Search results for " Transcription factor"

showing 10 items of 656 documents

Iwr1 facilitates RNA polymerase II dynamics during transcription elongation.

2017

Iwr1 is an RNA polymerase II (RNPII) interacting protein that directs nuclear import of the enzyme which has been previously assembled in the cytoplasm. Here we present genetic and molecular evidence that links Iwr1 with transcription. Our results indicate that Iwr1 interacts with RNPII during elongation and is involved in the disassembly of the enzyme from chromatin. This function is especially important in resolving problems posed by damage-arrested RNPII, as shown by the sensitivity of iwr1 mutants to genotoxic drugs and the Iwr1's genetic interactions with RNPII degradation pathway mutants. Moreover, absence of Iwr1 causes genome instability that is enhanced by defects in the DNA repair…

0301 basic medicineTranscription factoriesCytoplasmSaccharomyces cerevisiae ProteinsDNA RepairTranscription GeneticBiophysicsActive Transport Cell NucleusRNA polymerase IISaccharomyces cerevisiaeBiochemistryGenomic Instability03 medical and health sciencesStructural BiologyGeneticsMolecular BiologyRNA polymerase II holoenzymePolymeraseCell NucleusbiologyGeneral transcription factorMolecular biologyChromatinCell biology030104 developmental biologybiology.proteinTranscription factor II FRNA Polymerase IITranscription factor II DCarrier ProteinsTranscription factor II BDNA DamageBiochimica et biophysica acta. Gene regulatory mechanisms
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11q Deletion or ALK Activity Curbs DLG2 Expression to Maintain an Undifferentiated State in Neuroblastoma

2020

High-risk 11q deleted neuroblastomas typically display undifferentiated/poorly differentiated morphology. Neuroblastoma is thought to develop from Schwann cell precursors and undifferentiated neural crest (NC) derived cells. It is therefore vital to understand mechanisms involved in the block of differentiation. We identify an important role for oncogenic ALK-ERK1/2-SP1 signaling in maintenance of undifferentiated NC-derived progenitors via repression of DLG2, a tumor suppressor in neuroblastoma. DLG2 is expressed in the ‘bridge signature’ that represents the transcriptional transition state when neural crest cells or Schwann Cell Precursors become chromaffin cells of the adrenal gland. We …

0301 basic medicineTranscription GeneticCarcinogenesisChromaffin CellsRetinoic acidlaw.inventionNeuroblastomachemistry.chemical_compound0302 clinical medicinelawNerve Growth FactorMedicine and Health Sciencesretinoic acidAnaplastic Lymphoma Kinaselcsh:QH301-705.5NeuronsMice Inbred BALB CNeural crestCell DifferentiationPrognosisCandidate Tumor Suppressor GeneDLG2Up-RegulationCell biologyGene Expression Regulation NeoplasticERKPhenotypeTreatment Outcomemedicine.anatomical_structureFemaleChromosome Deletiontumor suppressorMAP Kinase Signaling SystemSp1 Transcription FactorSchwann cellGenetics and Molecular BiologyTretinoinBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesAdrenergic AgentsCell Line TumorNeuroblastomamedicineAnimalsHumansProgenitor cellGenePsychological repressionCell ProliferationChromosomes Human Pair 11Tumor Suppressor Proteinsmedicine.disease030104 developmental biologyALKlcsh:Biology (General)chemistryTrk receptorGeneral BiochemistrySuppressorSchwann CellsGuanylate Kinases030217 neurology & neurosurgerySSRN Electronic Journal
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E4BP4/NFIL3 modulates the epigenetically repressed RAS effector RASSF8 function through histone methyltransferases

2018

RAS proteins are major human oncogenes, and most of the studies are focused on enzymatic RAS effectors. Recently, nonenzymatic RAS effectors (RASSF, RAS association domain family) have garnered special attention because of their tumor-suppressive properties in contrast to the oncogenic potential of the classical enzymatic RAS effectors. Whereas most members of RASSF family are deregulated by promoter hypermethylation, RASSF8 promoter remains unmethylated in many cancers but the mechanism(s) of its down-regulation remains unknown. Here, we unveil E4BP4 as a critical transcriptional modulator repressing RASSF8 expression through histone methyltransferases, G9a and SUV39H1. In line with these …

0301 basic medicineTumor suppressor geneBreast NeoplasmsBiologyBiochemistryEpigenesis Genetic03 medical and health sciences0302 clinical medicineHistocompatibility AntigensHistone methylationHumansEpigeneticsMolecular BiologySUV39H1EffectorTumor Suppressor ProteinsNFIL3Molecular Bases of DiseaseCell BiologyHistone-Lysine N-MethyltransferaseMethyltransferasesCell biologyNeoplasm ProteinsGene Expression Regulation NeoplasticRepressor Proteins030104 developmental biologyBasic-Leucine Zipper Transcription FactorsHEK293 Cells030220 oncology & carcinogenesisHistone methyltransferaseMCF-7 CellsFemaleFunction (biology)
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Identification and Characterization of the Dermal Panniculus Carnosus Muscle Stem Cells

2016

Summary The dermal Panniculus carnosus (PC) muscle is important for wound contraction in lower mammals and represents an interesting model of muscle regeneration due to its high cell turnover. The resident satellite cells (the bona fide muscle stem cells) remain poorly characterized. Here we analyzed PC satellite cells with regard to developmental origin and purported function. Lineage tracing shows that they originate in Myf5+, Pax3/Pax7+ cell populations. Skin and muscle wounding increased PC myofiber turnover, with the satellite cell progeny being involved in muscle regeneration but with no detectable contribution to the wound-bed myofibroblasts. Since hematopoietic stem cells fuse to PC…

0301 basic medicineWOUNDSCellular differentiation[SDV]Life Sciences [q-bio]CellCell Culture TechniquesMuscle DevelopmentMOUSEBiochemistryMicelcsh:QH301-705.5ComputingMilieux_MISCELLANEOUSlcsh:R5-920Gene Expression Regulation DevelopmentalPAX7 Transcription FactorCell Differentiation3. Good healthPanniculus carnosusCell biologyHaematopoiesisPhenotypemedicine.anatomical_structureMOUSE;TISSUE;REPAIR;WOUNDS;MYOGENESIS;EXPRESSION;SKIN;MODEL;SATELLITE CELLS;SKELETAL-MUSCLESKELETAL-MUSCLEMYF5Stem celllcsh:Medicine (General)EXPRESSIONSatellite Cells Skeletal MuscleBone Marrow CellsMice TransgenicBiologyArticleMYOGENESIS03 medical and health sciencesSATELLITE CELLSGeneticsmedicineAnimalsRegenerationCell LineageMuscle SkeletalPAX3 Transcription FactorCell ProliferationREPAIR[ SDV ] Life Sciences [q-bio]Cell growthCell BiologyMODEL030104 developmental biologylcsh:Biology (General)Cell cultureTISSUEImmunologyBiomarkersSKINDevelopmental BiologyStem Cell Reports
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Waardenburg syndrome type I: dental phenotypes and genetic analysis of an extended family

2016

Background: The aim of this study was to describe the pattern of inheritance and the clinical features in a large family with Waardenburg syndrome type I (WS1), detailing the dental abnormalities and screening for PAX3 mutations. Material and Methods: To characterize the pattern of inheritance and clinical features, 29 family members were evaluated by dermatologic, ophthalmologic, otorhinolaryngologic and orofacial examination. Molecular analysis of the PAX3 gene was performed. Results: The pedigree of the family,including the last four generations, was constructed and revealed non-consanguineous marriages. Out of 29 descendants, 16 family members showed features of WS1, with 9 members show…

0301 basic medicineWaardenburg Syndrome Type IPAX3OdontologíaEsthetics DentalGenetic analysis03 medical and health sciencesMedicineHumansWaardenburg SyndromeGeneral DentistryPAX3 Transcription FactorGeneticsDental Enamel HypoplasiaOral Medicine and Pathologybusiness.industryWaardenburg syndromeResearchExtended familymedicine.disease:CIENCIAS MÉDICAS [UNESCO]PhenotypeCiencias de la saludPedigreestomatognathic diseases030104 developmental biologyPhenotypeOtorhinolaryngologyUNESCO::CIENCIAS MÉDICASSurgeryDental Enamel Hypoplasiabusiness
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Effects of muscular dystrophy, exercise and blocking activin receptor IIB ligands on the unfolded protein response and oxidative stress

2016

Protein homeostasis in cells, proteostasis, is maintained through several integrated processes and pathways and its dysregulation may mediate pathology in many diseases including Duchenne muscular dystrophy (DMD). Oxidative stress, heat shock proteins, endoplasmic reticulum (ER) stress and its response, i.e. unfolded protein response (UPR), play key roles in proteostasis but their involvement in the pathology of DMD are largely unknown. Moreover, exercise and activin receptor IIB blocking are two strategies that may be beneficial to DMD muscle, but studies to examine their effects on these proteostasis pathways are lacking. Therefore, these pathways were examined in the muscle of mdx mice, …

0301 basic medicineX-Box Binding Protein 1Activin Receptors Type IIEukaryotic Initiation Factor-2MyostatinUPRBiochemistryMiceeIF-2 KinaseThioredoxinsSirtuin 1ENDOPLASMIC-RETICULUM STRESSDISULFIDE-ISOMERASEPhosphorylationta315Endoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsIN-VIVOta3141Activin receptorMOUSE MODELER STRESSEndoplasmic Reticulum Stress3. Good healthmedicine.anatomical_structuremyostatinPRESERVES MUSCLE FUNCTIONER-stressSKELETAL-MUSCLEmdxSignal TransductionEXPRESSIONmedicine.medical_specialtyXBP1MDX MICEBiologyProtein Serine-Threonine Kinases03 medical and health sciencesPhysiology (medical)Internal medicineHeat shock proteinPhysical Conditioning AnimalEndoribonucleasesmedicineAnimalsHumansRNA MessengerMuscle SkeletalSkeletal muscleMyostatinGENEActivating Transcription Factor 6Immunoglobulin Fc FragmentsMuscular Dystrophy DuchenneDisease Models Animal030104 developmental biologyProteostasisEndocrinologyGene Expression RegulationUnfolded protein responsebiology.proteinMice Inbred mdxProteostasisUnfolded Protein Response3111 BiomedicineCarrier ProteinsACVR2B
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Impact of polymer-modified gold nanoparticles on brain endothelial cells: exclusion of endoplasmic reticulum stress as a potential risk factor

2016

A library of polymer-coated gold nanoparticles (AuNPs) differing in size and surface modifications was examined for uptake and induction of cellular stress responses in the endoplasmic reticulum (ER stress) in human brain endothelial cells (hCMEC/D3). ER stress is known to affect the physiology of endothelial cells (ECs) and may lead to inflammation or apoptosis. Thus, even if applied at non-cytotoxic concentrations ER stress caused by nanoparticles should be prevented to reduce the risk of vascular diseases and negative effects on the integrity of barriers (e.g. blood-brain barrier). We exposed hCMEC/D3 to twelve different AuNPs (three sizes: 18, 35, and 65 nm, each with four surface-modif…

0301 basic medicineXBP1BiPCell SurvivalPolymersBiomedical EngineeringMetal NanoparticlesApoptosis02 engineering and technologyBiologyEndoplasmic ReticulumToxicologyArticleCell LineProinflammatory cytokine03 medical and health sciencescell stressDownregulation and upregulationRisk FactorsHeat shock proteinAnimalsHumansHSP70 Heat-Shock ProteinsParticle SizeHeat-Shock ProteinsATF6Endoplasmic reticulumInterleukin-8ATF4Endothelial CellsMembrane Proteinsunfolded protein responseEndoplasmic Reticulum Stress021001 nanoscience & nanotechnologyQPActivating Transcription Factor 4Cell biology030104 developmental biologyBlood-Brain Barriertight junction proteinsImmunologyUnfolded protein responseGold0210 nano-technologyTranscription Factor CHOPNanotoxicology
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GDF11 exhibits tumor suppressive properties in hepatocellular carcinoma cells by restricting clonal expansion and invasion.

2019

Growth differentiation factor 11 (GDF11) has been characterized as a key regulator of differentiation in cells that retain stemness features, despite some controversies in age-related studies. GDF11 has been poorly investigated in cancer, particularly in those with stemness capacity, such as hepatocellular carcinoma (HCC), one of the most aggressive cancers worldwide. Here, we focused on investigating the effects of GDF11 in liver cancer cells. GDF11 treatment significantly reduced proliferation, colony and spheroid formation in HCC cell lines. Consistently, down-regulation of CDK6, cyclin D1, cyclin A, and concomitant upregulation of p27 was observed after 24 h of treatment. Interestingly,…

0301 basic medicine[SDV]Life Sciences [q-bio]Cyclin ACellChick EmbryoChorioallantoic Membrane0302 clinical medicineCell MovementCyclin D1HCCbiologyNeovascularization PathologicCell DifferentiationHep G2 CellsCell cycleCadherinsHuh7 cells3. Good health[SDV] Life Sciences [q-bio]Gene Expression Regulation NeoplasticGrowth Differentiation Factorsmedicine.anatomical_structure030220 oncology & carcinogenesisBone Morphogenetic ProteinsMolecular MedicineLiver cancerCyclin-Dependent Kinase Inhibitor p27Signal Transduction[SDV.CAN]Life Sciences [q-bio]/CancerCyclin ACell cycleHep3B cells03 medical and health sciencesCyclin D1Downregulation and upregulation[SDV.CAN] Life Sciences [q-bio]/CancerAntigens CDCell Line TumorOccludinSpheroids CellularmedicineAnimalsHumansViability assayMolecular BiologyCell Proliferation[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyCyclin-Dependent Kinase 6[SDV.MHEP.HEG] Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology030104 developmental biologyCell cultureGDF11biology.proteinCancer researchCyclin-dependent kinase 6Snail Family Transcription FactorsBiochimica et biophysica acta. Molecular basis of disease
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Enzymatic Activity of HPGD in Treg Cells Suppresses Tconv Cells to Maintain Adipose Tissue Homeostasis and Prevent Metabolic Dysfunction.

2019

Summary Regulatory T cells (Treg cells) are important for preventing autoimmunity and maintaining tissue homeostasis, but whether Treg cells can adopt tissue- or immune-context-specific suppressive mechanisms is unclear. Here, we found that the enzyme hydroxyprostaglandin dehydrogenase (HPGD), which catabolizes prostaglandin E2 (PGE2) into the metabolite 15-keto PGE2, was highly expressed in Treg cells, particularly those in visceral adipose tissue (VAT). Nuclear receptor peroxisome proliferator-activated receptor-γ (PPARγ)-induced HPGD expression in VAT Treg cells, and consequential Treg-cell-mediated generation of 15-keto PGE2 suppressed conventional T cell activation and proliferation. C…

0301 basic medicineanalogs & derivatives [Dinoprostone]Malemetabolism [Diabetes Mellitus Type 2]Adipose tissueLymphocyte Activation15-ketoprostaglandin E2T-Lymphocytes RegulatoryJurkat cellsJurkat CellsMice0302 clinical medicineimmunology [Lymphocyte Activation]genetics [Insulin Resistance]STAT5 Transcription FactorHomeostasisImmunology and AllergyTissue homeostasisgenetics [Hydroxyprostaglandin Dehydrogenases]Mice Knockoutcytology [Intra-Abdominal Fat]enzymology [T-Lymphocytes Regulatory]FOXP3hemic and immune systems3T3 CellsCell biologyInfectious Diseases030220 oncology & carcinogenesisHydroxyprostaglandin Dehydrogenasesmedicine.symptomimmunology [T-Lymphocytes Regulatory]metabolism [STAT5 Transcription Factor]Immunologymetabolism [Dinoprostone]chemical and pharmacologic phenomenaInflammationIntra-Abdominal FatBiologyDinoprostoneCell Line03 medical and health sciencesmetabolism [Hydroxyprostaglandin Dehydrogenases]immunology [Homeostasis]medicineAnimalsHumansddc:610immunology [Intra-Abdominal Fat]HEK 293 cells030104 developmental biologyHEK293 CellsDiabetes Mellitus Type 2Cell cultureInsulin ResistanceHomeostasis
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Effects of Pimozide Derivatives on pSTAT5 in K562 Cells

2017

STAT5 is a transcription factor, a member of the STAT family of signaling proteins. STAT5 is involved in many types of cancer, including chronic myelogenous leukemia (CML), in which this protein is found constitutively activated as a consequence of BCR-ABL expression. The neuroleptic drug pimozide was recently reported to act as an inhibitor of STAT5 phosphorylation and is capable of inducing apoptosis in CML cells in vitro. Our research group has synthesized simple derivatives of pimozide with cytotoxic activity and that are able to decrease the levels of phosphorylated STAT5. In this work we continued the search for novel STAT5 inhibitors, synthesizing compounds in which the benzoimidazol…

0301 basic medicineantiproliferationApoptosisPharmacologyBiochemistryAntineoplastic Agent0302 clinical medicinePimozidehemic and lymphatic diseasesDrug DiscoverySTAT5 Transcription FactorCytotoxic T cellPhosphorylationGeneral Pharmacology Toxicology and PharmaceuticsBCR-ABL-expressing leukemia; STAT5 inhibitors; antiproliferation; apoptosis; pimozideSTAT5Molecular StructurebiologyPimozidefood and beverages030220 oncology & carcinogenesisMolecular MedicinePhosphorylationHumanmedicine.drugAntineoplastic AgentsNOStructure-Activity Relationship03 medical and health sciencesK562 CellmedicineHumansTranscription factorCell ProliferationPharmacologyDose-Response Relationship DrugCell growthSTAT5 inhibitorsOrganic ChemistryApoptosiSTAT5 inhibitormedicine.disease030104 developmental biologyPharmacology Toxicology and Pharmaceutics (all)biology.proteinCancer researchBCR-ABL-expressing leukemiaDrug Screening Assays AntitumorK562 CellsK562 cellsChronic myelogenous leukemiaChemMedChem
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