Search results for "proteine"

showing 10 items of 179 documents

Six novel mutations of the LDL receptor gene in FH kindred of Sicilian and Paraguayan descent

2006

Familial hypercholesterolemia (FH) is an autosomal dominant inherited disease caused by mutations in the gene coding for the low density lipoprotein receptor (LDL-R). It is characterized by a high concentration of low density lipoprotein (LDL), which frequently gives rise to premature coronary artery disease. We studied the probands of five FH Sicilian families with 'definite' FH and one proband of Paraguayan descent with homozygous FH who has been treated with an effective living-donor liver transplantation. In order to seek the molecular defect in these six families, we used direct sequencing to define the molecular defects of the LDL-R gene responsible for the disease. We described three…

AdultProbandhypercholesterolemia LDL receptor gene mutation analysis direct sequencing splicing living-donor transplantationSettore MED/09 - Medicina InternaDNA Mutational AnalysisDirect sequencingHypercholesterolemiaFamilial hypercholesterolemiaBiologyGene mutationSplicingmedicine.disease_causeFrameshift mutationHyperlipoproteinemia Type IIExonGeneticsmedicineHumansMissense mutationRNA MessengerChildSicilyCells CulturedLiving-donor transplantationLDL receptor geneGeneticsMutationIntronExonsGeneral MedicineMiddle Agedmedicine.diseaseLipidsMolecular biologyPedigreeDirect sequencing; Hypercholesterolemia; LDL receptor gene; Living-donor transplantation; Mutation analysis; SplicingMutation analysisReceptors LDLParaguayChild PreschoolMutationBiological Assay
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A new PCSK9 gene promoter variant affects gene expression and causes autosomal dominant hypercholesterolemia.

2008

Autosomal dominant hypercholesterolemia (ADH) is a genetic disorder characterized by increased low-density lipoprotein (LDL)-cholesterol levels, leading to high risk of premature cardiovascular disease. More than 900 mutations in LDL receptor, six in APOB and 10 in PCSK9 have been identified as a cause of the disease in different populations. All known mutations in PCSK9 causing hypercholesterolemia produce an increase in the enzymatic activity of this protease. Up to now, there are data about the implication of PCSK9 in ADH in a low number of populations, not including a Spanish population.The objective of the study was to study the prevalence of PCSK9 mutations in ADH Spanish population.W…

Adultmedicine.medical_specialtyApolipoprotein BEndocrinology Diabetes and MetabolismClinical BiochemistryGene ExpressionTransfectionBiochemistryPolymorphism Single NucleotideHyperlipoproteinemia Type IIPCSK9 GeneMiceEndocrinologyGene FrequencyInternal medicinemedicineAnimalsHumansPromoter Regions GeneticAllele frequencyGeneCells CulturedGeneticsbiologyBase SequencePCSK9Biochemistry (medical)Serine EndopeptidasesGenetic disorderHyperlipoproteinemia Type IIaMiddle Agedmedicine.diseaseEndocrinologySpainCase-Control StudiesLDL receptorbiology.proteinNIH 3T3 Cellslipids (amino acids peptides and proteins)Mutant ProteinsProprotein ConvertasesProprotein Convertase 9The Journal of clinical endocrinology and metabolism
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Extracorporeal circuit heparinization in selective low density lipoprotein apheresis: changes in patient hemostasis and low molecular weight heparin …

1993

Treatment by low density lipoprotein (LDL) apheresis using dextran sulfate columns (DSC) leads to hemostasis alterations with prolonged activated partial thromboplastin time (APTT) of more than 120 seconds. In order to explain this hypocoagulability, we studied hemostasis parameters both in patients and in the extracorporeal circulation (ECC). Hemostasis changes are first related to unfractionated heparin (UFH)—needed to avoid circuit coagulation—which leads to high residual heparinemia in the patient (more than 3 times the recommended level for therapeutic use). Second, the hypocoagulability is induced by a coagulation factor decrease (primarily factors V, VIH, and X) mainly due to an adso…

Adultmedicine.medical_specialtyExtracorporeal Circulationmedicine.drug_classLow molecular weight heparinHyperlipoproteinemia Type IIInternal medicinemedicineHumansHemostasismedicine.diagnostic_testbusiness.industryExtracorporeal circulationAnticoagulantDextran SulfateNadroparinHematologyGeneral MedicineHeparinMiddle AgedBlood Coagulation FactorsSurgeryLipoproteins LDLApheresisLDL apheresisHemostasisCardiologyBlood Component RemovalbusinessPartial thromboplastin timemedicine.drugJournal of clinical apheresis
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Spectrum of mutations and phenotypic expression in patients with autosomal dominant hypercholesterolemia identified in Italy.

2013

Abstract Objective To determine the spectrum of gene mutations and the genotype–phenotype correlations in patients with Autosomal Dominant Hypercholesterolemia (ADH) identified in Italy. Methods The resequencing of LDLR , PCSK9 genes and a selected region of APOB gene were conducted in 1018 index subjects clinically heterozygous ADH and in 52 patients clinically homozygous ADH. The analysis was also extended to 1008 family members of mutation positive subjects. Results Mutations were detected in 832 individuals: 97.4% with LDLR mutations, 2.2% with APOB mutations and 0.36% with PCSK9 mutations. Among the patients with homozygous ADH, 51 were carriers of LDLR mutations and one was an LDLR / …

Adultmedicine.medical_specialtyHeterozygoteSettore MED/09 - Medicina InternaApolipoprotein BCoronary DiseaseBiologyGene mutationmedicine.disease_causeHyperlipoproteinemia Type IITendonschemistry.chemical_compoundReference ValuesInternal medicinemedicineXanthomatosisHumansGeneAllelesGenetic Association StudiesAgedGeneticsMutationCholesterolPCSK9Cholesterol HDLSerine EndopeptidasesSmokingAlcohol Dehydrogenasenutritional and metabolic diseasesCholesterol LDLMiddle AgedEndocrinologyPhenotypechemistryItalyLDL receptorMutationbiology.proteinAutosomal dominanthypercholesterolemia LDL receptor Apolipoprotein B PCSK9 Mutationslipids (amino acids peptides and proteins)Allelic heterogeneityFemaleProprotein ConvertasesProprotein Convertase 9Cardiology and Cardiovascular MedicineAtherosclerosis
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Plasma non-cholesterol sterols in primary hypobetalipoproteinemia

2011

Primary hypobetalipoproteinemia (pHBL) is characterized by plasma cholesterol levels ApoB48, and FHBL harbouring as yet unknown molecular defects. Not linked FHBL kindred are not homogeneous in terms of plasma NCS levels. NCS cannot replace genetic HBL analysis.

Adultmedicine.medical_specialtySettore MED/09 - Medicina InternaAdolescentNon-cholesterol sterolbehavioral disciplines and activitiesAbsorptionHypobetalipoproteinemiaschemistry.chemical_compoundHypolipemiafamilial hypobetalipoproteinemia; non-cholesterol sterols; geneticsPlasma cholesterolInternal medicinemental disordersGeneticsmedicinenon-cholesterol sterolsHumansgeneticsFamilial hypobetalipoproteinemiaIntestinal MucosaChildAgedAged 80 and overFamily HealthModels GeneticCholesterolFamilial HypobetalipoproteinemiaPhytosterolsMiddle Agedmedicine.diseaseSterolSterolsfamilial hypobetalipoproteinemiaCholesterolPhenotypeEndocrinologychemistryBiochemistryHomogeneousMutationHypobetalipoproteinemiaCardiology and Cardiovascular MedicineAtherosclerosis
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Amminoacidi e proteine

2020

Le proteine sono macromolecole che svolgono svariate e importanti funzioni sia dinamiche che strutturali all’interno degli organismi viventi. Le funzioni dinamiche comprendono la catalisi enzimatica, il trasporto, il controllo metabolico e la contrazione. Dal punto di vista strutturale, le proteine sono componenti fondamentali del tessuto muscolare, connettivo e della matrice delle ossa. Tutte le proteine sono polimeri non ramificati formati dalla combinazione di soli 20 diversi amminoacidi, detti proteici, uniti tra loro tramite il legame peptidico. La vasta gamma di attività che possono svolgere le proteine dipende proprio dalla loro composizione amminoacidica variabile. Lo studio delle p…

AmminoacidiSettore BIO/10 - Biochimicaproteine
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Influence of microsomal triglyceride transfer protein promoter polymorphism -493 GT on fasting plasma triglyceride values and interaction with treatm…

2005

Familial hypercholesterolaemia (FH) is an autosomal dominant disease characterized by elevated levels of low-density lipoprotein-cholesterol (LDL-C). Phenotypic expression is highly variable, being influenced by diet, age, gender, body mass index, apolipoprotein E genotype and type of LDL-receptor gene mutation. Microsomal triglyceride (TG) transfer protein (MTP) is a protein involved in lipid metabolism. Polymorphism MTP -493 GT has been shown to modulate lipid levels in several populations. To analyse the effect of this polymorphism in the lipid phenotype expression of FH and treatment response, we studied a sample of 222 Spanish FH patients, of whom 147 were studied before and after trea…

Apolipoprotein EMaleAtorvastatinPolymerase Chain ReactionMicrosomal triglyceride transfer proteinBody Mass Indexchemistry.chemical_compoundAtorvastatinGeneral Pharmacology Toxicology and PharmaceuticsPromoter Regions GeneticGenetics (clinical)Polymorphism Single-Stranded ConformationalGeneticsbiologyAutosomal dominant traitFastingLipoproteins LDLCholesterolPhenotypeMolecular Medicinelipids (amino acids peptides and proteins)Femalemedicine.drugmedicine.medical_specialtyHeterozygoteGenotypeLipoproteinsHyperlipoproteinemia Type IIApolipoproteins ESex FactorsInternal medicineGeneticsmedicineHumansPyrrolesMolecular BiologyAllelesTriglyceridesPolymorphism GeneticTriglycerideCholesterolGenetic VariationCholesterol LDLDNALipid MetabolismEndocrinologychemistryHeptanoic AcidsPharmacogeneticsMutationbiology.proteinHydroxymethylglutaryl-CoA Reductase InhibitorsCarrier ProteinsBody mass indexPharmacogeneticsPharmacogenetics and genomics
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Genetic polymorphisms affecting the phenotypic expression in familial hypercholesterolemia

2004

The clinical expression of heterozygous familial hypercholesterolemia (FH) is highly variable even in patients carrying the same LDL receptor (LDL-R) gene mutation. This variability might be due to environmental factors as well as to modifying genes affecting lipoprotein metabolism. We investigated Apo E (2, 3, 4), MTP (-493G/T), Apo B (-516C/T), Apo A-V (-1131T/C), HL (-514C/T and -250G/A), FABP-2 (A54T), LPL (D9N, N291S, S447X) and ABCA1 (R219K) polymorphisms in 221 unrelated FH index cases and 349 FH relatives with defined LDL-R gene mutations. We found a significant and independent effect of the following polymorphisms on: (i) plasma LDL-C (Apo E, MTP and Apo B); (ii) plasma HDL-C (HL, …

Apolipoprotein EMaleSettore MED/09 - Medicina InternaApolipoprotein BFamilial hypercholesterolemiaGene mutationPolymerase Chain ReactionCoronary artery diseasecoronary artery disease; familial hypercholesterolemia; genetic polymorphisms; plasma lipidsCohort Studieschemistry.chemical_compoundGenotypePlasma lipidsOdds RatiobiologyFamilial hypercholesterolemia Plasma lipids Genetic polymorphisms Coronary artery diseaseIncidenceMiddle AgedPhenotypelipids (amino acids peptides and proteins)FemaleCardiology and Cardiovascular MedicineAdultmedicine.medical_specialtyMolecular Sequence DataFamilial hypercholesterolemiaPlasma lipidGenetic polymorphismsRisk AssessmentHyperlipoproteinemia Type IIFamilial hypercholesterolemia; Plasma lipids; Genetic polymorphisms; Coronary artery diseasePredictive Value of TestsInternal medicinemedicineConfidence IntervalsHumansGenetic Predisposition to DiseaseGenetic polymorphismPolymorphism GeneticBase SequenceCholesterolCholesterol HDLCase-control studyCholesterol LDLmedicine.diseaseEndocrinologyApolipoproteinschemistrySettore MED/03 - Genetica MedicaGene Expression RegulationReceptors LDLCase-Control StudiesLDL receptorbiology.protein
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Two Italian kindreds carrying the Arg136--Ser mutation of the Apo E gene: development of premature and severe atherosclerosis in the presence of epsi…

2003

Abstract Background and Aims: Type III hyperlipoproteinemia, or dysbetalipoproteinemia, is commonly associated with apolipoprotein E2 homozygosity (Cy Background and Aims: 12, Cy Background and Aims: 58). Apo E2-Christchurch (Arg136→Ser), a rare mutation of the Apo E gene, located in the receptor-binding domain of the protein, has been found to be associated in the vast majority of cases of dysbetalipoproteinemia. Methods and Results: This is the first report of two Italian kindreds carrying the Arg136→Ser mutation. One family is a four-generation kindred from Genoa (Liguria, Italy) with a high rate of mortality due to coronary artery disease: the proband was a 51-year-old woman with previo…

Apolipoprotein EProbandMaleSettore MED/09 - Medicina InternaGenotypeApolipoprotein E2ArteriosclerosisEndocrinology Diabetes and MetabolismMedicine (miscellaneous)Sequence HomologyBiologyArteriosclerosiPolymerase Chain ReactionCoronary artery diseaseApolipoproteins EGenotypeHyperlipoproteinemia Type IIImedicineHaplotypeHumansAlleleGenotypingAllelesGeneticsAlleleNutrition and DieteticsBase SequenceHaplotypeLipidMiddle Agedmedicine.diseaseLipidsPedigreeSettore MED/03 - Genetica MedicaHaplotypesMutationFemaleCardiology and Cardiovascular MedicineApolipoprotein E2HumanNutrition, metabolism, and cardiovascular diseases : NMCD
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Ultrafast myoglobin structural dynamics observed with an X-ray free-electron laser.

2014

Light absorption can trigger biologically relevant protein conformational changes. The light-induced structural rearrangement at the level of a photoexcited chromophore is known to occur in the femtosecond timescale and is expected to propagate through the protein as a quake-like intramolecular motion. Here we report direct experimental evidence of such ‘proteinquake’ observed in myoglobin through femtosecond X-ray solution scattering measurements performed at the Linac Coherent Light Source X-ray free-electron laser. An ultrafast increase of myoglobin radius of gyration occurs within 1 picosecond and is followed by a delayed protein expansion. As the system approaches equilibrium it underg…

Biologia Strutturale[PHYS]Physics [physics]Quantitative Biology::BiomoleculesPhotolysisTime FactorsLight[SDV.BBM.BS]Life Sciences [q-bio]/Biochemistry Molecular Biology/Structural Biology [q-bio.BM]BiofisicaMyoglobinProtein ConformationLasers[PHYS.PHYS.PHYS-BIO-PH]Physics [physics]/Physics [physics]/Biological Physics [physics.bio-ph]Dinamica delle ProteineMolecular Dynamics SimulationCrystallography X-RayBiological sciences Biochemistry BiophysicsSettore FIS/07 - Fisica Applicata(Beni Culturali Ambientali Biol.e Medicin)Article[PHYS.PHYS.PHYS-GEN-PH]Physics [physics]/Physics [physics]/General Physics [physics.gen-ph][SDV.BBM.BP]Life Sciences [q-bio]/Biochemistry Molecular Biology/BiophysicsAnimalsHorsessense organsPhysics::Chemical Physics
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