Search results for "Endogenous Factors"

showing 10 items of 58 documents

Pancreatic Protein Tyrosine Phosphatase 1B Deficiency Exacerbates Acute Pancreatitis in Mice

2016

Acute pancreatitis (AP) is a common and devastating gastrointestinal disorder that causes significant morbidity. The disease starts as local inflammation in the pancreas that may progress to systemic inflammation and complications. Protein tyrosine phosphatase 1B (PTP1B) is implicated in inflammatory signaling, but its significance in AP remains unclear. To investigate whether PTP1B may have a role in AP, we used pancreas PTP1B knockout (panc-PTP1B KO) mice and determined the effects of pancreatic PTP1B deficiency on cerulein- and arginine-induced acute pancreatitis. We report that PTP1B protein expression was increased in the early phase of AP in mice and rats. In addition, histological an…

Male0301 basic medicineWistarSystemic inflammationMedical and Health SciencesOral and gastrointestinalMicePathology2.1 Biological and endogenous factorsAetiologyNon-Receptor Type 1CancerMice KnockoutProtein Tyrosine Phosphatase Non-Receptor Type 1Pancreatitis Acute NecrotizingReverse Transcriptase Polymerase Chain ReactionRegular Articlemedicine.anatomical_structureAcute NecrotizingGastrointestinal disorderAcute pancreatitisTumor necrosis factor alphamedicine.symptomPancreashormones hormone substitutes and hormone antagonistsmedicine.medical_specialtyKnockoutInflammationPathology and Forensic MedicineProinflammatory cytokinePancreatic Cancer03 medical and health sciencesRare DiseasesInternal medicinemedicineAnimalsRats WistarAnimalbusiness.industrymedicine.diseaseRatsDisease Models Animal030104 developmental biologyEndocrinologyPancreatitisDisease ModelsPancreatitisProtein Tyrosine PhosphataseDigestive DiseasesbusinessThe American Journal of Pathology
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NFIB Haploinsufficiency Is Associated with Intellectual Disability and Macrocephaly

2018

The nuclear factor I (NFI) family of transcription factors play an important role in normal development of multiple organs. Three NFI family members are highly expressed in the brain, and deletions or sequence variants in two of these, NFIA and NFIX, have been associated with intellectual disability (ID) and brain malformations. NFIB, however, has not previously been implicated in human disease. Here, we present a cohort of 18 individuals with mild ID and behavioral issues who are haploinsufficient for NFIB. Ten individuals harbored overlapping microdeletions of the chromosomal 9p23-p22.2 region, ranging in size from 225 kb to 4.3 Mb. Five additional subjects had point sequence variations c…

Male0301 basic medicinechromosome 9p23Medical and Health SciencesCorpus CallosumCohort StudiesMice2.1 Biological and endogenous factorsMegalencephalyAetiologyChildAgenesis of the corpus callosumGenetics (clinical)PediatricGenetics & HeredityCerebral CortexMice KnockoutGeneticsSingle Nucleotidenuclear factor IBiological SciencesNFIBNFIXdevelopmental delayMental HealthNFIBCodon NonsenseNFIAintellectual disabilityChild Preschoolchromosome 9p22.3NeurologicalSpeech delayFemalemedicine.symptomHaploinsufficiencyAdultAdolescentKnockoutIntellectual and Developmental Disabilities (IDD)[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human geneticsBiologymacrocephalyPolymorphism Single NucleotideArticleYoung Adult03 medical and health sciencesRare DiseasesBehavioral and Social ScienceGeneticsmedicinemegalencephalyAnimalsHumansPolymorphismCodonPreschoolNeurosciencesMacrocephalymedicine.diseaseBrain DisordershaploinsufficiencyNFI Transcription Factors030104 developmental biologyNonsense[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsbiology.proteinagenesis of the corpus callosumAmerican journal of human genetics
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Genome-wide Analyses Identify KIF5A as a Novel ALS Gene

2018

© 2018 Elsevier Inc.

MaleAls geneGenome-wide association studyFAMILIAL ALSALS; axonal transport; cargo; GWAS; KIF5A; WES; WGS0302 clinical medicine80 and overPsychologyGWASKIF5AAetiologycargoAged 80 and over0303 health sciencesFrench ALS ConsortiumKinesinKINESIN HEAVY-CHAINCognitive Sciencesaxonal transportHumanHereditary spastic paraplegiaNeuroscience(all)Single-nucleotide polymorphismTARGETED DISRUPTIONArticle03 medical and health sciencesGeneticsHumansAmino Acid SequenceLoss functionAgedHEXANUCLEOTIDE REPEATNeuroscience (all)MUTATIONSAmyotrophic Lateral Sclerosis3112 Neurosciences1702 Cognitive Sciencemedicine.diseaseITALSGEN ConsortiumAnswer ALS Foundation030104 developmental biologyALS Sequencing ConsortiumHuman medicine1109 Neurosciences030217 neurology & neurosurgery0301 basic medicineALS; GWAS; KIF5A; WES; WGS; axonal transport; cargo[SDV]Life Sciences [q-bio]KinesinsNeurodegenerativeGenetic analysisGenomeAMYOTROPHIC-LATERAL-SCLEROSIS3124 Neurology and psychiatryCohort StudiesPathogenesisLoss of Function MutationMissense mutation2.1 Biological and endogenous factorsAmyotrophic lateral sclerosisNYGC ALS ConsortiumGeneticsGeneral NeuroscienceALS axonal transport cargo GWAS KIF5A WES WGSMiddle AgedPhenotypeSettore MED/26 - NEUROLOGIANeurologicalProject MinE ALS Sequencing ConsortiumKinesinWESFemaleAdultBiologyGENOTYPE IMPUTATIONALS; axonal transport; cargo; GWAS; KIF5A; WES; WGS; Adult; Aged; Aged 80 and over; Amino Acid Sequence; Amyotrophic Lateral Sclerosis; Cohort Studies; Female; Genome-Wide Association Study; Humans; Kinesin; Loss of Function Mutation; Male; Middle Aged; Young AdultNOYoung AdultRare DiseasesmedicineSLAGEN ConsortiumGene030304 developmental biologyClinical Research in ALS and Related Disorders for Therapeutic Development (CReATe) ConsortiumNeurology & NeurosurgeryHuman GenomeNeurosciencesAXONAL-TRANSPORTBrain DisordersALS; axonal transport; cargo; GWAS; KIF5A; WES; WGS;Family memberDNA-DAMAGEMOTOR-NEURONS3111 BiomedicineCohort StudieALSGenomic Translation for ALS Care (GTAC) ConsortiumWGSAmyotrophic Lateral SclerosiGenome-Wide Association StudyALS; axonal transport; cargo; GWAS; KIF5A; WES; WGS; Neuroscience (all)
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The genomic landscape of the Ewing Sarcoma family of tumors reveals recurrent STAG2 mutation.

2014

The Ewing sarcoma family of tumors (EFT) is a group of highly malignant small round blue cell tumors occurring in children and young adults. We report here the largest genomic survey to date of 101 EFT (65 tumors and 36 cell lines). Using a combination of whole genome sequencing and targeted sequencing approaches, we discover that EFT has a very low mutational burden (0.15 mutations/Mb) but frequent deleterious mutations in the cohesin complex subunit STAG2 (21.5% tumors, 44.4% cell lines), homozygous deletion of CDKN2A (13.8% and 50%) and mutations of TP53 (6.2% and 71.9%). We additionally note an increased prevalence of the BRCA2 K3326X polymorphism in EFT patient samples (7.3%) compared …

MaleCancer ResearchCell Cycle Proteinsmedicine.disease_causeFusion geneCDKN2AMedicine and Health Sciences2.1 Biological and endogenous factorsAetiologyChildGenetics (clinical)CancerPediatricMutationTissue microarrayTumorGenomeSarcomasHigh-Throughput Nucleotide SequencingAntigens NuclearSarcomaNeoplasm ProteinsOncologyChild PreschoolFemaleSarcomaResearch ArticleBiotechnologyHumanAdultPediatric Research Initiativelcsh:QH426-470Cohesin complexAdolescentPediatric CancerEwing SarcomaSarcoma EwingBiologyDisease-Free SurvivalFrameshift mutationCell LineGermline mutationRare DiseasesCell Line TumorEwingCancer GeneticsmedicineGeneticsHumansNuclearGenetic TestingAntigensPreschoolMolecular BiologyEcology Evolution Behavior and SystematicsGenome HumanHuman GenomeBiology and Life SciencesCancers and NeoplasmsInfantmedicine.diseaselcsh:GeneticsOrphan DrugMutationCancer researchGene DeletionDevelopmental Biology
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Global, regional, and national incidence, prevalence, and years lived with disability for 301 acute and chronic diseases and injuries in 188 countrie…

2015

Summary Background Up-to-date evidence about levels and trends in disease and injury incidence, prevalence, and years lived with disability (YLDs) is an essential input into global, regional, and national health policies. In the Global Burden of Disease Study 2013 (GBD 2013), we estimated these quantities for acute and chronic diseases and injuries for 188 countries between 1990 and 2013. Methods Estimates were calculated for disease and injury incidence, prevalence, and YLDs using GBD 2010 methods with some important refinements. Results for incidence of acute disorders and prevalence of chronic disorders are new additions to the analysis. Key improvements include expansion to the cause an…

MaleGerontologyNutrition and DiseaseEpidemiologyyears lived with disability Global burden of disease acute and chronic diseases countriesPrevalenceDiseaseGlobal HealthMedical and Health SciencesConduct disorderOtitis-mediaCost of IllnessResidence CharacteristicsVoeding en ZiekteEpidemiologyPrevalence80 and overGlobal health2.2 Factors relating to the physical environment2.1 Biological and endogenous factorscountriesAetiologyChildAged 80 and overMedicine(all)education.field_of_studyATTENTION-DEFICIT/HYPERACTIVITY DISORDERIncidenceMortality rateIncidence (epidemiology)Pain ResearchNeglected DiseasesAlcohol dependenceGeneral MedicineMiddle AgedGlobal burden of diseaseGlobal Burden of Disease Study 2013 CollaboratorsMental HealthInfectious DiseasesAttention deficit/Hyperactivity disorderBurden of IllnessChild PreschoolAcute DiseaseFemaleLife Sciences & BiomedicineAdultmedicine.medical_specialtyAdolescentGBD 2013Populationacute and chronic diseasesYoung AdultMental-disordersAge DistributionMedicine General & InternalWeightsGeneral & Internal MedicinemedicineHumansLife ScienceDisabled PersonsSex DistributionPreschooleducationDeveloping CountriesVLAGAgedScience & Technologybusiness.industryDeveloped CountriesCutaneous LeishmaniasisInfant NewbornInfantHealth outcomesNewbornmedicine.diseaseComorbidityBrain Disordersyears lived with disabilityGood Health and Well BeingDisease injury incidence prevalence YLDs GBD 2010Chronic DiseaseWounds and Injuriesbusiness2.4 Surveillance and distributionIron-deficiencyDemography
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Cross-species transcriptomic analysis elucidates constitutive aryl hydrocarbon receptor activity

2014

Background Research on the aryl hydrocarbon receptor (AHR) has largely focused on variations in toxic outcomes resulting from its activation by halogenated aromatic hydrocarbons. But the AHR also plays key roles in regulating pathways critical for development, and after decades of research the mechanisms underlying physiological regulation by the AHR remain poorly characterized. Previous studies identified several core genes that respond to xenobiotic AHR ligands across a broad range of species and tissues. However, only limited inferences have been made regarding its role in regulating constitutive gene activity, i.e. in the absence of exogenous ligands. To address this, we profiled transc…

MaleHEPATIC GENE-EXPRESSION413 Veterinary scienceMedical and Health SciencesTranscriptomeDIOXIN RECEPTORMice0302 clinical medicineTCDD-induced toxicityReceptorsTranscriptional regulationABNORMAL LIVER DEVELOPMENT2.1 Biological and endogenous factorsCluster AnalysisAetiologyReceptorAH RECEPTORIN-VIVOAryl hydrocarbon receptorGeneticsRegulation of gene expression0303 health sciencesBiological Sciencesrespiratory systemCore-gene batteryAryl HydrocarbonOrgan Specificity030220 oncology & carcinogenesisAHR endogenous ligands2378-TETRACHLORODIBENZO-P-DIOXIN TCDDSignal transductionResearch ArticleBiotechnologySignal TransductionProtein BindingBioinformatics1.1 Normal biological development and functioningeducationRAT-LIVERConstitutive gene expressionBiologyMICE LACKING03 medical and health sciencesSpecies SpecificityUnderpinning researchInformation and Computing SciencesGeneticsAnimals030304 developmental biologyAryl hydrocarbon receptor activityGene Expression ProfilingComputational BiologyAryl hydrocarbon receptorCELL-CYCLE CONTROLRatsrespiratory tract diseasesGene expression profilingReceptors Aryl HydrocarbonGene Expression RegulationSUBCHRONIC EXPOSUREbiology.proteinDigestive DiseasesTranscriptome
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Widening of the genetic and clinical spectrum of Lamb-Shaffer syndrome, a neurodevelopmental disorder due to SOX5 haploinsufficiency

2020

International audience; PURPOSE: Lamb-Shaffer syndrome (LAMSHF) is a neurodevelopmental disorder described in just over two dozen patients with heterozygous genetic alterations involving SOX5, a gene encoding a transcription factor regulating cell fate and differentiation in neurogenesis and other discrete developmental processes. The genetic alterations described so far are mainly microdeletions. The present study was aimed at increasing our understanding of LAMSHF, its clinical and genetic spectrum, and the pathophysiological mechanisms involved.METHODS: Clinical and genetic data were collected through GeneMatcher and clinical or genetic networks for 41 novel patients harboring various ty…

MaleMedizinHaploinsufficiencyL-SOX5VARIANTS0302 clinical medicineNeurodevelopmental disorderIntellectual disabilityMissense mutation2.1 Biological and endogenous factorsAetiologyChildGenetics (clinical)GeneticsPediatricGenetics & Heredity0303 health sciencesPedigreeFAMILYDNA-Binding Proteinsdevelopmental delayTRANSCRIPTION FACTORSPhenotypeintellectual disabilityChild Preschoolmissense variantsFemalemissense variants.HaploinsufficiencySOXD Transcription FactorsAdultEXPRESSIONAdolescentIntellectual and Developmental Disabilities (IDD)Clinical SciencesMutation MissenseautismCell fate determinationBiologyLONG FORMSEQUENCEArticle03 medical and health sciencesYoung AdultRare DiseasesClinical ResearchCARTILAGEIntellectual DisabilitymedicineGeneticsAnimalsHumansLanguage Development DisordersGenetic Predisposition to DiseasePreschoolTranscription factorGene030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsMUTATIONSHuman GenomeInfantmedicine.diseaseBrain DisordersNeurodevelopmental DisordersDeciphering Developmental Disorder StudyMutationAutismepilepsyMissense030217 neurology & neurosurgeryGENERATIONGenetics in Medicine
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Disruption of the ASTN2 / TRIM32 locus at 9q33.1 is a risk factor in males for Autism Spectrum Disorders, ADHD and other neurodevelopmental phenotypes

2014

Rare copy number variants (CNVs) disrupting ASTN2 or both ASTN2 and TRIM32 have been reported at 9q33.1 by genome-wide studies in a few individuals with neurodevelopmental disorders (NDDs). The vertebrate-specific astrotactins, ASTN2 and its paralog ASTN1, have key roles in glial-guided neuronal migration during brain development. To determine the prevalence of astrotactin mutations and delineate their associated phenotypic spectrum, we screened ASTN2/TRIM32 and ASTN1 (1q25.2) for exonic CNVs in clinical microarray data from 89 985 individuals across 10 sites, including 64 114 NDD subjects. In this clinical dataset, we identified 46 deletions and 12 duplications affecting ASTN2. Deletions o…

MaleReceptors Cell Surface/geneticsAutismChild Development Disorders Pervasive/geneticsGene ExpressionGenome-wide association studyMedical and Health SciencesTripartite Motif ProteinsRisk FactorsReceptors2.1 Biological and endogenous factorsProtein IsoformsNerve Tissue Proteins/geneticsCopy-number variationAetiologyChildGenetics (clinical)Sequence DeletionPediatricGenetics & HeredityGeneticseducation.field_of_studySingle NucleotideArticlesGeneral MedicineExonsBiological SciencesMental HealthPhenotypeAutism spectrum disorderOrgan SpecificityCerebellar cortexChild PreschoolCell SurfaceSpeech delayFemalemedicine.symptomTranscription Initiation SiteAttention Deficit Disorder with Hyperactivity/geneticsChromosomes Human Pair 9HumanPair 9AdultPediatric Research InitiativeChild Development DisordersAdolescentDNA Copy Number VariationsIntellectual and Developmental Disabilities (IDD)Ubiquitin-Protein LigasesPopulationTranscription Factors/geneticsNerve Tissue ProteinsReceptors Cell SurfaceBiologyPolymorphism Single NucleotideChromosomesYoung AdultClinical ResearchProtein Isoforms/geneticsBehavioral and Social ScienceGeneticsmedicineAttention deficit hyperactivity disorderHumansGenetic Predisposition to DiseasePolymorphismPreschooleducationMolecular BiologyGenetic Association StudiesPervasiveGlycoproteinsHuman GenomeNeurosciencesInfant NewbornGlycoproteins/geneticsInfantNewbornmedicine.diseaseBrain DisordersAttention Deficit Disorder with HyperactivityChild Development Disorders PervasiveCase-Control StudiesAutismTranscription Factors
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Mechanism-based predictions of interactions.

1994

Abstract Exposure to more than one toxic compound is common in real life. The resulting toxic effects are often more than the simple sum of the effects of the individual compounds. It is unlikely that it will ever be possible to test all combinations. It is therefore highly desirable to improve or develop means for reasonably approximating predictions of interactions. In order to be valid and extrapolatable, these predictions are most promising if they are mechanism-based. Examples will be given for possibilities of mechanism-based predictions of interactions which exceed trivialities of simple increases by enzyme induction of enzymatic rates of a given biotransformation pathway leading to …

MaleSalmonella typhimuriumEndogenous FactorsHealth Toxicology and MutagenesisMetaboliteMechanism basedRats sprague dawleyXenobioticsRats Sprague-Dawleychemistry.chemical_compoundStilbenesBenzo(a)pyreneAnimalsIn real lifeDrug InteractionsPhosphorylationEpoxide HydrolasesMutagenicity TestsMechanism (biology)Public Health Environmental and Occupational HealthRatschemistryBiochemistryEnzyme InductionMicrosomes LiverBiochemical engineeringXenobioticMutagenicity TestResearch ArticleEnvironmental Health Perspectives
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Exome sequencing in suspected monogenic dyslipidemias.

2015

Background— Exome sequencing is a promising tool for gene mapping in Mendelian disorders. We used this technique in an attempt to identify novel genes underlying monogenic dyslipidemias. Methods and Results— We performed exome sequencing on 213 selected family members from 41 kindreds with suspected Mendelian inheritance of extreme levels of low-density lipoprotein cholesterol (after candidate gene sequencing excluded known genetic causes for high low-density lipoprotein cholesterol families) or high-density lipoprotein cholesterol. We used standard analytic approaches to identify candidate variants and also assigned a polygenic score to each individual to account for their burden of commo…

MaleSettore MED/09 - Medicina InternaMedical BiotechnologyDNA sequencing; exome; exome sequencing; genetics human; lipids; mendelian geneticsBiologyCardiorespiratory Medicine and HaematologyNovel genelipidsmendelian geneticsGene mappingClinical ResearchGenetics2.1 Biological and endogenous factorsHumansgeneticsExomeDNA sequencinghumanAetiologyMendelian disordersExomeGenetics (clinical)Exome sequencingDyslipidemiasGeneticsInborn ErrorsHuman GenomeHigh-Throughput Nucleotide SequencingAtherosclerosisMetabolismCardiovascular System & Hematologylipids (amino acids peptides and proteins)DNA sequencing; exome; genetics; human; lipidsFemalegeneticCardiology and Cardiovascular Medicineexome sequencingexomeMetabolism Inborn ErrorsCirculation. Cardiovascular genetics
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