Search results for "Zygote"

showing 10 items of 377 documents

Novel CREB3L3 Nonsense Mutation in a Family With Dominant Hypertriglyceridemia.

2015

Objective— Cyclic AMP responsive element–binding protein 3–like 3 ( CREB3L3 ) is a novel candidate gene for dominant hypertriglyceridemia. To date, only 4 kindred with dominant hypertriglyceridemia have been found to be carriers of 2 nonsense mutations in CREB3L3 gene (245fs and W46X). We investigated a family in which hypertriglyceridemia displayed an autosomal dominant pattern of inheritance. Approach and Results— The proband was a 49-year-old woman with high plasma triglycerides (≤1300 mg/dL; 14.68 mmol/L). Her father had a history of moderate hypertriglyceridemia, and her 51-year-old brother had triglycerides levels as high as 1600 mg/dL (18.06 mmol/L). To identify the causal mutation …

ProbandAdultMaleCandidate geneHeterozygoteSettore MED/09 - Medicina InternaHeredityAdolescentNonsense mutationDNA Mutational AnalysisPenetranceBiologymedicine.disease_causeSeverity of Illness IndexFrameshift mutationExonYoung AdultmedicineHumansGenetic Predisposition to DiseasetriglycerideCyclic AMP Response Element-Binding ProteinTriglyceridesAgedGeneticsAged 80 and overHypertriglyceridemiaMutationHypertriglyceridemiaMiddle Agedmedicine.diseasePenetrancePedigreePhenotypeCodon NonsenseFemalemutationCardiology and Cardiovascular MedicineBiomarkersArteriosclerosis, thrombosis, and vascular biology
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A family with various symptomatology suggestive of Anderson-Fabry disease and a genetic polymorphism of alpha galactosidase A gene.

2014

Background: Anderson/Fabry disease expresses a wide range of clinical variability in patients that it is possible to explain referring to a genetic variability with numerous mutations described in the literature (more than 600). Methods: We report some clinical cases of some members of a Sicilian family to express phenotypical variability of this disease in subjects with the same genetic mutation. Results: The first case was a 59-year-old female. Brain MRI revealed right frontal periventricular white matter of likely vascular-degenerative origin. The proband's alpha galactosidase A activity was 3.7. nmol/mL/h. Molecular genetics revealed a polymorphism: - 10 C. >. T; IVS 2-76_80del5; IVS…

ProbandAdultMalemedicine.medical_specialtyPathologySettore MED/09 - Medicina InternaAdolescentClinical BiochemistryMolecular Sequence DataBiologyAnderson-Fabry diseaseNucleic Acid DenaturationGastroenterologyPolymorphism (computer science)Internal medicineMolecular geneticsmedicineHaplotypeHumansFamilyGenetic Predisposition to DiseaseGenetic variabilitySymptomatologyChildPolymorphism GeneticBase SequenceHaplotypeHeterozygote advantageGeneral MedicineMiddle Agedmedicine.diseaseFabry diseaseMagnetic Resonance ImagingPedigreealpha-GalactosidaseFabry DiseaseMicroalbuminuriaFemaleHumanClinical biochemistry
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Additive effect of mutations in LDLR and PCSK9 genes on the phenotype of familial hypercholesterolemia.

2006

Patients homozygous or Compound heterozygous for LDLR mutations or double heterozygous for LDLR and apo B R3500Q mutation have higher LDL-C levels. more extensive xanthomatosis and more severe premature coronary disease (pCAD) than simple heterozygotes for mutations in either these genes or for missense mutations in PCSK9 gene. It is not known whether combined mutations in LDLR and PKCS9 are associated with such a severe phenotype. We sequenced Apo B and PCSK9 genes in two patients with the clinical diagnosis of homozygous FH who were heterozygous for LDLR gene mutations. Proband Z.P. (LDL-C 13.39 mmol/L and pCAD) was heterozygous for an LDLR mutation (p.E228K) inherited from her father (LD…

ProbandLDLR geneAdultMaleSettore MED/09 - Medicina InternaApolipoprotein BFamilial hypercholesterolemia (FH); Autosomal dominant hypercholesterolemia 3 (ADH3); LDLR gene; PCSK9 gene; Premature coronary artery diseasePremature coronary artery diseaseLDLR PCSK9Mutation MissenseFamilial hypercholesterolemiaCompound heterozygositymedicine.disease_causeHyperlipoproteinemia Type IIFamilial hypercholesterolemia (FH) Autosomal dominant hypercholesterolemia 3 (ADH3) LDLR gene PCSK9 gene Premature coronary artery diseaseFamilial hypercholesterolemia (FH)medicineMissense mutationHumansCells CulturedGeneticsMutationbiologybusiness.industrySerine EndopeptidasesHeterozygote advantageMiddle Agedmedicine.diseaseAutosomal dominant hypercholesterolemia 3 (ADH3)PedigreePhenotypeSettore MED/03 - Genetica MedicaAmino Acid SubstitutionReceptors LDLPCSK9 geneLDL receptorbiology.proteinlipids (amino acids peptides and proteins)FemaleProprotein ConvertasesProprotein Convertase 9Cardiology and Cardiovascular MedicinebusinessAtherosclerosis
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Lack of phenotypic additive effect of familial defective apolipoprotein B3531 in familial hypercholesterolaemia.

2020

Familial defective apolipoprotein (apo) B (FDB) and familial hypercholesterolaemia (FH) are the two common genetic conditions that cause hypercholesterolaemia. R3531C mutation of the APOB gene is a rare cause of FDB. Individuals with both FDB and FH are rare. A 51-year-old man with hypercholesterolaemia (11.4 mmol/L) and his family were studied. Low-density lipoprotein (LDL) receptor (LDLR) and APOB genes were analysed by direct sequencing. LDL of four subjects were studied in a fibroblast LDL receptor-binding displacement assay. We found a mutation of the LDLR gene (p.Y398X) in the proband and in four other family members: the p.R3531C APOB gene mutation was also found in the proband, his …

ProbandMalemedicine.medical_specialtyApolipoprotein B030204 cardiovascular system & hematologyCompound heterozygosityHyperlipoproteinemia Type II03 medical and health scienceschemistry.chemical_compoundFDB35310302 clinical medicineInternal medicineInternal MedicinemedicineHumans030212 general & internal medicineApolipoproteins Bdouble heterozygotebiologybusiness.industryCholesterolLDL receptornutritional and metabolic diseasesHeterozygote advantageMiddle AgedEndocrinologychemistryItalyReceptors LDLLDL receptorMutation (genetic algorithm)Mutationfamilial hypercholesterolaemiabiology.proteinlipids (amino acids peptides and proteins)businessLipoproteinInternal medicine journalReferences
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A homozygous mutation in the TUB gene associated with retinal dystrophy and obesity.

2013

Inherited retinal dystrophies are a major cause of childhood blindness. Here, we describe the identification of a homozygous frameshift mutation (c.1194_1195delAG, p.Arg398Serfs*9) in TUB in a child from a consanguineous UK Caucasian family investigated using autozygosity mapping and whole-exome sequencing. The proband presented with obesity, night blindness, decreased visual acuity, and electrophysiological features of a rod cone dystrophy. The mutation was also found in two of the proband's siblings with retinal dystrophy and resulted in mislocalization of the truncated protein. In contrast to known forms of retinal dystrophy, including those caused by mutations in the tubby-like protein …

ProbandMaleobesity030209 endocrinology & metabolismGenes RecessiveConsanguinityBiologymedicine.disease_causeWhite PeopleFrameshift mutation03 medical and health sciencesConsanguinity0302 clinical medicineRetinitis pigmentosaGeneticsRod-cone dystrophymedicineHomeostasisHumansretinal dystrophyTUBChildEye ProteinsFrameshift MutationGenetics (clinical)030304 developmental biologyAdaptor Proteins Signal TransducingGenetics0303 health sciencesMutationHomozygoteChildhood blindnessciliatubbyChromosome MappingProteinsmedicine.diseaseUnited Kingdom3. Good healthPedigreeBrief ReportsFemaleRetinal DystrophiesRetinitis Pigmentosa
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Null alleles of human complement C4. Evidence for pseudogenes at the C4A locus and for gene conversion at the C4B locus

1990

The two genes for the C4A and C4B isotypes of the fourth component of human complement are located in the MHC class III region. Previous studies have demonstrated the unusual expression of C4 genes in the form of aberrant or duplicated haplotypes. Null alleles of C4A or C4B (AQ0 or BQ0) have been defined by the absence of gene products and occur at frequencies of 0.1-0.3. However, only some C4 null alleles are due to gene deletions, the remainder were thought to be nonexpressed genes. We have analyzed the C4 gene structure of 26 individuals lacking either C4A or C4B protein. The DNA of individuals with apparently nonexpressed C4 genes was tested for the presence of C4A- and C4B-specific seq…

PseudogeneImmunologyMolecular Sequence DataGene ConversionLocus (genetics)chemical and pharmacologic phenomenaPolymerase Chain ReactionRestriction fragmentComplement C4bImmunology and AllergyHumansGene conversionAlleleGeneAllelesGeneticsbiologyBase SequenceHomozygoteC4AComplement C4aComplement C4ArticlesDNANull alleleMolecular biologyGenesbiology.proteinDNA ProbesOligonucleotide ProbesPseudogenesThe Journal of Experimental Medicine
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Cancer prevention with aspirin in hereditary colorectal cancer (Lynch syndrome), 10-year follow-up and registry-based 20-year data in the CAPP2 study…

2020

BACKGROUND: Lynch syndrome is associated with an increased risk of colorectal cancer and with a broader spectrum of cancers, especially endometrial cancer. In 2011, our group reported long-term cancer outcomes (mean follow-up 55·7 months [SD 31·4]) for participants with Lynch syndrome enrolled into a randomised trial of daily aspirin versus placebo. This report completes the planned 10-year follow-up to allow a longer-term assessment of the effect of taking regular aspirin in this high-risk population.METHODS: In the double-blind, randomised CAPP2 trial, 861 patients from 43 international centres worldwide (707 [82%] from Europe, 112 [13%] from Australasia, 38 [4%] from Africa, and four [&l…

RESISTANT STARCHPlacebo-controlled study030204 cardiovascular system & hematology0302 clinical medicineLife Tables030212 general & internal medicine11 Medical and Health Sciencesmedia_commonRISKAspirineducation.field_of_studyAnti-Inflammatory Agents Non-SteroidalLOW-DOSE ASPIRINGeneral MedicineLynch syndrome3. Good healthIntention to Treat AnalysisAnti-Inflammatory Agents Non-Steroidal/adverse effectsmedicine.drugCHEMOPREVENTIONmedicine.medical_specialtyHeterozygote3122 CancersPopulationNEOPLASIAAspirin/adverse effectsPlaceboCAPP2 InvestigatorsMedication Adherence03 medical and health sciencesDouble-Blind MethodInternal medicineGeneral & Internal MedicineColorectal Neoplasms Hereditary Nonpolyposis/geneticsBENEFITSmedicinemedia_common.cataloged_instanceHumansEuropean unioneducationProportional Hazards ModelsIntention-to-treat analysisCancer preventionAspirinbusiness.industryMORTALITY3126 Surgery anesthesiology intensive care radiologymedicine.diseaseColorectal Neoplasms Hereditary NonpolyposisbusinessFollow-Up Studies
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The induction of cytochrome P450 3A5 (CYP3A5) in the human liver and intestine is mediated by the xenobiotic sensors pregnane X receptor (PXR) and co…

2004

Induction of cytochrome P450 3A (CYP3A) by xenobiotics may lead to clinically relevant drug interactions. In contrast with other CYP3A family members, studies on the inducibility of CYP3A5 indicate conflicting results. We report the induction of CYP3A5 mRNA in 13 of 16 hepatocyte preparations exposed to rifampin. Furthermore, induction of CYP3A5 mRNA was observed in intestinal biopsies in three of eight probands following exposure to the antibiotic. The highest absolute levels of CYP3A5 transcripts were found following rifampin treatment in hepatocytes and intestines from carriers of CYP3A5*1 alleles. Elucidation of the mechanism involved in CYP3A5 induction revealed that constitutively act…

Receptors SteroidTime FactorsCYP3ABiopsyAmino Acid MotifsReceptors Cytoplasmic and NuclearPharmacology030226 pharmacology & pharmacyBiochemistryTransactivation0302 clinical medicineCytochrome P-450 Enzyme SystemGenes ReporterCytochrome P-450 CYP3AIntestinal MucosaReceptorPromoter Regions GeneticGenes Dominant0303 health sciencesPregnane X receptorPregnane X Receptor3. Good healthmedicine.anatomical_structureLiverHepatocyteRifampinPlasmidsProtein BindingTranscriptional ActivationHeterozygoteGenotypeBiologyTransfectionXenobiotics03 medical and health sciencesmedicineHumansRNA MessengerMolecular BiologyAllelesConstitutive Androstane Receptor030304 developmental biologyMessenger RNACYP3A4Cell BiologyMolecular biologyProtein Structure TertiaryHepatocytesRNADrug metabolismTranscription FactorsThe Journal of biological chemistry
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Neuroinflammation by cytotoxic T-lymphocytes impairs retrograde axonal transport in an oligodendrocyte mutant mouse.

2012

Mice overexpressing proteolipid protein (PLP) develop a leukodystrophy-like disease involving cytotoxic, CD8+ T-lymphocytes. Here we show that these cytotoxic T-lymphocytes perturb retrograde axonal transport. Using fluorogold stereotactically injected into the colliculus superior, we found that PLP overexpression in oligodendrocytes led to significantly reduced retrograde axonal transport in retina ganglion cell axons. We also observed an accumulation of mitochondria in the juxtaparanodal axonal swellings, indicative for a disturbed axonal transport. PLP overexpression in the absence of T-lymphocytes rescued retrograde axonal transport defects and abolished axonal swellings. Bone marrow tr…

Retinal Ganglion CellsProteolipid protein 1MouseCD8-Positive T-LymphocytesGranzymesMyelinMiceBone Marrow TransplantationNeuronsddc:616MultidisciplinarybiologyQRNeurodegenerative DiseasesAnimal ModelsCell biologyOligodendrogliamedicine.anatomical_structureNeurologyMedicineResearch ArticleHeterozygoteMultiple SclerosisProteolipidsScienceImmunologyMice Transgenicchemical and pharmacologic phenomenaAutoimmune DiseasesModel OrganismsmedicineAnimalsBiologyNeuroinflammationInflammationImmunityDemyelinating DisordersOligodendrocyteAxonsGranzyme BPerforinGranzymenervous systemImmune SystemImmunologyMutationAxoplasmic transportbiology.proteinClinical ImmunologyMolecular NeuroscienceT-Lymphocytes CytotoxicNeurosciencePLoS ONE
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The ATC1 gene encodes a cell wall-linked acid trehalase required for growth on trehalose in Candida albicans.

2004

After screening a Candida albicans genome data base, the product of an open reading frame (IPF 19760/CA2574) with 41% identity to Saccharomyces cerevisiae vacuolar acid trehalase (Ath1p) was identified and named Atc1p. The deduced amino acid sequence shows that Atc1p contains an N-terminal hydrophobic signal peptide and 20 potential sites for N-glycosylation. C. albicans homozygous mutants that lack acid trehalase activity were constructed by gene disruption at the two ATC chromosomal alleles. Analysis of these null mutants shows that Atc1p is localized in the cell wall and is required for growth on trehalose as a carbon source. An Atc1p endowed with acid trehalase activity was obtained by …

Saccharomyces cerevisiae ProteinsTime FactorsTranscription GeneticMutantBlotting WesternMolecular Sequence DataTrehalase activityBiologyBiochemistrychemistry.chemical_compoundOpen Reading FramesCell WallCandida albicansAmino Acid SequenceRNA MessengerTrehalaseTrehalaseCandida albicansMolecular BiologyPeptide sequenceAlleleschemistry.chemical_classificationCell-Free SystemModels GeneticSequence Homology Amino AcidReverse Transcriptase Polymerase Chain ReactionStructural geneHomozygoteNuclear ProteinsTrehaloseCell BiologyDNAbiology.organism_classificationPhosphoproteinsTrehaloseCarbonAmino acidProtein Structure TertiaryGlucosechemistryBiochemistryProtein BiosynthesisMutationElectrophoresis Polyacrylamide GelCell DivisionPlasmidsThe Journal of biological chemistry
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