Search results for "Intracellular signaling"

showing 10 items of 144 documents

SPRED1, a RAS MAPK pathway inhibitor that causes Legius syndrome, is a tumour suppressor downregulated in paediatric acute myeloblastic leukaemia

2013

Constitutional dominant loss-of-function mutations in the SPRED1 gene cause a rare phenotype referred as neurofibromatosis type 1 (NF1)-like syndrome or Legius syndrome, consisted of multiple café-au-lait macules, axillary freckling, learning disabilities and macrocephaly. SPRED1 is a negative regulator of the RAS MAPK pathway and can interact with neurofibromin, the NF1 gene product. Individuals with NF1 have a higher risk of haematological malignancies. SPRED1 is highly expressed in haematopoietic cells and negatively regulates haematopoiesis. SPRED1 seemed to be a good candidate for leukaemia predisposition or transformation. We performed SPRED1 mutation screening and expression status i…

MaleCancer ResearchAdolescentLoss of HeterozygosityFrameshift mutationGene productLoss of heterozygosityPrecursor B-Cell Lymphoblastic Leukemia-Lymphomahemic and lymphatic diseasesGeneticsmedicineHumansGenes Tumor SuppressorNeurofibromatosisChildMolecular BiologyAdaptor Proteins Signal TransducingLegius syndromeNeurofibromin 1biologyCafe-au-Lait SpotsInfant NewbornIntracellular Signaling Peptides and ProteinsMacrocephalyInfantMembrane Proteinsmedicine.diseaseNeurofibromin 1Gene Expression Regulation NeoplasticLeukemia Myeloid AcuteHaematopoiesisGenes rasChild PreschoolMutationCancer researchbiology.proteinFemalemedicine.symptomOncogene
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Integrating genome-wide genetic variations and monocyte expression data reveals trans-regulated gene modules in humans.

2011

One major expectation from the transcriptome in humans is to characterize the biological basis of associations identified by genome-wide association studies. So far, few cis expression quantitative trait loci (eQTLs) have been reliably related to disease susceptibility. Trans-regulating mechanisms may play a more prominent role in disease susceptibility. We analyzed 12,808 genes detected in at least 5% of circulating monocyte samples from a population-based sample of 1,490 European unrelated subjects. We applied a method of extraction of expression patterns—independent component analysis—to identify sets of co-regulated genes. These patterns were then related to 675,350 SNPs to identify maj…

MaleCancer ResearchGene ExpressionGenome-wide association studyGenetic NetworksCoronary Artery Disease[SDV.GEN] Life Sciences [q-bio]/GeneticsCardiovascularMESH: MonocytesMonocytesMESH: HypertensionTranscriptomes0302 clinical medicineMESH: ProteinsMESH: Genetic VariationGenetics (clinical)GeneticsMESH: Aged0303 health scienceseducation.field_of_studyMESH: Middle AgedMESH: Polymorphism Single NucleotideIntracellular Signaling Peptides and ProteinsMESH: Genetic Predisposition to DiseaseGenomicsMESH: Transcription FactorsMiddle AgedMESH: Ribosomal ProteinsMESH: Gene Expression Regulation3. Good healthHypertensionMedicineFemaleMESH: Diabetes Mellitus Type 1Research ArticleAdultRibosomal Proteinslcsh:QH426-470PopulationQuantitative Trait LociLocus (genetics)Single-nucleotide polymorphismBiologyQuantitative trait locusPolymorphism Single Nucleotide03 medical and health sciencesMESH: Gene Expression ProfilingGenome Analysis ToolsGeneticsGenome-Wide Association StudiesHumansGenetic Predisposition to DiseaseGene NetworkseducationMolecular BiologyBiologyEcology Evolution Behavior and SystematicsMESH: Genome Human030304 developmental biologyGenetic associationAdaptor Proteins Signal TransducingAged[SDV.GEN]Life Sciences [q-bio]/GeneticsMESH: HumansGenome HumanGene Expression ProfilingGenetic VariationProteinsHuman GeneticsMESH: AdultAtherosclerosisMESH: MaleMESH: Quantitative Trait LociGene expression profilingCeliac Diseaselcsh:GeneticsDiabetes Mellitus Type 1Gene Expression RegulationExpression quantitative trait lociGenetics of DiseaseMESH: Genome-Wide Association StudyMESH: MuramidaseMuramidaseGenome Expression AnalysisMESH: Female030217 neurology & neurosurgeryMESH: Celiac DiseaseGenome-Wide Association StudyTranscription Factors
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Inhibition of DNA methylation sensitizes glioblastoma for tumor necrosis factor-related apoptosis-inducing ligand-mediated destruction.

2005

AbstractLife expectancy of patients affected by glioblastoma multiforme is extremely low. The therapeutic use of tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) has been proposed to treat this disease based on its ability to kill glioma cell lines in vitro and in vivo. Here, we show that, differently from glioma cell lines, glioblastoma multiforme tumors were resistant to TRAIL stimulation because they expressed low levels of caspase-8 and high levels of the death receptor inhibitor PED/PEA-15. Inhibition of methyltransferases by decitabine resulted in considerable up-regulation of TRAIL receptor-1 and caspase-8, down-regulation of PED/PEA-15, inhibition of cell growth, and …

MaleCancer ResearchMethyltransferaseNudeDrug ResistanceApoptosisReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandCASPASE-8 EXPRESSIONMiceNude mouseSIGNALING COMPLEXReceptorsAntineoplastic Combined Chemotherapy ProtocolsTumor Cells CulturedDNA Modification MethylasesIN-VIVOHeterologousCaspase 8CulturedMembrane GlycoproteinsbiologyIntracellular Signaling Peptides and ProteinsMiddle AgedTumor CellsGene Expression Regulation NeoplasticMALIGNANT GLIOMA-CELLSOncologyCaspasesDNA methylationAzacitidineTumor necrosis factor alphaFemalemedicine.drugSignal TransductionAdultBRAIN-TUMORSTransplantation HeterologousCHEMOTHERAPEUTIC-AGENTSDecitabineMice NudeDecitabineDRUG-INDUCED APOPTOSISDEATH RECEPTOR5-AZA-2'-DEOXYCYTIDINEIn vivoSettore MED/04 - PATOLOGIA GENERALEmedicineAnimalsHumansneoplasmsAgedTransplantationNeoplasticCell growthTumor Necrosis Factor-alphaHistocompatibility Antigens Class IDNA Methylationbiology.organism_classificationPhosphoproteinsReceptors TNF-Related Apoptosis-Inducing LigandGene Expression RegulationApoptosisDrug Resistance NeoplasmImmunologyCancer researchNeoplasmAdult; Aged; Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Apoptosis Regulatory Proteins; Azacitidine; Caspase 8; Caspases; DNA Modification Methylases; Drug Resistance Neoplasm; Female; Glioblastoma; Histocompatibility Antigens Class I; Humans; Intracellular Signaling Peptides and Proteins; Male; Membrane Glycoproteins; Mice; Mice Nude; Middle Aged; Phosphoproteins; Receptors TNF-Related Apoptosis-Inducing Ligand; Receptors Tumor Necrosis Factor; Signal Transduction; TNF-Related Apoptosis-Inducing Ligand; Transplantation Heterologous; Tumor Cells Cultured; Tumor Necrosis Factor-alpha; DNA Methylation; Gene Expression Regulation Neoplastic; Cancer Research; OncologyTumor Necrosis FactorTRAIL-INDUCED APOPTOSISApoptosis Regulatory ProteinsGlioblastomaCancer research
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Meta-Analysis of the INSIG2 Association with Obesity Including 74,345 Individuals: Does Heterogeneity of Estimates Relate to Study Design?

2009

The INSIG2 rs7566605 polymorphism was identified for obesity (BMI≥30 kg/m2) in one of the first genome-wide association studies, but replications were inconsistent. We collected statistics from 34 studies (n = 74,345), including general population (GP) studies, population-based studies with subjects selected for conditions related to a better health status (‘healthy population’, HP), and obesity studies (OB). We tested five hypotheses to explore potential sources of heterogeneity. The meta-analysis of 27 studies on Caucasian adults (n = 66,213) combining the different study designs did not support overall association of the CC-genotype with obesity, yielding an odds ratio (OR) of 1.05 (p-va…

MaleCancer ResearchobesityLIVERMedizinPROTEINBioinformatics0302 clinical medicineINSIG2GENETICS & HEREDITYPOPULATIONGenetics (clinical)METABOLIC SYNDROME0303 health scienceseducation.field_of_studyINSIG2Intracellular Signaling Peptides and ProteinsUPSTREAMMiddle AgedINSULINResearch DesignMeta-analysisFemaleLife Sciences & BiomedicineMedical GeneticsResearch ArticleEXPRESSIONAdultAdolescentlcsh:QH426-470PopulationPublic Health and EpidemiologyCOMMON GENETIC VARIANTBiologyChildhood obesity03 medical and health sciencesYoung AdultGeneticsmedicineBiochemical Phenomena Metabolism and NutritionHumansObesityeducationMolecular BiologyEcology Evolution Behavior and Systematics030304 developmental biology0604 GeneticsScience & TechnologyPolymorphism GeneticMembrane ProteinsOdds ratioBODY-MASSmedicine.diseaseObesityPOLYMORPHISMlcsh:GeneticsGenetics PopulationMetabolic syndromeBody mass index030217 neurology & neurosurgeryDevelopmental BiologyDemographyGenome-Wide Association StudyPLoS Genetics
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Up-regulation of c-FLIPshort and reduction of activation-induced cell death in T-cells from patients with Type 1 diabetes

2004

AICD of T-cells is an efficient way of removing activated T-lymphocytes. In this study we investigated the molecular basis of AICD upon reactivation in peripheral T-lymphocytes from newly diagnosed T1DM patients and age-matched healthy controls. In an in vitro model system, PHA-stimulated T-cells, upon prolonged culture in IL-2, acquire a sensitive phenotype to Fas-mediated apoptosis. This phenomenon is less pronounced in T1DM T-cells. Moreover, the restimulation of activated T-cells via TCR/CD3 and/or via CD28 inhibits Fas-mediated apoptosis in T1DM in comparison to control T-cells. After Fas triggering, the generation of the active sub-units of caspase-8 is significantly reduced in T1DM T…

MaleCaspase 8Adolescenttype 1 diabetesT-LymphocytesCASP8 and FADD-Like Apoptosis Regulating ProteinIntracellular Signaling Peptides and ProteinsApoptosisLymphocyte ActivationCaspase InhibitorsSettore MED/13 - EndocrinologiaUp-RegulationDiabetes Mellitus Type 1CD28 AntigensReceptor-CD3 Complex Antigen T-CellCase-Control StudiesCaspasesHumansFemaleCarrier Proteins
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X-linked primary ciliary dyskinesia due to mutations in the cytoplasmic axonemal dynein assembly factor PIH1D3

2017

By moving essential body fluids and molecules, motile cilia and flagella govern respiratory mucociliary clearance, laterality determination and the transport of gametes and cerebrospinal fluid. Primary ciliary dyskinesia (PCD) is an autosomal recessive disorder frequently caused by non-assembly of dynein arm motors into cilia and flagella axonemes. Before their import into cilia and flagella, multi-subunit axonemal dynein arms are thought to be stabilized and pre-assembled in the cytoplasm through a DNAAF2–DNAAF4–HSP90 complex akin to the HSP90 co-chaperone R2TP complex. Here, we demonstrate that large genomic deletions as well as point mutations involving PIH1D3 are responsible for an X-li…

MaleCytoplasmProtein FoldingAxoneme[SDV]Life Sciences [q-bio][SDV.GEN] Life Sciences [q-bio]/Genetics[SDV.MHEP.PSR]Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tractouterGenes X-LinkedChilddefectsPhylogenyZebrafisharmsSequence DeletionvariantsIntracellular Signaling Peptides and ProteinsGenetic Diseases X-LinkedPedigreeMultidisciplinary Sciences[SDV] Life Sciences [q-bio]motilityChild PreschoolMicrotubule ProteinsSperm MotilityScience & Technology - Other TopicsFemaleAdultAdolescentinnerUK10K Rare Groupr2tp complexof-function mutationsArticleMicroscopy Electron TransmissionMD MultidisciplinaryExome SequencingAnimalsHumansPoint MutationCiliaHSP90 Heat-Shock Proteins[SDV.GEN]Life Sciences [q-bio]/GeneticsScience & TechnologyKartagener SyndromeInfant NewbornAxonemal DyneinsDisease Models AnimalHEK293 Cells[SDV.MHEP.PSR] Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tractidentifies mutationsproteinApoptosis Regulatory ProteinsSequence AlignmentMolecular ChaperonesNature Communications
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Postnatal Deletion of Numb/Numblike Reveals Repair and Remodeling Capacity in the Subventricular Neurogenic Niche

2006

Neural stem cells are retained in the postnatal subventricular zone (SVZ), a specialized neurogenic niche with unique cytoarchitecture and cell-cell contacts. Although the SVZ stem cells continuously regenerate, how they and the niche respond to local changes is unclear. Here we generated nestin-creERtm transgenic mice with inducible Cre recombinase in the SVZ, and removed Numb/Numblike, key regulators of embryonic neurogenesis from postnatal SVZ progenitors and ependymal cells. This resulted in severe damage to brain lateral ventricle integrity, and identified previously unknown roles for Numb/Numblike in regulating ependymal wall integrity and SVZ neuroblast survival. Surprisingly, the ve…

MaleEpendymal Cellanimal diseasesSubventricular zoneMice TransgenicNerve Tissue ProteinsCell CommunicationBiologyArticleGeneral Biochemistry Genetics and Molecular BiologyNestinMice03 medical and health sciences0302 clinical medicineIntermediate Filament ProteinsNeuroblastEpendymaLateral VentriclesmedicineAnimals030304 developmental biologyNeuronsGenetics0303 health sciencesIntegrasesBiochemistry Genetics and Molecular Biology(all)Stem CellsNeurogenesisIntracellular Signaling Peptides and ProteinsBrainMembrane ProteinsEmbryonic stem cellNeural stem cellCell biologyMice Inbred C57BLmedicine.anatomical_structureAnimals Newbornnervous systemNUMBFemaleStem cellGene Deletion030217 neurology & neurosurgeryCell
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Regional distribution of the leucine-rich glioma inactivated (LGI) gene family transcripts in the adult mouse brain

2009

25 p., figuras y bibliografía

MaleHippocampusSubstantia nigraNerve Tissue ProteinsHippocampal formationGene mutationBiologyReticular formationMiceC57BL/6J micemedicineGene familyAnimalsMolecular BiologyThalamic reticular nucleusBrain MappingGeneral NeuroscienceDentate gyrusIntracellular Signaling Peptides and ProteinsBrainProteinsMice Inbred C57BLmedicine.anatomical_structureLGI2LGI1Neurology (clinical)LGI4LGI3NeuroscienceIn situ hybridizationDevelopmental Biology
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IL-4 protects tumor cells from anti-CD95 and chemotherapeutic agents via up-regulation of antiapoptotic proteins

2004

Abstract We recently proposed that Th1 and Th2 cytokines exert opposite effects on the pathogenesis and clinical outcome of organ-specific autoimmunity by altering the expression of genes involved in target cell survival. Because a Th2 response against tumors is associated with poor prognosis, we investigated the ability of IL-4 to protect tumor cells from death receptor- and chemotherapy-induced apoptosis. We found that IL-4 treatment significantly reduced CD95 (Fas/APO-1)- and chemotherapeutic drug-induced apoptosis in prostate, breast, and bladder tumor cell lines. Analysis of antiapoptotic protein expression revealed that IL-4 stimulation resulted in up-regulation of cellular (c) FLIP/F…

MaleINFILTRATING LYMPHOCYTESCell SurvivalImmunologyCASP8 and FADD-Like Apoptosis Regulating Proteinbcl-X ProteinAntineoplastic AgentsApoptosisBreast NeoplasmsCARCINOMA-CELLSBiologySIGNALING PATHWAYSDownregulation and upregulationCell Line TumorImmunology and AllergyHumansfas ReceptorNON-HODGKINS-LYMPHOMACANCER PATIENTSReceptorBCL-2 PROTEINInterleukin 4EtoposideIL-4 apoptosis cancer stem cellsSettore MED/04 - Patologia GeneraleCHRONIC LYMPHOCYTIC-LEUKEMIAIntracellular Signaling Peptides and ProteinsAntibodies MonoclonalProstatic NeoplasmsFas receptorRecombinant ProteinsCell biologyUp-RegulationProto-Oncogene Proteins c-bcl-2ApoptosisCell cultureFlipCancer researchT-CELLSCamptothecinFemaleInterleukin-4FLICE-INHIBITORY PROTEINSignal transductionCarrier ProteinsRENAL-CELL
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The systemic lupus erythematosus IRF5 risk haplotype is associated with systemic sclerosis.

2013

Systemic sclerosis (SSc) is a fibrotic autoimmune disease in which the genetic component plays an important role. One of the strongest SSc association signals outside the human leukocyte antigen (HLA) region corresponds to interferon (IFN) regulatory factor 5 (IRF5), a major regulator of the type I IFN pathway. In this study we aimed to evaluate whether three different haplotypic blocks within this locus, which have been shown to alter the protein function influencing systemic lupus erythematosus (SLE) susceptibility, are involved in SSc susceptibility and clinical phenotypes. For that purpose, we genotyped one representative single-nucleotide polymorphism (SNP) of each block (rs10488631, r…

MaleLinkage disequilibrium:Phenomena and Processes::Genetic Phenomena::Phenotype [Medical Subject Headings]Polimorfismo de nucleótido simpleSLElcsh:MedicineAutoimmunityGenome-wide association studyLinkage DisequilibriumScleroderma:Phenomena and Processes::Genetic Phenomena::Genotype::Haplotypes [Medical Subject Headings]:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Primates::Haplorhini::Catarrhini::Hominidae::Humans [Medical Subject Headings]Gene Frequency:Named Groups::Persons::Population Groups::Continental Population Groups::European Continental Ancestry Group [Medical Subject Headings]Risk FactorsIRF5Genetics of the Immune SystemLupus Erythematosus Systemic:Diseases::Skin and Connective Tissue Diseases::Skin Diseases::Scleroderma Systemic [Medical Subject Headings]skin and connective tissue diseaseslcsh:ScienceMultidisciplinary:Diseases::Immune System Diseases::Autoimmune Diseases::Lupus Erythematosus Systemic [Medical Subject Headings]Predisposición genética a la enfermedad:Phenomena and Processes::Genetic Phenomena::Genetic Linkage::Linkage Disequilibrium [Medical Subject Headings]:Phenomena and Processes::Genetic Phenomena::Genotype::Genetic Predisposition to Disease [Medical Subject Headings]PhenotypeInterferon Regulatory FactorsSYSTEMIC SCLEROSISMedicineEvaluation of complex medical interventions Auto-immunity transplantation and immunotherapy [NCEBP 2]FemaleIRF5; SLE; TYPE I INTERFERON; SYSTEMIC SCLEROSISHaplotiposResearch ArticleFactores de riesgoImmunology:Chemicals and Drugs::Amino Acids Peptides and Proteins::Peptides::Intracellular Signaling Peptides and Proteins::Adaptor Proteins Signal Transducing::Interferon Regulatory Factors [Medical Subject Headings]:Check Tags::Male [Medical Subject Headings]:Health Care::Environment and Public Health::Public Health::Epidemiologic Factors::Causality::Risk Factors [Medical Subject Headings]Single-nucleotide polymorphismHuman leukocyte antigenBiologyPolymorphism Single NucleotideWhite PeopleAutoimmune DiseasesRheumatologyLupus eritematoso sistémicoGeneticsHumansGenetic Predisposition to DiseaseGrupo de ascendencia continental europeaAlleleBiologyAllele frequencyAllelesGenetic Association Studies:Phenomena and Processes::Genetic Phenomena::Genetic Structures::Genome::Genome Components::Genes::Alleles [Medical Subject Headings]Scleroderma SystemicHaplotypelcsh:R:Phenomena and Processes::Genetic Phenomena::Genetic Structures::Genome::Genome Components::Genetic Loci [Medical Subject Headings]Human Genetics:Phenomena and Processes::Genetic Phenomena::Genetic Variation::Polymorphism Genetic [Medical Subject Headings]Factores reguladores del interferónHaplotypesDesequilibrio de ligamiento:Check Tags::Female [Medical Subject Headings]Genetic LociTYPE I INTERFERONGenetics of DiseaseImmunologyGenetic PolymorphismClinical Immunologylcsh:Q:Phenomena and Processes::Genetic Phenomena::Gene Frequency [Medical Subject Headings]Population GeneticsIRF5PLoS ONE
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