Search results for "Maternal Inheritance"

showing 4 items of 4 documents

Maternal Inheritance of a Recessive RBP4 Defect in Canine Congenital Eye Disease

2018

SUMMARY Maternally skewed transmission of traits has been associated with genomic imprinting and oocyte-derived mRNA. We report canine congenital eye malformations, caused by an amino acid deletion (K12del) near the N terminus of retinol-binding protein (RBP4). The disease is only expressed when both dam and offspring are deletion homozygotes. RBP carries vitamin A (retinol) from hepatic stores to peripheral tissues, including the placenta and developing eye, where it is required to synthesize retinoic acid. Gestational vitamin A deficiency is a known risk factor for ocular birth defects. The K12del mutation disrupts RBP folding in vivo, decreasing its secretion from hepatocytes to serum. T…

0301 basic medicineMaleNon-Mendelian inheritanceProtein Foldingcongenital eye defectEye Diseasesgenetic structuresNATIVE DISULFIDE BONDSMedical PhysiologyRetinoic acidReproductive health and childbirth413 Veterinary scienceMicrophthalmiavitamin Achemistry.chemical_compoundPlasmaA-vitamiini2.1 Biological and endogenous factorsMicrophthalmosPrealbuminCRYSTAL-STRUCTUREAetiologyBase Pairinglcsh:QH301-705.5Sequence DeletionPediatricwhole genome sequencingVITAMIN-A-DEFICIENCYANOPHTHALMIAPenetrancePedigreemedicine.anatomical_structurePhenotypeFemalemedicine.medical_specialtyGenotypeENDOPLASMIC-RETICULUMGenes RecessiveMETABOLISMBiologyGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesDogscanine geneticsInternal medicinePlacentaRETINOL-BINDING-PROTEINGeneticsmedicineAnimalsHumansRecessiveMALFORMATIONSBIOCHEMICAL BASISAmino Acid SequenceAlleleEye Disease and Disorders of VisionNutritiongenome-wide association study030102 biochemistry & molecular biologywestern blottingMUTATIONSta1184RBP4maternal inheritancemedicine.diseaseRetinol-Binding ProteinsRetinol binding proteinnuclear magnetic resonance030104 developmental biologyEndocrinologychemistryGeneslcsh:Biology (General)microphthalmiaGenetic LociHela Cells1182 Biochemistry cell and molecular biologyCongenital Structural Anomalies3111 BiomedicineBiochemistry and Cell BiologyDigestive DiseasesGenomic imprintingRetinol-Binding Proteins PlasmaHeLa Cells
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Gender as a Modifying Factor Influencing Myotonic Dystrophy Type 1 Phenotype Severity and Mortality: A Nationwide Multiple Databases Cross-Sectional …

2016

International audience; BACKGROUND: Myotonic Dystrophy type 1 (DM1) is one of the most heterogeneous hereditary disease in terms of age of onset, clinical manifestations, and severity, challenging both medical management and clinical trials. The CTG expansion size is the main factor determining the age of onset although no factor can finely predict phenotype and prognosis. Differences between males and females have not been specifically reported. Our aim is to study gender impact on DM1 phenotype and severity.METHODS: We first performed cross-sectional analysis of main multiorgan clinical parameters in 1409 adult DM1 patients (\textgreater18y) from the DM-Scope nationwide registry and obser…

Male0301 basic medicineDatabases FactualPhysiologyCross-sectional studyMyotonic dystrophylcsh:MedicineDiseasecomputer.software_genreinfo:eu-repo/classification/mesh/Socioeconomic FactorsLaryngologyinfo:eu-repo/classification/mesh/Myotonic Dystrophy/epidemiology*0302 clinical medicineMedicine and Health SciencesEthnicitiesMedicineinfo:eu-repo/classification/mesh/FemaleFrench Peoplelcsh:Scienceinfo:eu-repo/classification/mesh/Adulteducation.field_of_studyMultidisciplinaryinfo:eu-repo/classification/mesh/Factual*Death ratesDatabaseCognitive NeurologyMortality rateDysphagia3. Good healthPhenotypeCognitive impairmentNeurologyPhysiological ParametersFemaleinfo:eu-repo/classification/mesh/Databasesinfo:eu-repo/classification/mesh/MaleResearch ArticleAdultMaternal inheritanceCognitive NeurosciencePopulation[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human geneticsMyotonic dystrophy03 medical and health sciencesPopulation MetricsAdultsHumansObesitySex DistributioneducationDemographyinfo:eu-repo/classification/mesh/Cross-Sectional StudiesPopulation BiologyCataractsbusiness.industrylcsh:RBody WeightBiology and Life Sciencesmedicine.diseaseMyotoniaThyroid disorderinfo:eu-repo/classification/mesh/Sex DistributionHealth CareOphthalmologyCross-Sectional Studies030104 developmental biologyOtorhinolaryngologySocioeconomic Factors[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAge Groups[SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologieLens DisordersPeople and Placesinfo:eu-repo/classification/mesh/Myotonic Dystrophy/mortalityCognitive Sciencelcsh:QPopulation Groupings[SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologieHealth StatisticsMorbidityAge of onsetbusinessinfo:eu-repo/classification/mesh/Phenotype*computerinfo:eu-repo/classification/mesh/Humans030217 neurology & neurosurgeryNeurosciencePLOS ONE
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Loss-of-function maternal-effect mutations of PADI6 are associated with familial and sporadic Beckwith-Wiedemann syndrome with multi-locus imprinting…

2020

Abstract Background PADI6 is a component of the subcortical maternal complex, a group of proteins that is abundantly expressed in the oocyte cytoplasm, but is required for the correct development of early embryo. Maternal-effect variants of the subcortical maternal complex proteins are associated with heterogeneous diseases, including female infertility, hydatidiform mole, and imprinting disorders with multi-locus imprinting disturbance. While the involvement of PADI6 in infertility is well demonstrated, its role in imprinting disorders is less well established. Results We have identified by whole-exome sequencing analysis four cases of Beckwith-Wiedemann syndrome with multi-locus imprintin…

MaleBeckwith-Wiedemann SyndromeGenomic imprintingMulti-locus imprinting disturbanceBeckwith–Wiedemann syndromeWhole Exome SequencingProtein-Arginine Deiminase Type 60302 clinical medicinePregnancyImprinting (psychology)ChildGenetics (clinical)Genetics0303 health sciencesDNA methylationPADI6Beckwith-Wiedemann syndrome; DNA methylation; Genomic imprinting; Infertility; Maternal-effect variants; Multi-locus imprinting disturbance; PADI6; Subcortical maternal complex; Adolescent; Adult; Beckwith-Wiedemann Syndrome; Child Preschool; DNA Methylation; Female; Genomic Imprinting; Heterozygote; Humans; Hydatidiform Mole; Infant; Infertility Female; Male; Maternal Inheritance; Mutation; Oocytes; Pedigree; Phenotype; Pregnancy; Protein-Arginine Deiminase Type 6; Siblings; Whole Exome SequencingFemale infertilityMaternal effectHydatidiform MolePedigreePhenotypeChild Preschool030220 oncology & carcinogenesisDNA methylationFemaleMaternal InheritanceInfertility FemaleAdultHeterozygoteAdolescentSubcortical maternal complexBiology03 medical and health sciencesExome SequencingGeneticsmedicineHumansMaternal-effect variantsPreschoolMolecular BiologyLoss function030304 developmental biologyMaternal-effect variantResearchSiblingsInfantmedicine.diseaseHuman geneticsInfertilityMutationOocytesGenomic imprintingDevelopmental BiologyClinical Epigenetics
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Maternal and fetal genetic effects on birth weight and their relevance to cardio-metabolic risk factors

2019

AbstractBirth weight (BW) variation is influenced by fetal and maternal genetic and non-genetic factors, and has been reproducibly associated with future cardio-metabolic health outcomes. These associations have been proposed to reflect the lifelong consequences of an adverse intrauterine environment. In earlier work, we demonstrated that much of the negative correlation between BW and adult cardio-metabolic traits could instead be attributable to shared genetic effects. However, that work and other previous studies did not systematically distinguish the direct effects of an individual’s own genotype on BW and subsequent disease risk from indirect effects of their mother’s correlated genoty…

MaleNetherlands Twin Register (NTR)LD SCORE REGRESSIONBirth Weight/geneticsPhysiologyGenome-wide association studyBLOOD-PRESSUREBlood PressureType 2 diabetesDISEASEFetal Development0302 clinical medicineModelsPregnancyRisk FactorsGenotypeBirth Weightmaternal genetic030212 general & internal medicineMaternal-Fetal Exchange0303 health sciencesBody Height/genetics1184 Genetics developmental biology physiologyHeart Diseases/etiologySingle NucleotideASSOCIATIONMetabolic Diseases/etiology3. Good healthType 2/etiologyMENDELIAN RANDOMIZATIONGROWTH/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingFemaleMaternal InheritanceMaternal Inheritance/geneticsAdultBlood Pressure/geneticsHeart DiseasesOffspringBirth weightcardio-metabolic health outcomesBiologyDiabetes Mellitus Type 2/etiologyPolymorphism Single NucleotideArticle03 medical and health sciencesGeneticMetabolic DiseasesSDG 3 - Good Health and Well-beingDiabetes mellitusMendelian randomizationGeneticsmedicineDiabetes Mellitus/dk/atira/pure/keywords/cohort_studies/netherlands_twin_register_ntr_HumansGenetic Predisposition to DiseasePolymorphism030304 developmental biologyGlycemicPregnancyFetusIDENTIFICATIONModels GeneticInfant NewbornInfantbirth weightDIABETES-MELLITUSmedicine.diseaseNewbornFetal Development/geneticsBody HeightMaternal-Fetal Exchange/geneticsLIFEBlood pressureDiabetes Mellitus Type 2ORIGINSInstitut für Ernährungswissenschaft030217 neurology & neurosurgeryGenome-Wide Association Study
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