Kinase InhibitorsneoplasmsbiologyGene Expression Regulation LeukemicKinaseNuclear ProteinsMyeloid leukemiaDrug SynergismHistone-Lysine N-MethyltransferaseCell BiologyHematologymedicine.diseaseCoculture TechniquesNeoplasm ProteinsLeukemia Myeloid AcuteLeukemiaKMT2Afms-Like Tyrosine Kinase 3biology.proteinCancer researchNucleophosminProtein Processing Post-TranslationalTyrosine kinaseMyeloid-Lymphoid Leukemia ProteinBlood
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Sodium chloride is an ionic checkpoint for human Th2 cell responses and shapes the atopic skin microenvironment

2018

One sentence summarySodium is an ionic checkpoint for the induction and amplification of human Th2 cell responses and shapes the atopic skin microenvironment, where it could serve as a novel therapeutic target for Th2 mediated diseases.AbstractThere has been a strong increase in the incidence of allergic diseases over the last 50 years. Environmental factors most likely account for this phenomenon. However, the nature of these factors and the mode of action by which they induce the type 2 immune deviation, which is characteristic of atopic diseases, remains unclear. It has previously been reported that dietary sodium chloride promotes the polarization of Th17 cells with implications for aut…

Naive T cellChemistryKinaseEffectorT cellSodiumCellchemistry.chemical_elementAtopic dermatitismedicine.diseasemedicine.anatomical_structureImmunologymedicineTranscription factor
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Redox signaling in acute pancreatitis

2015

Acute pancreatitis is an inflammatory process of the pancreatic gland that eventually may lead to a severe systemic inflammatory response. A key event in pancreatic damage is the intracellular activation of NF-κB and zymogens, involving also calcium, cathepsins, pH disorders, autophagy, and cell death, particularly necrosis. This review focuses on the new role of redox signaling in acute pancreatitis. Oxidative stress and redox status are involved in the onset of acute pancreatitis and also in the development of the systemic inflammatory response, being glutathione depletion, xanthine oxidase activation, and thiol oxidation in proteins critical features of the disease in the pancreas. On th…

NecrosisGSH reduced glutathioneSTAT3 signal transducer and activator of transcription 3ERK extracellular signal-regulated kinasesClinical BiochemistryCCK cholecystokininTRAFs TNF receptor associated factorsReview ArticleIκB kinasePharmacologymedicine.disease_causeBiochemistrySHP small heterodimer partnerSTIM1 stromal interaction molecule 1chemistry.chemical_compoundHATs histone acetyltransferasesMedicineASK1GCL glutamate cysteine ligaseTNF-α tumor necrosis factor alphaIKK IκB kinaseNOS nitric oxide synthaseAcute inflammationHIF hypoxia inducible factorlcsh:QH301-705.5NF-κB nuclear factor kappa BDAMPs damage-associated molecular pattern moleculeslcsh:R5-920biologyGSSG oxidized glutathioneNF-kappa BNLRs nucleotide-binding oligomerization domain (NOD) like receptorsTRADD tumor necrosis factor receptor type 1-associated DEATH domain proteinTRPC3 transient receptor potential channel 3VEGF vascular endothelial growth factorGlutathioneTNFR tumor necrosis factor receptorHMGB1 high-mobility group Box 1 proteinIP3R inositol 145-trisphosphate receptor type 3VCAM-1 Vascular Cell adhesion protein 1Acute DiseaseJNK c-Jun N-terminal kinaseAcute pancreatitisTLRs toll-like receptorsmedicine.symptomlcsh:Medicine (General)Oxidation-ReductionAP-1 activator protein-1Signal TransductionmRNA messenger ribonucleic acidHMGB1ASC apoptosis-associated speck-like protein containing a carboxy-terminal CARDRNS reactive nitrogen speciesPTPs protein tyrosine phosphatasesROS reactive oxygen speciesNADH nicotinamide adenine dinucleotidepHe extracellular pHFAEE fatty acid ethyl estersAP acute pancreatitisHumansXanthine oxidaseCBP CREB-binding proteinRyR endoplasmic reticulum membrane ryanodine receptorsMDA malondialdehydeNO nitric oxideXO xanthine oxidaseASK1 apoptosis signal-regulating kinase-1business.industryOrganic ChemistryAutophagyNADPH nicotinamide adenine dinucleotide phosphateHDACs histone deacetylasesmedicine.diseaseCARS compensatory anti-inflammatory response syndromeXDH xanthine dehydrogenaseIL interleukinIκB inhibitor of kappa BAcute pancreatitisETC Electron transport chainPancreatitisMKPs MAPK phosphatasesSAP severe acute pancreatitischemistrylcsh:Biology (General)DTT dithiothreitolOxidative stressNAC N-acetyl cysteineImmunologybiology.proteinCalciumLysosomesReactive Oxygen SpeciesbusinessMAPK mitogen-activated protein kinaseOxidative stressERCP endoscopic retrograde cholangiopancreatographyRedox Biology
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Adenoviral RB2/p130 gene transfer inhibits smooth muscle cell proliferation and prevents restenosis after angioplasty.

1999

Abstract —Smooth muscle cell (SMC) proliferation that results in neointima formation is implicated in the pathogenesis of atherosclerotic plaques and accounts for the high rates of restenosis that occur after percutaneous transluminal coronary angioplasty, a widespread treatment for coronary artery disease. Endothelial lesions trigger intense proliferative signals to the SMCs of the subintima, stimulating their reentry into the cell cycle from a resting G 0 state, resulting in neointima formation and vascular occlusion. Cellular proliferation is negatively controlled by growth-regulatory or tumor-suppressor genes, or both, such as the retinoblastoma gene family members ( RB/p105, p107, RB2…

NeointimaTranscriptional Activationmedicine.medical_specialtyPhysiologyadenovirus; cell cycle; gene therapy; p130; prb2; restenosisCellGenetic VectorsCell Cycle ProteinsPulmonary ArteryMuscle Smooth VascularAdenoviridaeCatheterizationPathogenesisRestenosisRecurrencemedicineAnimalsCarotid StenosisAngioplasty Balloon CoronaryGenes RetinoblastomaCells CulturedNeointimal hyperplasiaWound HealingRetinoblastoma-Like Protein p130business.industryCell growthGenetic transferCell CycleProteinsGenetic TherapyCell cyclemedicine.diseasePhosphoproteinsSurgeryE2F Transcription FactorsRatsDNA-Binding Proteinsmedicine.anatomical_structureCancer researchCardiology and Cardiovascular MedicinebusinessCarotid Artery InjuriesCarrier ProteinsTunica IntimaTranscription Factor DP1Cell DivisionRetinoblastoma-Binding Protein 1Transcription FactorsCirculation research
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Antagonistic roles for Ultrabithorax and Antennapedia in regulating segment-specific apoptosis of differentiated motoneurons in the Drosophila embryo…

2008

The generation of morphological diversity among segmental units of the nervous system is crucial for correct matching of neurons with their targets and for formation of functional neuromuscular networks. However, the mechanisms leading to segment diversity remain largely unknown. We report here that the Hox genes Ultrabithorax (Ubx) and Antennapedia (Antp) regulate segment-specific survival of differentiated motoneurons in the ventral nerve cord of Drosophilaembryos. We show that Ubx is required to activate segment-specific apoptosis in these cells, and that their survival depends on Antp. Expression of the Ubx protein is strongly upregulated in the motoneurons shortly before they undergo a…

Nervous systemCentral Nervous SystemProgrammed cell deathanimal structuresEmbryo NonmammalianApoptosisBiologyAntennapediaDownregulation and upregulationmedicineAnimalsDrosophila ProteinsHox geneMolecular BiologyUltrabithoraxGeneticsHomeodomain ProteinsGene Expression Regulation DevelopmentalCell DifferentiationEmbryonic stem cellCell biologymedicine.anatomical_structureVentral nerve cordembryonic structuresAntennapedia Homeodomain ProteinDrosophilaDevelopmental BiologyTranscription FactorsDevelopment (Cambridge, England)
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Expression of Drosophila Cabut during early embryogenesis, dorsal closure and nervous system development.

2010

cabut (cbt) encodes a transcription factor involved in Drosophila dorsal closure (DC), and it is expressed in embryonic epithelial sheets and yolk cell during this process upon activation of the Jun N-terminal kinase (JNK) signaling pathway. Additional studies suggest that cbt may have a role in multiple developmental processes. To analyze Cbt localization through embryogenesis, we generated a Cbt specific antibody that has allowed detecting new Cbt expression patterns. Immunohistochemical analyses on syncytial embryos and S2 cells reveal that Cbt is localized on the surface of mitotic chromosomes at all mitotic phases. During DC, Cbt is expressed in the yolk cell, in epidermal cells and in…

Nervous systemCentral Nervous SystemRecombinant Fusion ProteinsMitosisBiologybehavioral disciplines and activities03 medical and health sciencesGenes ReporterTubulinmental disordersPeripheral Nervous SystemGeneticsmedicineAnimalsDrosophila ProteinsPromoter Regions GeneticMolecular BiologyMitosis030304 developmental biologyRegulation of gene expressionGeneticsCell Nucleus0303 health sciencesSchneider 2 cells030302 biochemistry & molecular biologyEmbryogenesisGene Expression Regulation DevelopmentalEmbryoEmbryonic stem cellDorsal closureChromatin3. Good healthCell biologyProtein Structure Tertiarymedicine.anatomical_structureEpidermal CellsOrgan SpecificityDrosophilaLamininEpidermisDevelopmental BiologyTranscription FactorsGene expression patterns : GEP
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Spatio-temporal expression of Prospero is finely tuned to allow the correct development and function of the nervous system in Drosophila melanogaster.

2007

0012-1606 (Print) Comparative Study Journal Article Research Support, Non-U.S. Gov't; Adaptive animal behaviors depend upon the precise development of the nervous system that underlies them. In Drosophila melanogaster, the pan-neural prospero gene (pros), is involved in various aspects of neurogenesis including cell cycle control, axonal outgrowth, neuronal and glial cell differentiation. As these results have been generally obtained with null pros mutants inducing embryonic lethality, the role of pros during later development remains poorly known. Using several pros-Voila (prosV) alleles, that induce multiple developmental and behavioral anomalies in the larva and in adult, we explored the…

Nervous systemDrosophila melanogaster/*embryologyTranscription Factors/genetics/*metabolismNervous SystemPolymerase Chain Reaction0302 clinical medicineMessenger/*metabolismAntenno-maxillary complexNervous System/*embryologyDrosophila ProteinsProtein IsoformsRegulation of gene expressionGenetics0303 health sciencesbiologyProtein Isoforms/genetics/metabolismNeurogenesisGene Expression Regulation DevelopmentalNuclear ProteinsDrosophila Proteins/genetics/*metabolismPhenotypehumanitiesmedicine.anatomical_structureDrosophila melanogasterPhenotypeDrosophilaDrosophila melanogastereducationContext (language use)ProsperoNerve Tissue ProteinsNerve Tissue Proteins/genetics/*metabolism03 medical and health sciencesNuclear Proteins/genetics/*metabolismmedicineIn Situ Nick-End LabelingAnimalsRNA MessengerMolecular Biology030304 developmental biologyDNA PrimersDevelopmental/*physiologyProsperoCell Biologybiology.organism_classificationGlial cell differentiationMitotic activityGlial cellGene Expression RegulationCentral nervous systemNeuronal cellsRNANeuroscience030217 neurology & neurosurgeryDevelopmental BiologyTranscription FactorsDevelopmental biology
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Ems and Nkx6 are central regulators in dorsoventral patterning of the Drosophila brain

2009

In central nervous system development, the identity of neural stem cells (neuroblasts) critically depends on the precise spatial patterning of the neuroectoderm in the dorsoventral (DV) axis. Here, we uncover a novel gene regulatory network underlying DV patterning in the Drosophila brain, and show that the cephalic gap gene empty spiracles (ems) and the Nk6 homeobox gene (Nkx6) encode key regulators. The regulatory network implicates novel interactions between these and the evolutionarily conserved homeobox genes ventral nervous system defective (vnd), intermediate neuroblasts defective (ind) and muscle segment homeobox (msh). We show that Msh cross-repressively interacts with Nkx6 to sust…

Nervous systemEmbryo Nonmammaliananimal structuresBiologyNeuroblastmedicineAnimalsDrosophila ProteinsMolecular BiologyGap geneBody PatterningHomeodomain ProteinsGeneticsRegulation of gene expressionNeuroectodermNeural tubeBrainGene Expression Regulation DevelopmentalCell biologymedicine.anatomical_structureVentral nerve cordembryonic structuresHomeoboxDrosophilaTranscription FactorsDevelopmental BiologyDevelopment
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Thyroid hormones and the central nervous system of mammals (Review)

2008

Abstract. The thyroid hormones (THs) L-thyroxine (T4) and L-triiodothyronine (T3) have a profound influence on the development and maturation of the mammalian brain, both before and after birth. Any impairment in the supply of THs to the developing nervous system leads to severe and irreversible changes in both the overall architecture and functions of the brain and causes, in humans, neurological and motor deficits known as cretinism. Pronounced neurological symptoms are also commonly observed in adult patients suffering from both hyperthyroidism and hypothyroidism, and it has recently emerged that certain symptoms might result from the reduced brain uptake, rather than the insufficient pr…

Nervous systemGene isoformeffetti non-genomiciCancer Researchmedicine.medical_specialtyCentral nervous systemBiologyormoni tiroidei; sviluppo del cervello; sistema nervoso centrale (CNS); recettori nucleari; effetti non-genomiciBiochemistryormoni tiroideiInternal medicineSettore BIO/10 - BiochimicaGeneticsmedicineTranscriptional regulationsistema nervoso centrale (CNS)ReceptorMolecular Biologymedicine.diseaseEndocrinologymedicine.anatomical_structureOncologyNuclear receptorsviluppo del cervelloMolecular MedicineCretinismrecettori nucleariHormone
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The columnar gene vnd is required for tritocerebral neuromere formation during embryonic brain development of Drosophila.

2006

International audience; In Drosophila, evolutionarily conserved transcription factors are required for the specification of neural lineages along the anteroposterior and dorsoventral axes, such as Hox genes for anteroposterior and columnar genes for dorsoventral patterning. In this report, we analyse the role of the columnar patterning gene ventral nervous system defective (vnd) in embryonic brain development. Expression of vnd is observed in specific subsets of cells in all brain neuromeres. Loss-of-function analysis focussed on the tritocerebrum shows that inactivation of vnd results in regionalized axonal patterning defects, which are comparable with the brain phenotype caused by mutatio…

Nervous systemMutantApoptosis0302 clinical medicineMESH: Gene Expression Regulation DevelopmentalDrosophila ProteinsMESH: AnimalsAxonHox geneMESH: MelatoninGenetics0303 health sciencesMESH: Pineal GlandBrainGene Expression Regulation DevelopmentalMESH: Transcription FactorsNeuromerePhenotypeBiological EvolutionCell biologymedicine.anatomical_structureDrosophila melanogasterPhenotypeMESH: Photic StimulationMESH: Body PatterningMESH: MutationMESH: Drosophila ProteinsBiologyMESH: PhenotypeMESH: Drosophila melanogaster03 medical and health sciencesMESH: BrainNeuroblastMESH: EvolutionMESH: Homeodomain ProteinsmedicineAnimalsMESH: Circadian RhythmMolecular Biology030304 developmental biologyBody PatterningHomeodomain ProteinsMESH: HumansMESH: ApoptosisEmbryogenesis[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMESH: LightMutationMESH: SerotoninMESH: Seasons030217 neurology & neurosurgeryDevelopmental BiologyTranscription Factors
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