Search results for "Transducin"

showing 10 items of 169 documents

Caspase-8 prevents sustained activation of NF-kappaB in monocytes undergoing macrophagic differentiation.

2006

Abstract Caspases have demonstrated several nonapoptotic functions including a role in the differentiation of specific cell types. Here, we show that caspase-8 is the upstream enzyme in the proteolytic caspase cascade whose activation is required for the differentiation of peripheral-blood monocytes into macrophages. On macrophage colony-stimulating factor (M-CSF) exposure, caspase-8 associates with the adaptor protein Fas-associated death domain (FADD), the serine/threonine kinase receptor-interacting protein 1 (RIP1) and the long isoform of FLICE-inhibitory protein FLIP. Overexpression of FADD accelerates the differentiation process that does not involve any death receptor. Active caspase…

Macrophage colony-stimulating factorCellular differentiationFas-Associated Death Domain ProteinImmunologyCaspase 8BiochemistryMonocytesArticle03 medical and health sciences0302 clinical medicineCell Line TumormedicineHumansFADDCaspase030304 developmental biologyDeath domain0303 health sciencesCaspase 8biologyMonocyteMacrophage Colony-Stimulating FactorMacrophagesNF-kappa BSignal transducing adaptor proteinRNA-Binding ProteinsCell DifferentiationCell BiologyHematologyMolecular biologyNuclear Pore Complex Proteinsmedicine.anatomical_structure030220 oncology & carcinogenesisbiology.proteinBlood
researchProduct

Genome- wide association study with additional genetic and post-transcriptional analyses reveals novel regulators of plasma factor XI levels

2017

International audience; Coagulation factor XI (FXI) has become increasingly interesting for its role in pathogenesis of thrombosis. While elevated plasma levels of FXI have been associated with venous thromboembolism and ischemic stroke, its deficiency is associated with mild bleeding. We aimed to determine novel genetic and post-transcriptional plasma FXI regulators.We performed a genome-wide association study (GWAS) for plasma FXI levels, using novel data imputed to the 1000 Genomes reference panel. Individual GWAS analyses, including a total of 16,169 European individuals from the ARIC, GHS, MARTHA and PROCARDIS studies, were meta-analysed and further replicated in 2,045 individuals from…

Male0301 basic medicineIn silicoReceptors Cell SurfaceSingle-nucleotide polymorphismGenome-wide association study030204 cardiovascular system & hematologyBiologyPolymorphism Single Nucleotide03 medical and health sciences0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]GeneticsmedicineHumansComputer SimulationGene Regulatory NetworksGenetic Predisposition to Disease1000 Genomes ProjectMolecular BiologyGeneGenetics (clinical)Adaptor Proteins Signal TransducingGeneticsmedicine.diagnostic_testKininogensAssociation Studies ArticlesHaplotypeThrombosisGeneral Medicine3. Good health030104 developmental biologyGene Expression RegulationFemalePartial Thromboplastin TimeCell Adhesion MoleculesProtein Processing Post-TranslationalImputation (genetics)Genome-Wide Association StudyPartial thromboplastin time
researchProduct

Homozygous Familial Hypercholesterolemia in Spain Prevalence and Phenotype-Genotype Relationship

2016

Background— Homozygous familial hypercholesterolemia (HoFH) is a rare disease characterized by elevated plasma levels of low-density lipoprotein cholesterol (LDL-C) and extremely high risk of premature atherosclerotic cardiovascular disease. HoFH is caused by mutations in several genes, including LDL receptor ( LDLR ), apolipoprotein B ( APOB ), proprotein convertase subtilisin/kexin type 9 ( PCSK9 ), and LDL protein receptor adaptor 1 ( LDLRAP1 ). No epidemiological studies have assessed HoFH prevalence or the clinical and molecular characteristics of this condition. Here, we aimed to characterize HoFH in Spain. Methods and Results— Data were collected from the Spanish Dyslipidemia Regist…

Male0301 basic medicineOncologyLdl receptor geneApolipoprotein BLipid-lowering therapyFamilial hypercholesterolemia030204 cardiovascular system & hematologyCompound heterozygosity0302 clinical medicineAutosomal-dominant hypercholesterolemiaRisk FactorsEpidemiologyPrevalenceDiseaseRegistriesGenetics (clinical)Molecular EpidemiologybiologyhypercholesterolemiaHomozygoteDouble-blindMiddle AgedPhenotypeCardiovascular DiseasesApolipoprotein B-100allelesFemalelipids (amino acids peptides and proteins)Proprotein Convertase 9Cardiology and Cardiovascular MedicineMutationsAdultGenetic MarkersHeterozygotemedicine.medical_specialtyInhibitorAdolescentPlacebo-controlled trialHyperlipoproteinemia Type IIlipidsYoung Adult03 medical and health sciencesInternal medicineGeneticsmedicineHumansGenetic Predisposition to DiseaseAlleleAdaptor Proteins Signal TransducingRecessive hypercholesterolemiaPCSK9registriesCholesterol LDLApolipoprotein-bmedicine.disease030104 developmental biologyEndocrinologyReceptors LDLSpainMutationLDL receptorbiology.proteinmutationDyslipidemia
researchProduct

CpG islands in MyD88 and ASC/PYCARD/TMS1 promoter regions are differentially methylated in head and neck squamous cell carcinoma and primary lung squ…

2021

Abstract Background Patients with head and neck squamous cell carcinoma (HNSCC) can develop lung squamous cell carcinoma (LuSCC), which could be the second primary tumor or HNSCC metastasis. Morphologically it is difficult to distinguish metastatic HNSCC from a second primary tumor which presents a significant diagnostic challenge. Differentiation of those two malignancies is important because the recommended treatments for metastatic HNSCC and primary LuSCC differ significantly. We investigated if the quantification of the promotor methylation status in HNSCC and LuSCC differs. Methods Primary HNSCC (N = 36) and LuSCC (N = 17) were included in this study. Methylation status in the ASC/TMS1…

Male0301 basic medicinePathologyLung NeoplasmsHNSCCEpigenesis GeneticMetastasis0302 clinical medicinePromoter Regions GeneticLungDiagnostic biomarkerPYCARDGeneral MedicineMethylationMiddle AgedGene Expression Regulation NeoplasticBisulfiteCpG siteHead and Neck Neoplasms030220 oncology & carcinogenesisCarcinoma Squamous CellSecond primary tumorFemalelcsh:RB1-214Adultmedicine.medical_specialtyHistologyShort ReportBiologyMethylationPathology and Forensic Medicine03 medical and health sciencesCpG ; diagnostic biomarker ; HNSCC ; lung ; methylation ; second primary tumorCpGClinical Medical Scienceslcsh:PathologymedicineHumansGeneAdaptor Proteins Signal TransducingAgedSquamous Cell Carcinoma of Head and NeckPromotermedicine.diseaseHead and neck squamous-cell carcinomastomatognathic diseases030104 developmental biologyMyeloid Differentiation Factor 88Cancer researchCpG IslandsDiagnostic Pathology
researchProduct

Skraban‐Deardorff syndrome: Six new cases of WDR 26 ‐related disease and expansion of the clinical phenotype

2021

International audience; Skraban-Deardorff syndrome (a disease related to variations in the WDR26 gene; OMIM #617616) was first described in a cohort of 15 individuals in 2017. The syndrome comprises intellectual deficiency, severe speech impairment, ataxic gait, seizures, mild hypotonia with feeding difficulties during infancy, and dysmorphic features. Here, we report on six novel heterozygous de novo pathogenic variants in WDR26 in six probands. The patients’ phenotypes were consistent with original publication. One patient displayed marked hypotonia with an abnormal muscle biopsy; this finding warrants further investigation. Gait must be closely monitored, in order to highlight any muscul…

Male0301 basic medicineProbandPediatricsmedicine.medical_specialtyAdolescent[SDV]Life Sciences [q-bio]Developmental DisabilitiesSkraban-Deardorff syndromeDisease030105 genetics & heredityYoung Adult03 medical and health sciencesIntellectual disabilityGeneticsmedicineWDR26HumansAbnormalities MultiplehypotoniaAtaxic GaitChildGenetics (clinical)Adaptor Proteins Signal Transducing[SDV.GEN]Life Sciences [q-bio]/GeneticsMuscle biopsymedicine.diagnostic_testbusiness.industryInfantSyndromemedicine.diseaseGaitHypotonia3. Good health[SDV] Life Sciences [q-bio]Phenotype030104 developmental biologyspeech therapyintellectual disabilityChild PreschoolMutationCohortlanguage development disordersFemalemedicine.symptombusinessClinical Genetics
researchProduct

Proprotein Convertase Subtilisin Kexin Type 9 Inhibition for Autosomal Recessive Hypercholesterolemia—Brief Report

2016

Objective— Proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitors lower low-density lipoprotein (LDL) cholesterol in the vast majority of patients with autosomal dominant familial hypercholesterolemia. Will PCSK9 inhibition with monoclonal antibodies, in particular alirocumab, be of therapeutic value for patients with autosomal recessive hypercholesterolemia (ARH)? Approach and Results— Primary lymphocytes were obtained from 28 genetically characterized ARH patients and 11 controls. ARH lymphocytes treated with mevastatin were incubated with increasing doses of recombinant PCSK9 with or without saturating concentrations of alirocumab. Cell surface LDL receptor expression measured…

Male0301 basic medicineSettore MED/09 - Medicina Interna[SDV]Life Sciences [q-bio]receptorsalirocumabFamilial hypercholesterolemia030204 cardiovascular system & hematologyproprotein convertase subtilisin kexin type 90302 clinical medicinetherapeuticsLymphocytesCells CulturedhypercholesterolemiaAnticholesteremic AgentsPCSK9 InhibitorsAntibodies MonoclonalMiddle Aged3. Good healthPhenotypeAutosomal Recessive HypercholesterolemiaKexinDrug Therapy CombinationFemalelipids (amino acids peptides and proteins)LovastatinProprotein Convertase 9Cardiology and Cardiovascular Medicinemedicine.drugAdultmedicine.medical_specialtySerine Proteinase InhibitorsAdolescentBiologyAntibodies Monoclonal HumanizedLDLYoung Adult03 medical and health sciencesInternal medicinemedicineHumansGenetic Predisposition to DiseaseLovastatinAdaptor Proteins Signal TransducingAlirocumabPCSK9receptors LDLCholesterol LDLmedicine.diseaseProprotein convertasetherapeutic030104 developmental biologyEndocrinologyCase-Control Studiesalirocumab; hypercholesterolemia; proprotein convertase subtilisin kexin type 9; receptors LDL; therapeutics; Cardiology and Cardiovascular MedicineMutationLDL receptorHydroxymethylglutaryl-CoA Reductase InhibitorsArteriosclerosis, Thrombosis, and Vascular Biology
researchProduct

Neuropeptide FF increases M2 activation and self-renewal of adipose tissue macrophages

2017

The quantity and activation state of adipose tissue macrophages (ATMs) impact the development of obesity-induced metabolic diseases. Appetite-controlling hormones play key roles in obesity; however, our understanding of their effects on ATMs is limited. Here, we have shown that human and mouse ATMs express NPFFR2, a receptor for the appetite-reducing neuropeptide FF (NPFF), and that NPFFR2 expression is upregulated by IL-4, an M2-polarizing cytokine. Plasma levels of NPFF decreased in obese patients and high-fat diet-fed mice and increased following caloric restriction. NPFF promoted M2 activation and increased the proliferation of murine and human ATMs. Both M2 activation and increased ATM…

Male0301 basic medicinemedicine.medical_specialty[SDV.BIO]Life Sciences [q-bio]/BiotechnologyUbiquitin-Protein LigasesAdipose tissue macrophagesMafB Transcription FactorAdipose tissueMice TransgenicReceptors Cell SurfaceSelf renewalMice03 medical and health sciencesClinical investigationInternal medicinemedicineAnimalsNeuropeptide FFTranscription factorAdaptor Proteins Signal TransducingCell ProliferationSTAT62. Zero hungerArginasebiologybusiness.industryChemistryMacrophagesProteinsSciences du Vivant [q-bio]/BiotechnologiesGeneral MedicineMacrophage ActivationInterleukin-10Ubiquitin ligaseCell biologyEndocrinology030104 developmental biologyAdipose TissueMAFBbiology.proteinInterleukin-4CorrigendumbusinessOligopeptidesMacrophage proliferationResearch ArticleJournal of Clinical Investigation
researchProduct

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
researchProduct

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
researchProduct

Promoter methylation of MGMT, MLH1 and RASSF1A tumor suppressor genes in head and neck squamous cell carcinoma: Pharmacological genome demethylation …

2012

Promoter hypermethylation of tumor suppressor genes (TSGs) is a common feature of primary cancer cells. However, to date the somatic epigenetic events that occur in head and neck squamous cell carcinoma (HNSCC) tumorigenesis have not been well-defined. In the present study, we analyzed the promoter methylation status of the genes mutL homolog 1 (MLH1), Ras-association domain family member 1 (RASSF1A) and O-6-methylguanine-DNA methyltransferase (MGMT) in 23 HNSCC samples, three control tissues and one HNSCC cell line (UM-SCC 33) using methylation-specific PCR (MSP). The expression of the three proteins was quantified by semi-quantitative immunohistochemical analysis. The cell line was treate…

MaleCancer Researchmedicine.disease_causePolymerase Chain Reactionchemistry.chemical_compoundRas association domain family member 1Genes Tumor Suppressortumor suppressor geneEnzyme InhibitorsPromoter Regions GeneticDNA Modification MethylasesAged 80 and overNuclear ProteinsArticlesGeneral MedicineMethylationMiddle AgedImmunohistochemistryPrimary tumorOncologyDealkylationHead and Neck NeoplasmsDNA methylationAzacitidineCarcinoma Squamous CellFemaleMutL Protein Homolog 1Molecular Sequence DataDown-RegulationBiologyhead and neck squamous cell carcinomamutL homolog 15-azacytidineCell Line TumormedicineHumansEpigeneticsneoplasmsO-6-methylguanine-DNA methyltransferaseAdaptor Proteins Signal TransducingAgedCell ProliferationBase SequenceDose-Response Relationship DrugTumor Suppressor ProteinsSequence Analysis DNADNA Methylationmedicine.diseaseHead and neck squamous-cell carcinomaMolecular biologyDemethylating agentSquamous carcinomastomatognathic diseasesDNA Repair EnzymeschemistryCase-Control StudiesCpG IslandsCarcinogenesisOncology Reports
researchProduct