Search results for "ApoB"

showing 10 items of 32 documents

Spectrum of mutations in Italian patients with familial hypercholesterolemia: New results from the LIPIGEN study

2017

Abstract Background Familial hypercholesterolemia (FH) is an autosomal dominant disease characterized by elevated plasma levels of LDL-cholesterol that confers an increased risk of premature atherosclerotic cardiovascular disease. Early identification and treatment of FH patients can improve prognosis and reduce the burden of cardiovascular mortality. Aim of this study was to perform the mutational analysis of FH patients identified through a collaboration of 20 Lipid Clinics in Italy (LIPIGEN Study). Methods We recruited 1592 individuals with a clinical diagnosis of definite or probable FH according to the Dutch Lipid Clinic Network criteria. We performed a parallel sequencing of the major…

0301 basic medicineApolipoprotein ECandidate geneSettore MED/09 - Medicina InternaDatabases FactualApolipoprotein BDNA Mutational AnalysisFamilial hypercholesterolemia030204 cardiovascular system & hematologyCompound heterozygosityPCSK90302 clinical medicineRisk FactorsReceptorsGeneticsHomozygoteAutosomal dominant traitPathogenic variantsGeneral MedicinePrognosisAPOB; Familial hypercholesterolemia; LDLR; PCSK9; Pathogenic variantsCholesterolPhenotypeItalyAutosomal Recessive HypercholesterolemiaApolipoprotein B-100lipids (amino acids peptides and proteins)Proprotein Convertase 9APOBCardiology and Cardiovascular MedicinePreliminary DataGenetic MarkersFamilial hypercholesterolemiaLDLRPCSK9APOBPathogenic variantsHeterozygoteFamilial hypercholesterolemiaBiologyPathogenic variantLDLHyperlipoproteinemia Type II03 medical and health sciencesDatabasesmedicineInternal MedicineHumansAPOB; Familial hypercholesterolemia; LDLR; Pathogenic variants; PCSK9; Internal Medicine; Cardiology and Cardiovascular MedicineGenetic Predisposition to DiseaseFactualPCSK9Settore MED/13 - ENDOCRINOLOGIAAPOB; Familial hypercholesterolemia; LDLR; Pathogenic variants; PCSK9; Cardiology and Cardiovascular Medicine; Internal Medicinemedicine.diseaseAtherosclerosis030104 developmental biologyLDLRReceptors LDLMutationbiology.proteinAPOB; Familial hypercholesterolemia; LDLR; Pathogenic variants; PCSK9; Apolipoprotein B-100; Atherosclerosis; Cholesterol; DNA Mutational Analysis; Databases Factual; Genetic Markers; Genetic Predisposition to Disease; Heterozygote; Homozygote; Humans; Hyperlipoproteinemia Type II; Italy; Phenotype; Preliminary Data; Prognosis; Proprotein Convertase 9; Receptors LDL; Risk Factors; Mutation; Internal Medicine; Cardiology and Cardiovascular Medicine
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APOBEC3-mediated restriction of RNA virus replication

2018

AbstractAPOBEC3 family members are cytidine deaminases with roles in intrinsic responses to infection by retroviruses and retrotransposons, and in the control of other DNA viruses, such as herpesviruses, parvoviruses and hepatitis B virus. Although effects of APOBEC3 members on viral DNA have been demonstrated, it is not known whether they edit RNA genomes through cytidine deamination. Here, we investigated APOBEC3-mediated restriction of Coronaviridae. In experiments in vitro, three human APOBEC3 proteins (A3C, A3F and A3H) inhibited HCoV-NL63 infection and limited production of progeny virus, but did not cause hypermutation of the coronaviral genome. APOBEC3-mediated restriction was parti…

0301 basic medicineHepatitis B virusviruseslcsh:MedicineGenome Viralmedicine.disease_causeVirus ReplicationVirusArticleCell LineCytosine Deaminase03 medical and health scienceschemistry.chemical_compoundCytidine deaminationCytidine DeaminasemedicineCoronaviridaeHumansRNA VirusesAPOBEC Deaminaseslcsh:ScienceCoronavirusMultidisciplinarybiology630 Agriculturelcsh:RDNA VirusesRNARNA virusbiochemical phenomena metabolism and nutritionbiology.organism_classificationVirology3. Good health030104 developmental biologyNucleoproteinschemistryViral replicationRNA570 Life sciences; biologylcsh:QDNA
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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
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Distinct immune evasion in APOBEC-enriched, HPV-negative HNSCC

2019

Immune checkpoint inhibition leads to response in some patients with head and neck squamous cell carcinoma (HNSCC). Robust biomarkers are lacking to date. We analyzed viral status, gene expression signatures, mutational load and mutational signatures in whole exome and RNA-sequencing data of the HNSCC TCGA dataset (N = 496) and a validation set (DKTK MASTER cohort, N = 10). Public single-cell gene expression data from 17 HPV-negative HNSCC were separately re-analyzed. APOBEC3-associated TCW motif mutations but not total single nucleotide variant burden were significantly associated with inflammation. This association was restricted to HPV-negative HNSCC samples. An APOBEC-enriched, HPV-nega…

APOBECmedicine.medical_treatmentImmunotherapyBiologymedicine.diseaseHead and neck squamous-cell carcinomaPhenotypeImmune checkpointstomatognathic diseasesImmune systemGene expressionCancer researchmedicineTechnology PlatformsExome
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Role of APOBEC3H in the Viral Control of HIV Elite Controller Patients

2017

Background APOBEC3H (A3H) gene presents variation at 2 positions (rs139297 and rs79323350) leading to a non-functional protein. So far, there is no information on the role played by A3H in spontaneous control of HIV. The aim of this study was to evaluate the A3H polymorphisms distribution in a well-characterized group of Elite Controller (EC) subjects. Methods We analyzed the genotype distribution of two different SNPs (rs139297 and rs79323350) of A3H in 30 EC patients and compared with 11 non-controller (NC) HIV patients. Genotyping was performed by PCR, cloning and Sanger sequencing. Both polymorphisms were analyzed jointly in order to adequately attribute the active or inactive status of…

AdultCD4-Positive T-LymphocytesMalers139297HIV InfectionsSingle-nucleotide polymorphismBiologyVirus ReplicationPolymorphism Single NucleotideAPOBEC3H polymorphisms03 medical and health sciencessymbols.namesake0302 clinical medicineGene FrequencyAminohydrolasesGenotypeHumansAlleleGenotypingGeneSanger sequencingCloningelite controllers.HaplotypeHIVGeneral MedicineMiddle AgedCross-Sectional StudiesHaplotypesImmunologyrs79323350symbolsFemaleResearch Paper030215 immunologyInternational Journal of Medical Sciences
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L’obesità viscerale ed un aumentato rapporto ApoB/ApoA1 fanno perdere la protezione cardiovascolare di genere nelle donne diabetiche tipo 2.

2012

ApoB ApoA1 diabete
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Luminal Lipid Regulates CD36 Levels and Downstream Signaling to Stimulate Chylomicron Synthesis

2011

International audience; The membrane glycoprotein CD36 binds nanomolar concentrations of long chain fatty acids (LCFA) and is highly expressed on the luminal surface of enterocytes. CD36 deficiency reduces chylomicron production through unknown mechanisms. In this report, we provide novel insights into some of the underlying mechanisms. Our in vivo data demonstrate that CD36 gene deletion in mice does not affect LCFA uptake and subsequent esterification into triglycerides by the intestinal mucosa exposed to the micellar LCFA concentrations prevailing in the intestine. In rodents, the CD36 protein disappears early from the luminal side of intestinal villi during the postprandial period, but …

CD36 AntigensMaleMTPCD36[SDV]Life Sciences [q-bio]BiochemistryMicrosomal triglyceride transfer proteinMice0302 clinical medicineIntestinal mucosaCricetinaeChylomicronsLipoproteinHypertriglyceridemiaMice Knockout0303 health sciencesMitogen-Activated Protein Kinase 3biologyPostprandial PeriodLipid-binding ProteinIntestineApoB48ERKmedicine.anatomical_structurePostprandialBiochemistrylipids (amino acids peptides and proteins)Apolipoprotein B-48MAP Kinase Signaling SystemEnterocyteCHO CellsChylomicron03 medical and health sciencesCricetulusparasitic diseasesmedicineAnimalsRats WistarMolecular Biology030304 developmental biologyUbiquitinationLipid absorptionLipid metabolismCell BiologyLipid MetabolismRatsEnterocytesMetabolismbiology.proteinApolipoprotein B-48CD36[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition030217 neurology & neurosurgeryChylomicron
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A new triple fluorescence reporter system for discrimination of Apobec1 and Apobec3 C-to-U RNA editing activities and editing-dependent protein expre…

2021

AbstractThe human body is composed of many different cell types which communicate with each other. In particular, the brain consists of billions of neurons and non-neuronal cells which are interconnected and require tight and precise regulation of cellular processes. RNA editing is a cellular process that diversifies gene function by enzymatic deamination of cytidine or adenine. This can result in changes of protein structure and function. Altered RNA editing is becoming increasingly associated with all kind of disease, but most approaches use advanced sequencing technologies to analyze bulk material. However, it is also becoming progressively evident that changes in RNA editing have to be …

Cell typeAPOBEC1RNACytidineBiologyCell biologychemistry.chemical_compoundmedicine.anatomical_structurechemistryRNA editingmedicineNeuronGeneFunction (biology)
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SHORT APOB TRUNCATIONS SHOW IMPAIRE CHYLOMICRON EXPORT AND ENTEROCYTE TRIGLYCERIDE ACCUMULATION. IN VIVO AND IN VITRO EVIDENCE ON A APOB 28.25 STABLE…

2007

FHBLCHYLOMICRONAPOB
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Familial hypobetalipoproteinemia: Analysis by next generation sequencing and identification of a novel frameshift mutation in the apoB gene

2017

GeneticsNutrition and DieteticsApob geneEndocrinology Diabetes and MetabolismFamilial HypobetalipoproteinemiaMedicine (miscellaneous)Identification (biology)BiologyCardiology and Cardiovascular MedicineDNA sequencingFrameshift mutationNutrition, Metabolism and Cardiovascular Diseases
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