Search results for " Pair 3"

showing 10 items of 21 documents

New susceptibility locus for coronary artery disease on chromosome 3q22.3

2009

We present a three-stage analysis of genome-wide SNP data in 1,222 German individuals with myocardial infarction and 1,298 controls, in silico replication in three additional genome-wide datasets of coronary artery disease (CAD) and subsequent replication in approximately 25,000 subjects. We identified one new CAD risk locus on 3q22.3 in MRAS (P = 7.44 x 10(-13); OR = 1.15, 95% CI = 1.11-1.19), and suggestive association with a locus on 12q24.31 near HNF1A-C12orf43 (P = 4.81 x 10(-7); OR = 1.08, 95% CI = 1.05-1.11).

medicine.medical_specialtyQuantitative Trait LociLocus (genetics)Single-nucleotide polymorphismGenome-wide association studyCoronary Artery DiseaseQuantitative trait locusBiologyBioinformaticsPolymorphism Single NucleotideArticleCoronary artery diseaseGermanyInternal medicineGeneticsmedicineHumansGenetic Predisposition to DiseaseHepatocyte Nuclear Factor 1-alphaMyocardial infarctionCase-control studyChromosomemedicine.diseaseCase-Control Studiesras ProteinsCardiologyChromosomes Human Pair 3Genome-Wide Association Study
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Genome-wide analysis of multi-ancestry cohorts identifies new loci influencing intraocular pressure and susceptibility to glaucoma

2014

Elevated intraocular pressure (IOP) is an important risk factor in developing glaucoma, and variability in IOP might herald glaucomatous development or progression. We report the results of a genome-wide association study meta-analysis of 18 population cohorts from the International Glaucoma Genetics Consortium (IGGC), comprising 35,296 multi-ancestry participants for IOP. We confirm genetic association of known loci for IOP and primary open-angle glaucoma (POAG) and identify four new IOP-associated loci located on chromosome 3q25.31 within the FNDC3B gene (P = 4.19 x 10(-8) for rs6445055), two on chromosome 9 (P = 2.80 x 10(-11) for rs2472493 near ABCA1 and P = 6.39 x 10(-11) for rs8176693…

MaleIntraocular pressuregenetic structuresGlaucomaGenome-wide association studyCohort Studies0302 clinical medicinePolymorphism (computer science)Risk FactorsPOPULATIONGeneticsAged 80 and overRISK0303 health scienceseducation.field_of_studyCOMMON VARIANTSASSOCIATIONMiddle AgedFemaleTRIALChromosomes Human Pair 3OPEN-ANGLE GLAUCOMAChromosomes Human Pair 9Glaucoma Open-AngleATP Binding Cassette Transporter 1AdultEXPRESSIONmedicine.medical_specialtyOpen angle glaucomaGenotypePopulationChromosome 9BiologyPolymorphism Single NucleotideArticleABO Blood-Group System03 medical and health sciencesYoung AdultMeta-Analysis as TopicOphthalmologyGeneticsmedicineHumansGenetic Predisposition to DiseaseeducationCENTRAL CORNEAL THICKNESSIntraocular PressureMETAANALYSIS030304 developmental biologyGenetic associationAgedChromosomes Human Pair 11Glaucomamedicine.diseaseeye diseasesFibronectinsREDUCTIONGenetic Loci030221 ophthalmology & optometrysense organsGenome-Wide Association StudyNature Genetics
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Delineation of the 3p14.1p13 microdeletion associated with syndromic distal limb contractures

2014

International audience; Distal limb contractures (DLC) represent a heterogeneous clinical and genetic condition. Overall, 20–25% of the DLC are caused by mutations in genes encoding the muscle contractile apparatus. Large interstitial deletions of the 3p have already been diagnosed by standard chromosomal analysis, but not associated with a specific phenotype. We report on four patients with syndromic DLC presenting with a de novo 3p14.1p13 micro-deletion. The clinical features associated multiple contractures, feeding problems, developmental delay, and intellectual disability. Facial dysmorphism was constant with low-set posteriorly rotated ears and blepharophimosis. Review of previously r…

MalePathologymedicine.medical_specialtyContracture[SDV]Life Sciences [q-bio]Locus (genetics)FOXP1BiologyMicedistal limb contracturessymbols.namesakeExonEIF4E3Intellectual disabilityGeneticsmedicineAnimalsHumans[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]3p141p13 microdeletionGenetics (clinical)ArthrogryposisChromosome AberrationsMice KnockoutSanger sequencingGeneticsComparative Genomic Hybridization[ SDV ] Life Sciences [q-bio]ExtremitiesForkhead Transcription FactorsSyndromeFOXP1Microdeletion syndromemedicine.diseaseBlepharophimosisPhenotypeRepressor Proteins[SDV] Life Sciences [q-bio]array-CGH[ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]symbolsFemale[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Chromosomes Human Pair 3FranceCarrier Proteinsintronic regulatory sequenceAmerican Journal of Medical Genetics Part A
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Genomic structure and paralogous regions of the inversion breakpoint occurring between human chromosome 3p12.3 and orangutan chromosome 2.

2003

Intrachromosomal duplications play a significant role in human genome pathology and evolution. To better understand the molecular basis of evolutionary chromosome rearrangements, we performed molecular cytogenetic and sequence analyses of the breakpoint region that distinguishes human chromosome 3p12.3 and orangutan chromosome 2. FISH with region-specific BAC clones demonstrated that the breakpoint-flanking sequences are duplicated intrachromosomally on orangutan 2 and human 3q21 as well as at many pericentromeric and subtelomeric sites throughout the genomes. Breakage and rearrangement of the human 3p12.3-homologous region in the orangutan lineage were associated with a partial loss of dup…

Genome evolutionHerpesvirus 4 HumanPan troglodytesBiologyHybrid CellsChimpanzee genome projectEvolution MolecularContig MappingChromosome 19Pongo pygmaeusGeneticsAnimalsHumansLymphocytesMolecular BiologyGenetics (clinical)In Situ Hybridization FluorescenceChromosomal inversionCell Line TransformedSequence DeletionGeneticsHuman evolutionary geneticsCercopithecidaeChromosome BreakageGenome projectChromosomes MammalianChromosome InversionChromosomes Human Pair 3Chromosome breakageChromosome 21Cytogenetic and genome research
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Isolation and differential expression of two isoforms of the ROBO2/Robo2 axon guidance receptor gene in humans and mice.

2006

AbstractExpression of Robo receptor molecules is important for axon guidance across the midline of the mammalian central nervous system. Here we describe novel isoform a of human ROBO2, which is initially strongly expressed in the fetal human brain but thereafter only weakly expressed in adult brain and a few other tissues. The known isoform b of ROBO2 shows a more or less ubiquitous expression pattern, suggesting diverse functional roles. The genomic structure and distinct expression patterns of Robo2a and Robo2b have been conserved in the mouse, but in contrast to human ROBO2a mouse Robo2a is also abundant in adult brain. Exons 1 and 2 of human ROBO2a lie in an inherently unstable DNA seg…

Fetal brain developmentGene isoformSegmental duplicationMolecular Sequence DataBreak in syntenyBiologyLoss of heterozygosity03 medical and health sciencesMice0302 clinical medicineChromosome 3p12.3GeneticsAnimalsHumansProtein IsoformsAmino Acid SequenceReceptors ImmunologicGene030304 developmental biologySegmental duplicationSyntenyEvolutionary breakpointGenetics0303 health sciencesAxon guidanceChromosomeBrainGene Expression Regulation DevelopmentalROBO2ExonsChromosomes MammalianHuman genomeAxon guidanceChromosomes Human Pair 3030217 neurology & neurosurgeryGenomics
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3q27.3 microdeletional syndrome: a recognisable clinical entity associating dysmorphic features, marfanoid habitus, intellectual disability and psych…

2013

Abstract: Background Since the advent of array-CGH, numerous new microdeletional syndromes have been delineated while others remain to be described. Although 3q29 subtelomeric deletion is a well-described syndrome, there is no report on 3q interstitial deletions. Methods We report for the first time seven patients with interstitial deletions at the 3q27.3q28 locus gathered through the Decipher database, and suggest this locus as a new microdeletional syndrome. Results The patients shared a recognisable facial dysmorphism and marfanoid habitus, associated with psychosis and mild to severe intellectual disability (ID). Most of the patients had no delay in gross psychomotor acquisition, but ha…

AdultMalePsychosisCandidate genePediatricsmedicine.medical_specialtyAdolescentLocus (genetics)ArachnodactylyYoung AdultIntellectual DisabilityIntellectual disabilityGeneticsMedicineHumansAbnormalities MultipleGenetics (clinical)GeneticsComparative Genomic Hybridizationbusiness.industryMood DisordersMarfanoidChromosome MappingFaciesInfantSyndromemedicine.diseasePhenotypeMood disordersChild PreschoolBone maturationFemaleHuman medicineChromosomes Human Pair 3Chromosome DeletionbusinessJournal of medical genetics
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The gene encoding the transcriptional repressor BERF-1 maps to a region of conserved synteny on mouse chromosome 16 and human chromosome 3 and a rela…

1999

We have recently identified and characterized a Kruppel-like zinc finger protein (BERF-1), that functions as a repressor of β enolase gene transcription. By interspecific backcross analysis the gene encoding BERF-1 was localized 4.7 cM proximal to the <i>Mtv6</i> locus on mouse chromosome 16, and an isolated pseudogene was localized to mouse chromosome 8, about 5.3 cM distal to the D8Mit4 marker. Nucleotide sequence identity and chomosome location indicate that the gene encoding BERF-1 is the mouse homologue (<i>Zfp148</i>) of ZNF148 localized to human chromosome 3q21, a common translocation site in acute myeloid leukemia patients.

Genetic MarkersDNA ComplementaryTranscription GeneticKruppel-Like Transcription FactorsBiologyHybrid CellsPolymerase Chain ReactionGene Expression Regulation EnzymologicMiceChromosome 16GeneticsAnimalsHumansMolecular BiologyGenetics (clinical)Conserved SequenceSyntenyDNA PrimersGeneticsBase SequenceYY1Chromosome MappingTAF9Zinc FingersTCF4DNA-Binding ProteinsRepressor ProteinsChromosome 3GATAD2BPhosphopyruvate Hydratasecardiovascular systemChromosomes Human Pair 3Chromosome 22PseudogenesTranscription FactorsCytogenetics and cell genetics
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Detection of a germline mutation and somatic homozygous loss of the von Hippel-Lindau tumor-suppressor gene in a family with a de novo mutation

1996

von Hippel-Lindau (VHL) disease is a pleiotropic disorder featuring a variety of malignant and benign tumors of the eye, central nervous system, kidney, and adrenal gland. Recently the VHL gene has been identified in the chromosomal region 3p25-26. Prognosis and successful management of VHL patients and their descendants depend on unambiguous diagnosis. Due to recurrent hemangioblastomas, a29-year-old patient without familial history of VHL disease was diagnosed to be at risk for the disease. Histopathological examination of a small renal mass identified a clear cell tumor with a G1 grading. Genetic characterization of the germline and of the renal tumor was performed. Polymerase chain reac…

AdultMalemedicine.medical_specialtyvon Hippel-Lindau DiseaseTumor suppressor geneDNA Mutational AnalysisMolecular Sequence Dataurologic and male genital diseasesPolymerase Chain ReactionGermlineGermline mutationVon Hippel–Lindau tumor suppressorGeneticsmedicineHumansGenes Tumor SuppressorSpinal Cord NeoplasmsVon Hippel–Lindau diseaseGerm-Line MutationPolymorphism Single-Stranded ConformationalGenetics (clinical)Sequence Deletionbiologymedicine.diagnostic_testHomozygoteCytogeneticsExonsmedicine.diseaseKidney Neoplasmsfemale genital diseases and pregnancy complicationsHemangioblastomaPedigreeKaryotypingChromosomal regionbiology.proteinCancer researchFemaleChromosomes Human Pair 3Chromosome DeletionFluorescence in situ hybridizationHuman Genetics
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Aceruloplasminaemia: a family with a novel mutation and long-term therapy with deferasirox.

2014

Ceruloplasmin is a member of the multicopper oxidase family that plays a major role in the transport of iron in the body. Aceruloplasminaemia (ACP) is a rare disease and is clinically identified by iron overload in liver, pancreas, brain, and other organs, and by microcytic anaemia. So far, the iron chelator deferasirox was given for therapy only up to 6 months due to side effects. Here, we describe a novel mutation leading to ACP and report for the first time a long-term therapy, that is, 2 years with deferasirox. ACP was diagnosed in 3 siblings using clinical and biochemical characteristics, HFE and ceruloplasmin mutational analysis, liver biopsy, brain-, liver-, and heart-MRI. For iron d…

AdultBlood GlucoseMalemedicine.medical_specialtyEndocrinology Diabetes and MetabolismIronClinical BiochemistryCarbohydrate metabolismBiochemistryBenzoatesEndocrinologyInsulin resistanceHepcidinInternal medicineGermanyMedicineHumansChelating Agentsbiologymedicine.diagnostic_testbusiness.industryBiochemistry (medical)DeferasiroxCeruloplasminNeurodegenerative DiseasesGeneral MedicineTriazolesmedicine.diseaseIron Metabolism DisordersMagnetic Resonance ImagingPedigreeDeferasiroxEndocrinologymedicine.anatomical_structureTreatment OutcomeLiverLiver biopsyMutationbiology.proteinFemaleChromosomes Human Pair 3businessCeruloplasminPancreasmedicine.drugRare diseaseHormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme
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Replication of linkage of familial hypobetalipoproteinemia to chromosome 3p in six kindreds

2002

Familial hypobetalipoproteinemia (FHBL) is a genetically heterogeneous condition characterized by very low apolipoprotein B (apoB) concentrations in plasma and/or low levels of LDL-cholesterol (LDL-C) with a propensity to developing fatty liver. In a minority of cases, truncation-specifying mutations of the apoB gene (APOB) are etiologic, but the genetic basis of most cases is unknown. We previously reported linkage of FHBL to a 10 cM region on 3p21.1-22 in one kindred. The objectives of the current study were to identify other FHBL families with linkage to 3p and to narrow the FHBL susceptibility region on 3p. Six additional FHBL kindreds unlinked to the APOB region on chromosome 2 were ge…

Genetic MarkersAdultMaleMeiosiSettore MED/09 - Medicina InternaApolipoprotein BGenotypeGenetic LinkageQD415-436BiologyBiochemistryChromosomal crossoverHypobetalipoproteinemiasEndocrinologyQuantitative Trait HeritableGenetic linkageGenetic MarkerHaplotypeHumanslinkage analysisCrossing Over GeneticChildAgedAdult; Aged; Aged 80 and over; Child; Chromosome Mapping; Chromosomes Human Pair 3; Crossing Over Genetic; Female; Genetic Linkage; Genetic Markers; Genotype; Haplotypes; Humans; Hypobetalipoproteinemias; Male; Meiosis; Middle Aged; Pedigree; Quantitative Trait HeritableGeneticsAged 80 and overGenetic heterogeneityHaplotypeChromosomeChromosome MappingCell BiologyoligogenicMiddle AgedPedigreeMeiosisMarkov chain Monte CarloChromosome 3HaplotypesGenetic markerbiology.proteinvariance componentslipids (amino acids peptides and proteins)FemaleChromosomes Human Pair 3geneticHypobetalipoproteinemiaHuman
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