Search results for "L3"

showing 10 items of 80 documents

KIR2DL3 and the KIR ligand groups HLA-A-Bw4 and HLA-C2 predict the outcome of hepatitis B virus infection.

2017

Killer immunoglobulin-like receptors (KIRs) regulate the activation of Natural Killer cells through their interaction with human leukocyte antigens (HLA). KIR and HLA loci are highly polymorphic and certain HLA-KIR combinations have been found to protect against viral infections. In this study we analyzed whether the KIR/HLA repertoire may influence the course of hepatitis B virus (HBV) infection. Fifty-seven subjects with chronic hepatitis B (CHB), 44 subjects with resolved HBV infection, and 60 healthy uninfected controls (HC) were genotyped for KIR and their HLA ligands. The frequency of the HLA-A-Bw4 ligand group was higher in CHB (58%) than subjects with resolved infection (23%) (crude…

0301 basic medicineAdultMaleSettore MED/09 - Medicina InternaGenotypeSettore MED/17 - Malattie InfettiveKIR LigandHuman leukocyte antigenHLA-C AntigensBiologymedicine.disease_cause03 medical and health sciencesYoung Adult0302 clinical medicineHepatitis B ChronicVirologymedicineHumansGenetic Predisposition to DiseaseAlleleReceptorGeneAgedSettore MED/04 - Patologia GeneraleHepatitis B virusHepatologyHLA-A AntigensMiddle AgedVirologyHLA-AKIRs HLAA HBV030104 developmental biologyInfectious DiseasesTreatment OutcomeHLA-B AntigensReceptors KIR2DL3ImmunologyFemalePredictive variables030215 immunology
researchProduct

The immunoglobulin γ marker 17 allotype and KIR/HLA genes prevent the development of chronic hepatitis B in humans

2020

Hepatitis B virus (HBV) infection causes a self-limiting disease in most individuals. However, < 10% of infected subjects develop a chronic disease. Genetic host variability of polymorphic genes at the interface of innate and acquired immunity, such as killer immunoglobulin-like receptors (KIR), their human leucocyte antigen (HLA) and IgG allotypes (GM), could explain this different clinical picture. We previously showed a protective role of the KIR2DL3 gene for the development of chronic hepatitis B (CHB), and a detrimental role of the KIR ligand groups, HLA-A-Bw4 and HLA-C2. We have expanded the previous analysis genotyping patients for GM23 and GM3/17 allotypes. The comparison of the …

0301 basic medicineHepatitis B virusKIR LigandImmunologyhepatitis B viruHuman leukocyte antigenHLA-C Antigensmedicine.disease_causeRisk Assessment03 medical and health sciences0302 clinical medicineHepatitis B ChronicGene FrequencyImmunoglobulin Gm AllotypesRisk Factorskiller immunoglobulin-like receptorImmunology and AllergyMedicineHumansGenetic Predisposition to DiseaseGenotypingHepatitis B virusSettore MED/04 - Patologia Generalebiologybusiness.industryOriginal ArticlesProtective FactorsAcquired immune systemAllotypeγ marker030104 developmental biologyPhenotypeHLA-B AntigensReceptors KIR2DL3Case-Control StudiesImmunologyHost-Pathogen Interactionsbiology.proteinGene polymorphismAntibodyhepatitis B virus; human leucocyte antigen; killer immunoglobulin-like receptor; ? markerbusiness030215 immunologyhuman leucocyte antigen
researchProduct

Lysyl Oxidase (LOX) Family Members: Rationale and Their Potential as Therapeutic Targets for Liver Fibrosis.

2019

The cross-linking of structural extracellular matrix (ECM) components, especially fibrillar collagens and elastin, is strongly implicated in fibrosis progression and resistance to fibrosis reversal. Lysyl oxidase family members (LOX and LOXL1 [lysyl oxidase-like 1], LOXL2 [lysyl oxidase-like 2], LOXL3 [lysyl oxidase-like 3], and LOXL4 [lysyl oxidase like 4]) are extracellular copper-dependent enzymes that play a key role in ECM cross-linking, but have also other intracellular functions relevant to fibrosis and carcinogenesis. Although the expression of most LOX family members is elevated in experimental liver fibrosis of diverse etiologies, their individual contribution to fibrosis is incom…

0301 basic medicineLiver CirrhosisLysyl oxidaseExtracellular matrixProtein-Lysine 6-Oxidase03 medical and health sciences0302 clinical medicineFibrosisExtracellularmedicineAnimalsHumansLOXL3integumentary systemHepatologyLOXL2biologybusiness.industrymedicine.diseaseenzymes and coenzymes (carbohydrates)030104 developmental biologySimtuzumabCancer researchbiology.protein030211 gastroenterology & hepatologyAmino Acid OxidoreductasesbusinessElastinHepatology (Baltimore, Md.)References
researchProduct

Threshold Effects of Circulating Angiopoietin-Like 3 Levels on Plasma Lipoproteins.

2017

Abstract Context Angiopoietin-like 3 (ANGPTL3) deficiency in plasma due to loss-of-function gene mutations results in familial combined hypobetalipoproteinemia type 2 (FHBL2) in homozygotes. However, the lipid phenotype in heterozygotes is much milder and does not appear to relate directly to ANGPTL3 levels. Furthermore, the low-density lipoprotein (LDL) phenotype in carriers of ANGPTL3 mutations is unexplained. Objective To determine whether reduction below a critical threshold in plasma ANGPTL3 levels is a determinant of lipoprotein metabolism in FHBL2, and to determine whether proprotein convertase subtilisin kexin type 9 (PCSK9) is involved in determining low LDL levels in this conditio…

0301 basic medicineMaleApolipoprotein BEndocrinology Diabetes and MetabolismClinical BiochemistryBiochemistryLipoprotein particlePCSK9Cohort StudiesHypobetalipoproteinemiaschemistry.chemical_compoundEndocrinologyANGPTL3biologyChemistryMiddle AgedPedigreeLipoproteins LDLPhenotypeKexinlipids (amino acids peptides and proteins)FemaleANGPTL3; familial combined hypolipidemia; PCSK9Lipoproteins HDLAdultmedicine.medical_specialtyHeterozygoteBlotting Western03 medical and health sciencesInternal medicinemedicineHumansGenetic Predisposition to DiseaseClinical Research ArticlesAgedAngiopoietin-Like Protein 3Apolipoproteins BCholesterolPCSK9Biochemistry (medical)medicine.disease030104 developmental biologyEndocrinologyAngiopoietin-like ProteinsLDL receptorMultivariate AnalysisMutationbiology.proteinLinear Modelsfamilial combined hypobetalipoproteinemiaHypobetalipoproteinemiaAngiopoietinsLipoprotein
researchProduct

Novel multiple sclerosis susceptibility loci implicated in epigenetic regulation

2016

Genome-wide study in Germans identifies four novel multiple sclerosis risk genes and confirms already known gene loci.

0301 basic medicineMaleDLEU1MedizinGenome-wide association studyEpigenesis GeneticCohort StudiesResearch ArticlesTranscriptional Regulator ERGGeneticsAged 80 and overGlycine Hydroxymethyltransferaseeducation.field_of_studyMultidisciplinaryDNA methylationSciAdv r-articlesMiddle AgedSHMT13. Good healthddc:DNA-Binding ProteinsERGDNA methylationFemaleMAZFunction and Dysfunction of the Nervous SystemResearch ArticleAdultAdolescentPopulationQuantitative Trait Loci610 Medicine & healthDleu1 ; Dna Methylation ; Erg ; L3mbtl3 ; Maz ; Multiple Sclerosis ; Shmt1 ; Genome-wide Association StudyQuantitative trait locusBiologyMajor histocompatibility complexNeurological DisordersMultiple sclerosis03 medical and health sciencesYoung AdultTranscriptional Regulator ERGHumansGenetic Predisposition to DiseaseL3MBTL3EpigeneticsAlleleeducationAllelesAgedgenome-wide association study030104 developmental biologyGenetic LociCase-Control Studiesbiology.proteinTranscription Factors
researchProduct

Clinical and biochemical characteristics of individuals with low cholesterol syndromes: A comparison between familial hypobetalipoproteinemia and fam…

2017

Background The most frequent monogenic causes of low plasma cholesterol are familial hypobetalipoproteinemia (FHBL1) because of truncating mutations in apolipoprotein B coding gene (APOB) and familial combined hypolipidemia (FHBL2) due to loss-of-function mutations in ANGPTL3 gene. Objective A direct comparison of lipid phenotypes of these 2 conditions has never been carried out. In addition, although an increased prevalence of liver steatosis in FHBL1 has been consistently reported, the hepatic consequences of FHBL2 are not well established. Methods We investigated 350 subjects, 67 heterozygous carriers of APOB mutations, 63 carriers of the p.S17* mutation in ANGPTL3 (57 heterozygotes and …

0301 basic medicineMaleHepatic steatosisSettore MED/09 - Medicina InternaApolipoprotein BEndocrinology Diabetes and Metabolism030204 cardiovascular system & hematologymedicine.disease_causeANGPTL3 gene; APOB gene; Familial combined hypolipidemia; Familial hypobetalipoproteinemia; HDL cholesterol; Hepatic steatosis; Low cholesterol syndromesHypobetalipoproteinemiasExon0302 clinical medicineHDL cholesterolANGPTL3Nutrition and DieteticFamilial hypobetalipoproteinemiaGeneticsMutationNutrition and Dieteticsbiologyhepatic steatosisHomozygoteANGPTL3 geneMiddle AgedLow cholesterol syndromesPhenotypePhenotypelipids (amino acids peptides and proteins)FemaleCardiology and Cardiovascular MedicineANGPTL3 gene; APOB gene; familial combined hypolipidemia; familial hypobetalipoproteinemia; HDL cholesterol; hepatic steatosis; low cholesterol syndromesmedicine.medical_specialtyHeterozygoteLow cholesterol syndromeHepatic steatosi03 medical and health sciencesInternal medicineInternal MedicinemedicineHumansAPOB geneFamilial combined hypolipidemiaGeneAgedAngiopoietin-Like Protein 3Apolipoproteins Bbusiness.industryHeterozygote advantagemedicine.disease030104 developmental biologyEndocrinologyAngiopoietin-like ProteinsMutationbiology.proteinlow cholesterol syndromesSteatosisbusiness
researchProduct

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)
researchProduct

L'efficacité des privatisations françaises : une vision dynamique à travers la théorie de la gouvernance

2004

International audience; A reading of the process of privatization through the corporate governance theory leads to propose a model taking into account, on the one hand, the time dimension of the process of privatization, on the other hand, the contextual, organizational, governance and strategic variables which influence this process. After replicating some traditional tests, we test this model on a sample of French privatized firms and on a seven years horizon. The positive effect traditionally attributed to privatizations is not confirmed. The importance of the effect is subordinated to some of the suggested variables.; Une lecture du processus de privatisation à travers la théorie de la …

050208 financePrivatisationprivatisation;efficacité statique;efficacité dynamique; gouvernance des entreprises.05 social sciencesjel:G30050801 communication & media studies0506 political sciencejel:L33jel:G390508 media and communicationsJEL: G - Financial Economics/G.G3 - Corporate Finance and Governance/G.G3.G39 - Other8. Economic growth0502 economics and business050602 political science & public administrationJEL: L - Industrial Organization/L.L3 - Nonprofit Organizations and Public Enterprise/L.L3.L33 - Comparison of Public and Private Enterprises and Nonprofit Institutions • Privatization • Contracting Out[SHS.GESTION]Humanities and Social Sciences/Business administrationGouvernance des entreprisesGeneral Economics Econometrics and Finance050203 business & management
researchProduct

Embeddings of a family of Danielewski hypersurfaces and certain \C^+-actions on \C^3

2006

International audience; We consider the family of complex polynomials in \C[x,y,z] of the form x^2y-z^2-xq(x,z). Two such polynomials P_1 and P_2 are equivalent if there is an automorphism \varphi of \C[x,y,z] such that \varphi(P_1)=P_2. We give a complete classification of the equivalence classes of these polynomials in the algebraic and analytic category.

14R10; 14R05 ; 14L30equivalence of polynomialsDanielewski surfacesstable equivalence[MATH.MATH-AG] Mathematics [math]/Algebraic Geometry [math.AG][MATH.MATH-AG]Mathematics [math]/Algebraic Geometry [math.AG]Physics::Atomic Physicsalgebraic embeddings[ MATH.MATH-AG ] Mathematics [math]/Algebraic Geometry [math.AG]
researchProduct

CLINICAL CHARACTERISTICS AND PLASMA LIPIDS IN SUBJECTS WITH FAMILIAL COMBINED HYPOLIPIDEMIA: A POOLED ANALYSIS

2013

Background. Angiopoietin-like 3 (ANGPTL3) regulates lipoprotein metabolism by modulating extracellular lipases. Loss-of function mutations in ANGPTL3 gene cause familial combined hypolipidemia (FHBL2). The mode of inheritance and hepatic and vascular consequences of FHBL2 have not been fully elucidated. To get further insights on these aspects, we re-evaluated the clinical and the biochemical characteristics of all reported cases of FHBL2. Methods and Results. One hundred fteen FHBL2 individuals carrying 13 different mutations in the ANGPTL3 gene (14 homozygotes, 8 compound heterozygotes and 93 heterozygotes) and 402 controls were considered. Carriers of 2 mutant alleles had undetectable pl…

ANGPTL3 mutations; angiopoietin-like 3; cardiovascular disease; diabetes mellitus; fatty liverSettore MED/09 - Medicina InternaCompound heterozygosityBiochemistryCohort StudiesHypobetalipoproteinemiasEndocrinologyANGPTL3cardiovascular diseaseGenotypeChildLipoproteinclinical characteristicsAged 80 and overbiologydiabetes mellituFatty liverHomozygoteLipoprotein(a)Middle AgedANGPTL3 mutationLipidsCardiovascular Diseasesdiabetes mellitusANGPTL3 Familial combined hypolipidemia LipoproteinAdultmedicine.medical_specialtyHeterozygoteANGPTL3; Familial combined hypolipidemia; clinical characteristicsAdolescentEvinacumabQD415-436Young AdultDiabetes mellitusInternal medicinemedicineHumansANGPTL3 mutationsAlleleFamilial combined hypolipidemiaAgedAngiopoietin-Like Protein 3fatty liverangiopoietin-like 3Cell Biologymedicine.diseaseEndocrinologyAngiopoietin-like ProteinsGene Expression RegulationMutationbiology.proteinPatient-Oriented and Epidemiological ResearchAngiopoietinsLipoproteinLipoprotein(a)
researchProduct