Search results for "epigenetic pathways"

showing 10 items of 41 documents

Epigenetic Regulation in the Pathogenesis of Sjögren Syndrome and Rheumatoid Arthritis

2019

Autoimmune rheumatic diseases, such as Sjögren syndrome (SS) and rheumatoid arthritis (RA), are characterized by chronic inflammation and autoimmunity, which cause joint tissue damage and destruction by triggering reduced mobility and debilitation in patients with these diseases. Initiation and maintenance of chronic inflammatory stages account for several mechanisms that involve immune cells as key players and the interaction of the immune cells with other tissues. Indeed, the overlapping of certain clinical and serologic manifestations between SS and RA may indicate that numerous immunologic-related mechanisms are involved in the physiopathology of both these diseases. It is widely accept…

0301 basic medicinelcsh:QH426-470InflammationReviewmedicine.disease_causeAutoimmunityPathogenesis03 medical and health sciences0302 clinical medicineImmune systemImmunitymicroRNAGeneticsmedicineautoimmune diseasesEpigeneticsepigenetic pathwaysGenetics (clinical)DNA methylationepigeneticshistone modificationsbusiness.industrylcsh:Genetics030104 developmental biology030220 oncology & carcinogenesismiRNAsDNA methylationImmunologyrheumatic diseasesMolecular Medicinemedicine.symptombusinessFrontiers in Genetics
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The influence of serotonin- and other genes on impulsive behavioral aggression and cognitive impulsivity in children with attention-deficit/hyperacti…

2008

Contains fulltext : 70708.pdf (Publisher’s version ) (Open Access) ABSTRACT: BACKGROUND: Low serotonergic (5-HT) activity correlates with increased impulsive-aggressive behavior, while the opposite association may apply to cognitive impulsiveness. Both types of impulsivity are associated with attention-deficit/hyperactivity disorder (ADHD), and genes of functional significance for the 5-HT system are implicated in this disorder. Here we demonstrate the separation of aggressive and cognitive components of impulsivity from symptom ratings and test their association with 5-HT and functionally related genes using a family-based association test (FBAT-PC). METHODS: Our sample consisted of 1180 o…

2805 Cognitive Neurosciencemedicine.medical_specialtyNeurologyGenetics and epigenetic pathways of disease [NCMLS 6]Cognitive NeuroscienceMedizin610 Medicine & healthNeuroinformatics [DCN 3]SerotonergicImpulsivityMental health [NCEBP 9]lcsh:RC346-429Genomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesBehavioral Neuroscience0302 clinical medicineCognitive neurosciences [UMCN 3.2]2802 Behavioral NeurosciencePerception and Action [DCN 1]medicineAttention deficit hyperactivity disorderddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und JugendaltersAssociation (psychology)Psychiatrylcsh:Neurology. Diseases of the nervous systemBiological PsychiatryAggressionResearchCognitionGeneral Medicine10058 Department of Child and Adolescent Psychiatrymedicine.disease030227 psychiatryAutism spectrum disordermedicine.symptomPsychologyFunctional Neurogenomics [DCN 2]2803 Biological Psychiatry030217 neurology & neurosurgeryClinical psychology
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CNGB3 mutations account for 50% of all cases with autosomal recessive achromatopsia

2005

Contains fulltext : 47591.pdf (Publisher’s version ) (Closed access) Achromatopsia is a congenital, autosomal recessively inherited disorder characterized by a lack of color discrimination, low visual acuity (<0.2), photophobia, and nystagmus. Mutations in the genes for CNGA3, CNGB3, and GNAT2 have been associated with this disorder. Here, we analyzed the spectrum and prevalence of CNGB3 gene mutations in a cohort of 341 independent patients with achromatopsia. In 163 patients, CNGB3 mutations could be identified. A total of 105 achromats carried apparent homozygous mutations, 44 were compound (double) heterozygotes, and 14 patients had only a single mutant allele. The derived CNGB3 mutatio…

AchromatopsiaGenetics and epigenetic pathways of disease [NCMLS 6]genetic structuresGATED CATION CHANNELCNGB3 mutationsNonsense mutationMutantCyclic Nucleotide-Gated Cation ChannelsColor Vision DefectsGenes RecessiveLocus (genetics)Gene mutationBiologyTOTAL COLOURBLINDNESSIon ChannelsCLONINGDogscyclic nucleotide-gated channelGNAT2GeneticsmedicineLOCUSAnimalsHumansMissense mutationNeurosensory disorders [UMCN 3.3]ACHM3 locusDog DiseasesAlleleAllelesGenetics (clinical)Geneticstotal colorblindnessGNAT2PHOTORECEPTORSDYSTROPHYmedicine.diseaseCONE DEGENERATIONGENEeye diseasesPhenotypeEvaluation of complex medical interventions [NCEBP 2]MutationRetinal Cone Photoreceptor Cellssense organsachromatopsiarod monochromacyALPHA-SUBUNIThuman activities
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Translocations Disrupting PHF21A in the Potocki-Shaffer-Syndrome Region Are Associated with Intellectual Disability and Craniofacial Anomalies

2012

Contains fulltext : 110038.pdf (Publisher’s version ) (Closed access) Potocki-Shaffer syndrome (PSS) is a contiguous gene disorder due to the interstitial deletion of band p11.2 of chromosome 11 and is characterized by multiple exostoses, parietal foramina, intellectual disability (ID), and craniofacial anomalies (CFAs). Despite the identification of individual genes responsible for multiple exostoses and parietal foramina in PSS, the identity of the gene(s) associated with the ID and CFA phenotypes has remained elusive. Through characterization of independent subjects with balanced translocations and supportive comparative deletion mapping of PSS subjects, we have uncovered evidence that t…

AdultMaleAdolescentGenotypePotocki–Shaffer syndromeChromosome DisordersHaploinsufficiencyBiologyHistone DeacetylasesSodium ChannelsTranslocation GeneticArticleChromatin remodelingCraniofacial Abnormalities03 medical and health sciencesSCN3A0302 clinical medicineIntellectual DisabilityNAV1.3 Voltage-Gated Sodium ChannelmedicineTranscriptional regulationGeneticsAnimalsHumansDeletion mappingGenetics(clinical)CraniofacialZebrafishGenetics (clinical)030304 developmental biologyGenetics0303 health sciencesChromosomes Human Pair 11Infant Newbornmedicine.diseaseGenetics and epigenetic pathways of disease DCN MP - Plasticity and memory [NCMLS 6]Child PreschoolHomeoboxFemaleChromosome DeletionHaploinsufficiencyExostoses Multiple Hereditary030217 neurology & neurosurgeryThe American Journal of Human Genetics
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Mutations in the gene encoding the basal body protein RPGRIP1L, a nephrocystin-4 interactor, cause Joubert syndrome.

2007

Peters, T.A./0000-0001-8443-5500; van Beersum, Sylvia E.C./0000-0002-4552-2908; Cremers, Frans/0000-0002-4954-5592; Roepman, Ronald/0000-0002-5178-8163 WOS: 000247619800019 PubMed: 17558407 Protein- protein interaction analyses have uncovered a ciliary and basal body protein network that, when disrupted, can result in nephronophthisis ( NPHP), Leber congenital amaurosis, Senior- Loken syndrome ( SLSN) or Joubert syndrome ( JBTS)(1-6). However, details of the molecular mechanisms underlying these disorders remain poorly understood. RPGRIP1- like protein ( RPGRIP1L) is a homolog of RPGRIP1 ( RPGR-interacting protein 1), a ciliary protein defective in Leber congenital amaurosis(7,8). We show t…

AdultMaleHealth aging / healthy living [IGMD 5]Eye DiseasesGenetics and epigenetic pathways of disease [NCMLS 6]TMEM67Molecular Sequence DataMembrane transport and intracellular motility [NCMLS 5]Biologymedicine.disease_causeJoubert syndromeCell LineGenomic disorders and inherited multi-system disorders [IGMD 3]NephronophthisisCerebellar DiseasesGeneticsmedicinePerception and Action [DCN 1]Basal bodyAnimalsHumansNeurosensory disorders [UMCN 3.3]CiliaAdaptor Proteins Signal TransducingRenal disorder [IGMD 9]GeneticsMutationCiliumCiliary transition zoneProteinsSyndromemedicine.diseasePedigreeRatsCytoskeletal ProteinsGenetic defects of metabolism [UMCN 5.1]RPGRIP1LFemaleKidney DiseasesFunctional Neurogenomics [DCN 2]Ciliary Motility Disorders
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The analysis of 51 genes in DSM-IV combined type attention deficit hyperactivity disorder: association signals in DRD4, DAT1 and 16 other genes.

2006

Contains fulltext : 35205.pdf (Publisher’s version ) (Closed access) Attention deficit hyperactivity disorder (ADHD) is a common neurodevelopmental disorder, starting in early childhood and persisting into adulthood in the majority of cases. Family and twin studies have demonstrated the importance of genetic factors and candidate gene association studies have identified several loci that exert small but significant effects on ADHD. To provide further clarification of reported associations and identify novel associated genes, we examined 1,038 single-nucleotide polymorphisms (SNPs) spanning 51 candidate genes involved in the regulation of neurotransmitter pathways, particularly dopamine, nor…

Candidate geneGenetics and epigenetic pathways of disease [NCMLS 6]MedizinReceptors NicotinicTryptophan HydroxylaseNeuroinformatics [DCN 3]0302 clinical medicinePerception and Action [DCN 1]Determinants in Health and Disease [EBP 1]ChildOncogene ProteinsGenetics0303 health sciencesbiologyDNA POOLING ANALYSISPedigree3. Good healthserotoninPsychiatry and Mental healthConduct disorderChild Preschool/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingMonoamine oxidase AdopaminePsychologyFunctional Neurogenomics [DCN 2]Genetic MarkersAdolescentSynaptosomal-Associated Protein 25Single-nucleotide polymorphismassociation studyPolymorphism Single NucleotideMental health [NCEBP 9]Genetic determinismGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesCellular and Molecular NeuroscienceMONOAMINE-OXIDASE-ACognitive neurosciences [UMCN 3.2]SDG 3 - Good Health and Well-beingmental disordersmedicineHumansAttention deficit hyperactivity disorderADHDGenetic Predisposition to Disease5-HT1B RECEPTOR GENEddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und JugendaltersMonoamine OxidaseMolecular Biology030304 developmental biologyGenetic associationDopamine Plasma Membrane Transport ProteinsSEROTONIN TRANSPORTER GENEDOPAMINE-BETA-HYDROXYLASESiblingsReceptors Dopamine D4candidate genemedicine.diseaseTwin studyPREFERENTIAL TRANSMISSIONHaplotypesCATECHOL-O-METHYLTRANSFERASEAttention Deficit Disorder with HyperactivityCONDUCT DISORDERbiology.proteinnoradrenalineDEFICIT/HYPERACTIVITY DISORDERNO EVIDENCE030217 neurology & neurosurgerylinkage disequilibriumMolecular Psychiatry
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Genome-wide association scan of attention deficit hyperactivity disorder

2008

Contains fulltext : 70191.pdf (Publisher’s version ) (Closed access) Results of behavioral genetic and molecular genetic studies have converged to suggest that genes substantially contribute to the development of attention deficit/hyperactivity disorder (ADHD), a common disorder with an onset in childhood. Yet, despite numerous linkage and candidate gene studies, strongly consistent and replicable association has eluded detection. To search for ADHD susceptibility genes, we genotyped approximately 600,000 SNPs in 958 ADHD affected family trios. After cleaning the data, we analyzed 438,784 SNPs in 2,803 individuals comprising 909 complete trios using ADHD diagnosis as phenotype. We present t…

Candidate geneLinkage disequilibriumGenetics and epigenetic pathways of disease [NCMLS 6]Medizin2804 Cellular and Molecular NeuroscienceGenome-wide association studyNeuroinformatics [DCN 3]Linkage Disequilibrium2738 Psychiatry and Mental Health0302 clinical medicinePerception and Action [DCN 1]Genetics(clinical)ChildGenetics (clinical)Genetics0303 health sciencesHomozygote10058 Department of Child and Adolescent PsychiatrySNP genotypingPsychiatry and Mental healthChild PreschoolData Interpretation Statistical/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingFunctional Neurogenomics [DCN 2]Algorithms2716 Genetics (clinical)AdolescentSingle-nucleotide polymorphism610 Medicine & healthBiologyMental health [NCEBP 9]Polymorphism Single NucleotideGenetic determinismArticleGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesCellular and Molecular NeuroscienceCognitive neurosciences [UMCN 3.2]SDG 3 - Good Health and Well-beingmedicineSNPAttention deficit hyperactivity disorderHumansddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und JugendaltersAlleles030304 developmental biologyGenome Humanmedicine.diseaseGenetic defects of metabolism [UMCN 5.1]Attention Deficit Disorder with HyperactivityCase-Control Studies030217 neurology & neurosurgeryGenome-Wide Association Study
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Usher syndrome and Leber congenital amaurosis are molecularly linked via a novel isoform of the centrosomal ninein-like protein.

2009

Contains fulltext : 80984.pdf (Publisher’s version ) (Closed access) Usher syndrome (USH) and Leber congenital amaurosis (LCA) are autosomal recessive disorders resulting in syndromic and non-syndromic forms of blindness. In order to gain insight into the pathogenic mechanisms underlying retinal degeneration, we searched for interacting proteins of USH2A isoform B (USH2A(isoB)) and the LCA5-encoded protein lebercilin. We identified a novel isoform of the centrosomal ninein-like protein, hereby named Nlp isoform B (Nlp(isoB)), as a common interactor. Although we identified the capacity of this protein to bind calcium with one of its three EF-hand domains, the interacton with USH2A(isoB) did …

Gene isoformRetinal degenerationCandidate geneGenetics and epigenetic pathways of disease [NCMLS 6]Usher syndromeMolecular Sequence DataOptic Atrophy Hereditary LeberBiologyIn Vitro TechniquesNeuroinformatics [DCN 3]CiliopathiesRetinaCell LineMiceCiliogenesisTwo-Hybrid System TechniquesGeneticsmedicineotorhinolaryngologic diseasesAnimalsHumansProtein IsoformsPhotoreceptor CellsAmino Acid SequenceNuclear proteinRats WistarEye ProteinsMolecular BiologyGenetics (clinical)GeneticsExtracellular Matrix ProteinsCiliumNuclear ProteinsGeneral MedicineArticlesmedicine.diseaseRatsMice Inbred C57BLMicrotubule-Associated ProteinsSequence AlignmentUsher SyndromesFunctional Neurogenomics [DCN 2]Protein BindingHuman Molecular Genetics
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Conduct disorder and ADHD: evaluation of conduct problems as a categorical and quantitative trait in the international multicentre ADHD genetics stud…

2008

Contains fulltext : 71374.pdf (Publisher’s version ) (Closed access) Attention-deficit/hyperactivity disorder (ADHD) is typically characterized by inattention, excessive motor activity, impulsivity, and distractibility. Individuals with ADHD have significant impairment in family and peer relations, academic functioning, and show high co-morbidity with a wide range of psychiatric disorders including oppositional defiant disorder (ODD), conduct disorder (CD), anxiety disorder, depression, substance abuse, and pervasive developmental disorder (PDD). Family studies suggest that ADHD + CD represents a specific subtype of the ADHD disorder with familial risk factors only partly overlapping with t…

Genetics and epigenetic pathways of disease [NCMLS 6]2804 Cellular and Molecular NeuroscienceMedizinPoison controlComorbidityNeuroinformatics [DCN 3]Linkage DisequilibriumCohort Studies2738 Psychiatry and Mental Health0302 clinical medicinePerception and Action [DCN 1]Genetics(clinical)ChildGenetics (clinical)Oligonucleotide Array Sequence Analysis0303 health sciencesAntisocial Personality Disorder10058 Department of Child and Adolescent Psychiatry3. Good healthPedigreeEuropePsychiatry and Mental healthConduct disorderAttention Deficit and Disruptive Behavior DisordersADHD -- conduct disorder -- genome wide association study -- genetic association information networkmedicine.symptomPsychologyFunctional Neurogenomics [DCN 2]Anxiety disorderAlgorithmsClinical psychologyConduct DisorderGenetic Markers2716 Genetics (clinical)Quantitative Trait LociContext (language use)610 Medicine & healthChild Behavior DisordersImpulsivityPolymorphism Single NucleotideMental health [NCEBP 9]behavioral disciplines and activitiesGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesCellular and Molecular NeuroscienceCognitive neurosciences [UMCN 3.2]mental disordersmedicinePervasive developmental disorderHumansddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und Jugendalters030304 developmental biologyPsychiatric Status Rating ScalesGenome HumanAntisocial personality disordermedicine.diseaseComorbidityGenetic defects of metabolism [UMCN 5.1]Attention Deficit Disorder with Hyperactivity030217 neurology & neurosurgeryGenome-Wide Association Study
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Association of Whirlin with Cav1.3 (α1D) Channels in Photoreceptors, Defining a Novel Member of the Usher Protein Network

2010

Contains fulltext : 88383.pdf (Publisher’s version ) (Closed access) PURPOSE: Usher syndrome is the most common form of hereditary deaf-blindness. It is both clinically and genetically heterogeneous. The USH2D protein whirlin interacts via its PDZ domains with other Usher-associated proteins containing a C-terminal type I PDZ-binding motif. These proteins co-localize with whirlin at the region of the connecting cilium and at the synapse of photoreceptor cells. This study was undertaken to identify novel, Usher syndrome-associated, interacting partners of whirlin and thereby obtain more insights into the function of whirlin. METHODS: The database of ciliary proteins was searched for proteins…

Genetics and epigenetic pathways of disease [NCMLS 6]Calcium Channels L-TypeUsher syndromeProtein subunitImmunoelectron microscopyBlotting WesternPDZ domainRetinaCav1.3MiceTwo-Hybrid System TechniquesChlorocebus aethiopsmedicineAnimalsInner earRNA MessengerRats WistarDatabases ProteinMicroscopy ImmunoelectronPhotoreceptor Connecting CiliumIn Situ HybridizationRenal disorder [IGMD 9]RetinaVoltage-dependent calcium channelbiologyComputational BiologyMembrane Proteinsmedicine.diseaseeye diseasesRatsCell biologyMice Inbred C57BLmedicine.anatomical_structureCOS Cellsbiology.proteinsense organsFunctional Neurogenomics [DCN 2]Photoreceptor Cells VertebrateInvestigative Opthalmology &amp; Visual Science
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