Search results for " Cytoplasmic and Nuclear"

showing 10 items of 80 documents

Dynamic intracellular survivin in oral squamous cell carcinoma: underlying molecular mechanism and potential as an early prognostic marker

2007

Survivin functions as an apoptosis inhibitor and a regulator of cell division in many tumours. The intracellular localization of survivin in tumours has been suggested as a prognostic marker. However, current reports are inconsistent and the underlying molecular mechanisms are not understood. The present study has examined the localization and prognostic value of nuclear and cytoplasmic survivin in the pre-therapeutic biopsies from 71 oral and oropharyngeal squamous carcinoma (OSCC) patients. Statistical analysis indicated that preferential nuclear versus cytoplasmic survivin correlated with favourable versus unfavourable disease outcome. Uni- and multi-variate analysis showed that in contr…

CytoplasmProgrammed cell deathPathologymedicine.medical_specialtySurvivinReceptors Cytoplasmic and NuclearApoptosisKaplan-Meier EstimateCysteine Proteinase InhibitorsKaryopherinsInhibitor of Apoptosis ProteinsPathology and Forensic MedicineCell Line TumorSurvivinBiomarkers TumorCarcinomaHumansMedicineNuclear export signalneoplasmsCell NucleusNuclear Export SignalsPredictive markerbusiness.industryCell cyclePrognosismedicine.diseaseImmunohistochemistryNeoplasm ProteinsSquamous carcinomaOropharyngeal NeoplasmsHead and Neck NeoplasmsApoptosisCarcinoma Squamous CellCancer researchMouth NeoplasmsbusinessMicrotubule-Associated ProteinsThe Journal of Pathology
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T helper 17 lineage differentiation is programmed by orphan nuclear receptors ROR alpha and ROR gamma.

2007

T cell functional differentiation is mediated by lineage-specific transcription factors. T helper 17 (Th17) has been recently identified as a distinct Th lineage mediating tissue inflammation. Retinoic acid receptor-related orphan receptor gamma (ROR gamma) was shown to regulate Th17 differentiation; ROR gamma deficiency, however, did not completely abolish Th17 cytokine expression. Here, we report Th17 cells highly expressed another related nuclear receptor, ROR alpha, induced by transforming growth factor-beta and interleukin-6 (IL-6), which is dependent on signal transducer and activator of transcription 3. Overexpression of ROR alpha promoted Th17 differentiation, possibly through the c…

Encephalomyelitis Autoimmune ExperimentalReceptors Retinoic AcidT cellImmunologyRetinoic acidReceptors Cytoplasmic and NuclearElectrophoretic Mobility Shift AssayBiology03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineT-Lymphocyte SubsetsmedicineT helper 17 cellImmunology and AllergyAnimalsCell LineageReceptorMOLIMMUNOTranscription factor030304 developmental biologyOrphan receptor0303 health sciencesReceptors Thyroid HormoneReverse Transcriptase Polymerase Chain ReactionInterleukin-17Cell DifferentiationNuclear Receptor Subfamily 1 Group F Member 1T-Lymphocytes Helper-InducerNuclear Receptor Subfamily 1 Group F Member 3Molecular biologyMice Mutant StrainsCell biologymedicine.anatomical_structureInfectious DiseaseschemistryNuclear receptorSTAT proteinTrans-ActivatorsFemale030215 immunologyImmunity
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The cyclopentenone-type prostaglandin 15-deoxy-delta12,14-prostaglandin J2 inhibits CD95 ligand gene expression in T lymphocytes: interference with p…

2003

Abstract 15-Deoxy-Δ12,14-PGJ2 (15d-PGJ2) is a cyclopentenone-type PG endowed with anti-inflammatory properties and produced by different cells, including those of the immune system. 15d-PGJ2 is a natural ligand of the peroxisome proliferator-activated receptor (PPAR)-γ nuclear receptor, but relevant PPARγ-independent actions mediated by this prostanoid have been described. Fas (APO-1/CD95) and its ligand (Fas-L) are cell surface proteins whose interaction activates apoptosis of Fas-expressing targets. In T cells, the Fas-Fas-L system regulates activation-induced cell death and has been implicated in diseases in which lymphocyte homeostasis is compromised. Moreover, several studies have desc…

Fas Ligand ProteinNerve growth factor IBT-LymphocytesImmunologyPeroxisome proliferator-activated receptorReceptors Cytoplasmic and NuclearApoptosisCyclopentanesBiologyLigandsLymphocyte ActivationJurkat cellsImmediate-Early ProteinsTransactivationchemistry.chemical_compoundJurkat CellsMiceHeat Shock Transcription FactorsPeroxisomesImmunology and AllergyAnimalsHumansHSP70 Heat-Shock ProteinsGene Silencingfas ReceptorReceptorPromoter Regions GeneticCell Line TransformedEarly Growth Response Protein 1chemistry.chemical_classificationHybridomasMembrane GlycoproteinsProstaglandin D2Fas receptorMolecular biologyDNA-Binding ProteinschemistryNuclear receptorlipids (amino acids peptides and proteins)Prostaglandin D2Transcription Factors
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Neuronal Cell Nuclear Factor. A Nuclear Receptor Possibly Involved in the Control of Neurogenesis and Neuronal Differentiation

1997

We have cloned from a cDNA library of neuronal derivatives of retinoic-acid-induced embryonic carcinoma cells a nuclear receptor that may be involved in the control of late neurogenesis and early neuronal differentiation. The receptor which is practically identical in sequence with germ cell nuclear factor, has been designated neuronal cell nuclear factor (NCNF). NCNF is exclusively expressed in the neuronal derivatives of PCC7-Mz1 cells, with the expression beginning within hours of exposure to retinoic acid. In the developing mouse brain, NCNF is expressed in the marginal zones of the neuroepithelium which are known to contain young postmitotic neurons. NCNF binds to the DRO sequence ther…

Germ cell nuclear factorRetinoic acidReceptors Cytoplasmic and NuclearTretinoinBiologyLigandsBiochemistryMicechemistry.chemical_compoundNuclear Receptor Subfamily 6 Group A Member 1Tumor Cells CulturedAnimalsCloning MolecularReceptorIn Situ HybridizationNuclear receptor co-repressor 1NeuronsNeurogenesisBrainGene Expression Regulation DevelopmentalCell DifferentiationDNABlotting NorthernMolecular biologyDNA-Binding ProteinsRepressor ProteinsNeuroepithelial cellNuclear receptor coactivator 1Blotting SouthernOligodeoxyribonucleotidesnervous systemchemistryNuclear receptorEuropean Journal of Biochemistry
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The germ cell nuclear factor (GCNF)

2005

The germ cell nuclear factor (GCNF), which is also known as RTR (retinoid receptor-related testis-associated receptor) is a member of the nuclear receptor superfamily. As a natural ligand remains to be discovered, GCNF is referred to as an orphan receptor. Owing to GCNF's unique features and its distant relation to any other known nuclear receptor it has been classified as the only member of the subgroup six and designated NR6A1 by the Receptor Nomenclature Committee (Duarte et al., 2002: Nucleic Acids Res 30: 364-368). To date, GCNF has been cloned from distinct vertebrate species, including zebrafish, Xenopus laevis, mouse, rat, and human. Cloning and characterization of the gene, domain …

Germ cell nuclear factorXenopusEmbryonic DevelopmentReceptors Cytoplasmic and NuclearNuclear Receptor Subfamily 6 Group A Member 1GeneticsmedicineAnimalsHumansZebrafishGeneGeneticsOrphan receptorCloningbiologyGene Expression Regulation DevelopmentalCell DifferentiationCell Biologybiology.organism_classificationDNA-Binding ProteinsGerm Cellsmedicine.anatomical_structureNuclear receptorVertebratesGerm cellDevelopmental BiologyMolecular Reproduction and Development
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NR1H4 rs35724 G>C variant modulates liver damage in nonalcoholic fatty liver disease

2021

Background and Aims: Farnesoid X receptor (FXR) plays a key role in bile acid and lipid homeostasis. Experimental evidence suggests that it can modulate liver damage related to nonalcoholic fatty liver disease (NAFLD). We examined the impact of the NR1H4 rs35724 G>C, encoding for FXR, on liver damage in a large cohort of patients at risk of steatohepatitis. Methods: We considered 2,660 consecutive individuals at risk of steatohepatitis with liver histology. The rs35724 G>C polymorphisms were genotyped by TaqMan assays. Gene expression was evaluated by RNASeq in a subset of patients (n = 124). Results: The NR1H4 rs35724 CC genotype, after adjusting for clinic-metabolic and genetic conf…

Liver Cirrhosismedicine.medical_specialtymedicine.drug_classReceptors Cytoplasmic and NuclearGastroenterologyBile Acids and Saltschemistry.chemical_compoundNon-alcoholic Fatty Liver DiseaseFibrosisSettore BIO/13 - Biologia ApplicataInternal medicineNAFLDNonalcoholic fatty liver diseasemedicineHumansReceptor Fibroblast Growth Factor Type 4Settore MED/12 - GastroenterologiaHepatologyBile acidCholesterolbusiness.industryNASHObeticholic acidmedicine.diseaseNR1H4LiverchemistryFXRSteroid HydroxylasesFarnesoid X receptorSteatohepatitisSteatosisbusiness
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Recent advances in 2D and 3D in vitro systems using primary hepatocytes, alternative hepatocyte sources and non-parenchymal liver cells and their use…

2013

This review encompasses the most important advances in liver functions and hepatotoxicity and analyzes which mechanisms can be studied in vitro. In a complex architecture of nested, zonated lobules, the liver consists of approximately 80 % hepatocytes and 20 % non-parenchymal cells, the latter being involved in a secondary phase that may dramatically aggravate the initial damage. Hepatotoxicity, as well as hepatic metabolism, is controlled by a set of nuclear receptors (including PXR, CAR, HNF-4α, FXR, LXR, SHP, VDR and PPAR) and signaling pathways. When isolating liver cells, some pathways are activated, e.g., the RAS/MEK/ERK pathway, whereas others are silenced (e.g. HNF-4α), resulting in…

MAPK/ERK pathwayHealth Toxicology and MutagenesisNF-KAPPA-BReceptors Cytoplasmic and NuclearReview ArticlePharmacologyToxicologyToxicogeneticsNon-parenchymal cells0302 clinical medicineInduced pluripotent stem cellANION-TRANSPORTING POLYPEPTIDECONSTITUTIVE ANDROSTANE RECEPTOR0303 health sciencesGeneral Medicine3. Good healthCell biologymedicine.anatomical_structureLiver030220 oncology & carcinogenesisHepatocyte[SDV.TOX]Life Sciences [q-bio]/ToxicologyInactivation MetabolicClearanceDILIStem cellPLURIPOTENT STEM-CELLSFARNESOID-X-RECEPTORSignal TransductionMechanisms of gene regulationARYL-HYDROCARBON RECEPTORCell signalingPharmacology and ToxicologyHEPATIC STELLATE CELLSBiology03 medical and health sciencesOrgan Culture TechniquesIn vivoCulture TechniquesToxicity TestsmedicineMathematical modeling.AnimalsHumansLiver X receptorDRUG-DRUG INTERACTIONS030304 developmental biologyCryopreservation[INFO.INFO-MO]Computer Science [cs]/Modeling and Simulation3D ModelsCoculture TechniquesHigh-Throughput Screening AssaysSALT EXPORT PUMPGene Expression RegulationHepatic stellate cellHepatocytes[SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologyPRIMARY RAT HEPATOCYTESMathematical modeling
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TBL1XR1 mutations in Pierpont syndrome are not restricted to the recurrent p.Tyr446Cys mutation

2018

IF 2.264; International audience; Pierpont syndrome is a rare and sporadic syndrome, including developmental delay, facial characteristics, and abnormal extremities. Recently, a recurrent de novo TBL1XR1 variant (c.1337A > G; p.Tyr446Cys) has been identified in eight patients by whole‐exome sequencing. A dominant‐negative effect of this mutation is strongly suspected, since patients with TBL1XR1 deletion and other variants predicting loss of function do not share the same phenotype. We report two patients with typical Pierpont‐like syndrome features. Exome sequencing allowed identifying a de novo heterozygous missense TBL1XR1 variant in both patients, different from those already reported: …

Male0301 basic medicineAdolescentGenotypeReceptors Cytoplasmic and NuclearBiology03 medical and health sciences0302 clinical medicinePIERPONT SYNDROMEGeneticsHumansTBL1XR1Missense mutationAbnormalities MultipleRecurrent mutationGenetic TestingAllelesGenetics (clinical)Exome sequencingLoss functionUltrasonographyGeneticsComparative Genomic Hybridization[SDV.GEN]Life Sciences [q-bio]/GeneticsBrainFaciesNuclear ProteinsSyndromeMagnetic Resonance ImagingPhenotype3. Good healthRepressor ProteinsPhenotype030104 developmental biologyAmino Acid Substitution030220 oncology & carcinogenesisMutationMutation (genetic algorithm)Pierpont syndromeAmerican Journal of Medical Genetics Part A
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Muricholic Acids Promote Resistance to Hypercholesterolemia in Cholesterol-Fed Mice

2021

International audience; Background and aims: Hypercholesterolemia is a major risk factor for atherosclerosis and cardiovascular diseases. Although resistant to hypercholesterolemia, the mouse is a prominent model in cardiovascular research. To assess the contribution of bile acids to this protective phenotype, we explored the impact of a 2-week-long dietary cholesterol overload on cholesterol and bile acid metabolism in mice. Methods: Bile acid, oxysterol, and cholesterol metabolism and transport were assessed by quantitative real-time PCR, western blotting, GC-MS/MS, or enzymatic assays in the liver, the gut, the kidney, as well as in the feces, the blood, and the urine. Results: Plasma tr…

Male0301 basic medicineMuricholic acidDrug Evaluation PreclinicalReceptors Cytoplasmic and NuclearCholesterol Dietarychemistry.chemical_compound0302 clinical medicineBiology (General)Spectroscopy2. Zero hungerKidney[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyBile acidChemistryGeneral Medicine3. Good healthComputer Science ApplicationsBlotChemistrymedicine.anatomical_structureCholesterolFXR030220 oncology & carcinogenesislipids (amino acids peptides and proteins)LXRmedicine.medical_specialtyOxysterolQH301-705.5medicine.drug_classHypercholesterolemiaArticleCatalysisBile Acids and SaltsInorganic Chemistry03 medical and health sciencesIn vivoInternal medicinemedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyPhysical and Theoretical ChemistryLiver X receptorQD1-999Molecular BiologyCholesterolOrganic ChemistryCholic AcidsBile acidsMice Inbred C57BL030104 developmental biologyEndocrinology[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Lean NAFLD: A Distinct Entity Shaped by Differential Metabolic Adaptation

2020

Background and Aims: Nonalcoholic fatty liver disease (NAFLD) affects a quarter of the adult population. A significant subset of patients are lean, but their underlying pathophysiology is not well understood. Approach and Results: We investigated the role of bile acids (BAs) and the gut microbiome in the pathogenesis of lean NAFLD. BA and fibroblast growth factor (FGF) 19 levels (a surrogate for intestinal farnesoid X receptor [FXR] activity), patatin-like phospholipase domain containing 3 (PNPLA3), and transmembrane 6 superfamily member 2 (TM6SF2) variants, and gut microbiota profiles in lean and nonlean NAFLD were investigated in a cohort of Caucasian patients with biopsy-proven NAFLD (n …

Male0301 basic medicineReceptors Cytoplasmic and NuclearGut floraMice0302 clinical medicineNon-alcoholic Fatty Liver DiseaseFibrosisNonalcoholic fatty liver diseasebiologyMiddle AgedNAFLD; bile acids; fibrosis; gut microbiota; leanPhospholipases A2 Calcium-IndependentFemale030211 gastroenterology & hepatologyfibrosiAdultmedicine.medical_specialtydigestive systemBile Acids and SaltsCyclic N-Oxides03 medical and health sciencesThinnessInternal medicineNAFLDmedicinebile acidAnimalsHumansbile acidsHepatologygut microbiotabusiness.industryFGF15fibrosisnutritional and metabolic diseasesFGF19leanmedicine.diseasebiology.organism_classificationNAFLD fibrosis lean bile acids gut microbiotadigestive system diseasesGastrointestinal MicrobiomeFibroblast Growth FactorsMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinologyFarnesoid X receptorSteatohepatitisbusinessTropanesTM6SF2
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