Search results for "610"

showing 10 items of 1353 documents

Genetic heterogeneity in ADHD: DAT1 gene only affects probands without CD

2008

Contains fulltext : 70183.pdf (Publisher’s version ) (Closed access) Previous studies have found heterogeneous association between DAT1-3'-UTR-VNTR and attention deficit hyperactivity disorder (ADHD). Various proportions of conduct disorder (CD) comorbidity in their ADHD samples may partially explain the observational discrepancies. Evidence for this comes from family and twin studies which found ADHD probands with CD (ADHD + CD) are genetically different from those without CD (ADHD - CD). Genotypes of 20 DAT1 markers were analyzed in 576 trios, consisting of 141 ADHD + CD and 435 ADHD - CD. In addition to the classical TDT test, a specific genetic heterogeneity test was performed to identi…

ProbandMaleLinkage disequilibriumGenetics and epigenetic pathways of disease [NCMLS 6]2804 Cellular and Molecular NeuroscienceMedizinComorbidityNeuroinformatics [DCN 3]Linkage Disequilibrium2738 Psychiatry and Mental Health0302 clinical medicineGene FrequencyPerception and Action [DCN 1]Genetics(clinical)ChildGenetics (clinical)GeneticsIncidence10058 Department of Child and Adolescent PsychiatryEuropePsychiatry and Mental healthConduct disorder/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingFemaleFunctional Neurogenomics [DCN 2]Conduct DisorderGenetic Markers2716 Genetics (clinical)GenotypeSingle-nucleotide polymorphism610 Medicine & healthBiologyMental health [NCEBP 9]Polymorphism Single Nucleotidebehavioral disciplines and activitiesGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesGenetic HeterogeneityCellular and Molecular NeuroscienceCognitive neurosciences [UMCN 3.2]SDG 3 - Good Health and Well-beingmental disordersmedicineAttention deficit hyperactivity disorderHumansddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und JugendaltersAlleleAllelesDopamine Plasma Membrane Transport ProteinsChi-Square DistributionGenetic heterogeneitymedicine.diseaseTwin study030227 psychiatryGenetic defects of metabolism [UMCN 5.1]HaplotypesAttention Deficit Disorder with Hyperactivity030217 neurology & neurosurgery
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Separation of Cognitive Impairments in Attention-Deficit/Hyperactivity Disorder Into 2 Familial Factors

2010

Contains fulltext : 89304.pdf (Publisher’s version ) (Open Access) CONTEXT: Attention-deficit/hyperactivity disorder (ADHD) is associated with widespread cognitive impairments, but it is not known whether the apparent multiple impairments share etiological roots or separate etiological pathways exist. A better understanding of the etiological pathways is important for the development of targeted interventions and for identification of suitable intermediate phenotypes for molecular genetic investigations. OBJECTIVES: To determine, by using a multivariate familial factor analysis approach, whether 1 or more familial factors underlie the slow and variable reaction times, impaired response inhi…

ProbandMaleMedizinComorbidityNeuropsychological TestsChoice BehaviorDevelopmental psychology2738 Psychiatry and Mental HealthMOLECULAR-GENETICS0302 clinical medicinePerception and Action [DCN 1]GENETIC INFLUENCES10. No inequalityChildMental Health [NCEBP 9]Cognitive disorderCognition10058 Department of Child and Adolescent PsychiatryPedigreePsychiatry and Mental healthPhenotype1201 Arts and Humanities (miscellaneous)Femalemedicine.symptomPsychologyFunctional Neurogenomics [DCN 2]AdolescentDEFICIT HYPERACTIVITY DISORDERContext (language use)610 Medicine & healthImpulsivityArticleREACTION-TIME PERFORMANCE03 medical and health sciencesArts and Humanities (miscellaneous)medicineReaction TimeAttention deficit hyperactivity disorderHumansINTRA-SUBJECT VARIABILITYFamilyINHIBITORY CONTROLGENOME-WIDE ASSOCIATIONDELAY AVERSIONSiblingsSocial environmentmedicine.diseaseComorbidity030227 psychiatryAttention Deficit Disorder with HyperactivityImpulsive BehaviorRESPONSE VARIABILITYSUSTAINED ATTENTIONCognition DisordersFactor Analysis Statistical030217 neurology & neurosurgery
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The impact of study design and diagnostic approach in a large multi-centre ADHD study: Part 2: Dimensional measures of psychopathology and intelligen…

2011

Contains fulltext : 97437.pdf (Publisher’s version ) (Open Access) BACKGROUND: The International Multi-centre ADHD Genetics (IMAGE) project with 11 participating centres from 7 European countries and Israel has collected a large behavioural and genetic database for present and future research. Behavioural data were collected from 1068 probands with ADHD and 1446 unselected siblings. The aim was to describe and analyse questionnaire data and IQ measures from all probands and siblings. In particular, to investigate the influence of age, gender, family status (proband vs. sibling), informant, and centres on sample homogeneity in psychopathological measures. METHODS: Conners' Questionnaires, St…

ProbandResearch designMale110 012 Social cognition of verbal communicationIntelligencePerception and Actions Mental Health [DCN 1]MedizinSocial Sciencescentre effectsDevelopmental psychology2738 Psychiatry and Mental Health0302 clinical medicinelcsh:PsychiatryMulticenter Studies as Topicsibling designChildATTENTION-DEFICIT/HYPERACTIVITY DISORDERMental DisordersWechsler ScalesWechsler Adult Intelligence Scale10058 Department of Child and Adolescent PsychiatryDiagnostic and Statistical Manual of Mental DisordersPsychiatry and Mental healthPhenotypeConduct disorderResearch DesignRELIABILITYFemaleFamily RelationsPsychologyClinical psychologyPsychopathologyResearch ArticleAdultlcsh:RC435-571DEFICIT HYPERACTIVITY DISORDERTWIN610610 Medicine & health150 000 MR Techniques in Brain Function03 medical and health sciencesmulti-centre studyADHD multi-centre studymedicineCriterion validityAttention deficit hyperactivity disorderHumansADHDGenetic Predisposition to Diseaseddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und JugendaltersSiblingMETAANALYSISFamily HealthPsychiatric Status Rating ScalesCHILD PSYCHIATRIC-PATIENTSSiblingsPARENTmedicine.disease030227 psychiatryAttention Deficit Disorder with HyperactivityCONDUCT DISORDERCRITERION VALIDITY030217 neurology & neurosurgery
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Cell fate regulation upon DNA damage : p53 Serine 46 kinases pave the cell death road

2019

Mild and massive DNA damage are differentially integrated into the cellular signaling networks and, in consequence, provoke different cell fate decisions. After mild damage, the tumor suppressor p53 directs the cellular response to cell cycle arrest, DNA repair, and cell survival, whereas upon severe damage, p53 drives the cell death response. One posttranslational modification of p53, phosphorylation at Serine 46, selectively occurs after severe DNA damage and is envisioned as a marker of the cell death response. However, the molecular mechanism of action of the p53 Ser46 phospho-isomer, the molecular timing of this phosphorylation event, and its activating effects on apoptosis and ferropt…

Programmed cell deathCell signalingCell cycle checkpointDNA RepairDNA repairDNA damage610 MedizinApoptosisCell fate determinationBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciences0302 clinical medicine610 Medical sciencesAnimalsHumansPhosphorylation030304 developmental biology0303 health sciencesKinaseCell Cycle CheckpointsCell biologyPhosphorylationTumor Suppressor Protein p53030217 neurology & neurosurgeryDNA Damage
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Knockout of myeloid cell leukemia-1 induces liver damage and increases apoptosis susceptibility of murine hepatocytes

2008

Apoptosis, or programmed cell death, regulates tissue development and homeostasis in multi-cellular organisms. Extrinsic or intrinsic death signals activate pro-apoptotic pathways, resulting in the activation of caspases and finally in cell death. An important event during apoptosis process is the permeabilization of the outer mitochondrial membrane (OMM). Integrity of the OMM is regulated by the Bcl-2 protein family, which is divided into three groups: anti-apoptotic members Bcl-2, Bcl-xL and myeloid cell leukemia-1 (Mcl-1), pro-apoptotic multidomain members Bax and Bak, and pro-apoptotic BH3-only proteins. Mitochondrial activation is regulated by selective interactions of Bcl-2 proteins v…

Programmed cell deathGenotypeCellular differentiation610 Medicine & healthApoptosisBiologyPolymerase Chain ReactionArticleMiceimmune system diseases10049 Institute of Pathology and Molecular Pathologyhemic and lymphatic diseasesmedicineAnimalsAspartate AminotransferasesneoplasmsDNA PrimersHepatologyCaspase 3Alanine TransaminaseCell DifferentiationDNAFas receptorCell biologyMyeloid Cell Leukemia Sequence 1 ProteinHaematopoiesisGene Expression RegulationLiverProto-Oncogene Proteins c-bcl-2ApoptosisHepatocytesMyeloid Cell Leukemia Sequence 1 ProteinRNA2721 HepatologyHepatocyte growth factorStem cellmedicine.drugHepatology
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Hepatocyte-specific deletion of the antiapoptotic protein myeloid cell leukemia-1 triggers proliferation and hepatocarcinogenesis in mice

2010

Regulation of hepatocellular apoptosis is crucial for liver homeostasis. Increased sensitivity of hepatocytes toward apoptosis results in chronic liver injury, whereas apoptosis resistance is linked to hepatocarcinogenesis and nonresponsiveness to therapy-induced cell death. Recently, we have demonstrated an essential role of the antiapoptotic Bcl-2 family member Myeloid cell leukemia-1 (Mcl-1) in hepatocyte survival. In mice lacking Mcl-1 specifically in hepatocytes (Mcl-1Δhep), spontaneous apoptosis caused severe liver damage. Here, we demonstrate that chronically increased apoptosis of hepatocytes coincides with strong hepatocyte proliferation resulting in hepatocellular carcinoma (HCC).…

Programmed cell deathPathologymedicine.medical_specialty10208 Institute of NeuropathologyApoptosis610 Medicine & health10071 Functional Genomics Center ZurichBiologyArticleMiceLiver Neoplasms Experimental10049 Institute of Pathology and Molecular PathologySurvivinmedicineAnimalsneoplasmsCell ProliferationChromosome AberrationsMice KnockoutHepatologyCell growthLiver cellmedicine.diseaseMyeloid Cell Leukemia Sequence 1 ProteinLeukemiamedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2ApoptosisHepatocyteHepatocytesCancer researchMyeloid Cell Leukemia Sequence 1 Protein570 Life sciences; biology2721 HepatologyU7 Systems Biology / Functional GenomicsHepatology
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Pathogens and host immunity in the ancient human oral cavity.

2014

Calcified dental plaque (dental calculus) preserves for millennia and entraps biomolecules from all domains of life and viruses. We report the first high-resolution taxonomic and protein functional characterization of the ancient oral microbiome and demonstrate that the oral cavity has long served as a reservoir for bacteria implicated in both local and systemic disease. We characterize: (i) the ancient oral microbiome in a diseased state, (ii) 40 opportunistic pathogens, (iii) the first evidence of ancient human-associated putative antibiotic resistance genes, (iv) a genome reconstruction of the periodontal pathogen Tannerella forsythia, (v) 239 bacterial and 43 human proteins, allowing co…

ProteomeMolecular Sequence Data610 Medicine & health10071 Functional Genomics Center ZurichDental plaqueArticlePrehistòriaBacterial geneticsPeriodontal pathogenMicrobiology1311 GeneticsTandem Mass SpectrometryGermanyRNA Ribosomal 16SGeneticsmedicineTannerella forsythiaHumansDental CalculusMicrobiomePathogenPhylogenyMouthbiologyBase SequenceEcologyBacteroidetesMicrobiotaSequence Analysis DNAbiology.organism_classificationmedicine.diseaseRed complexHistory Medieval10182 Institute of Oral Biologystomatognathic diseasesArchaeology10076 Center for Integrative Human Physiology11294 Institute of Evolutionary Medicine570 Life sciences; biologyOral MicrobiomeFood AnalysisGenome BacterialNature genetics
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Proteomic analysis of tyrosine phosphorylation induced by exogenous expression of oncogenic kinase fusions identified in lung adenocarcinoma.

2021

Kinase fusions are considered oncogenic drivers in numerous types of cancer. In lung adenocarcinoma 5-10% of patients harbor kinase fusions. The most frequently detected kinase fusion involves the Anaplastic Lymphoma Kinase (ALK) and Echinoderm Microtubule-associated protein-Like 4 (EML4). In addition, oncogenic kinase fusions involving the tyrosine kinases RET and ROS1 are found in smaller subsets of patients. In this study, we employed quantitative mass spectrometry-based phosphoproteomics to define the cellular tyrosine phosphorylation patterns induced by different oncogenic kinase fusions identified in patients with lung adenocarcinoma. We show that exogenous expression of the kinase fu…

ProteomicsLung NeoplasmsOncogene Proteins FusionAdenocarcinoma of LungBiologyBiochemistry03 medical and health scienceschemistry.chemical_compoundProto-Oncogene ProteinsmedicineROS1Anaplastic lymphoma kinaseHumansddc:610PhosphorylationLung cancerMolecular Biology030304 developmental biology0303 health sciencesKinase030302 biochemistry & molecular biologyProto-Oncogene Proteins c-retPhosphoproteomicsTyrosine phosphorylationProtein-Tyrosine Kinasesmedicine.diseasechemistryCancer researchPhosphorylationTyrosineTyrosine kinaseProteomicsREFERENCES
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Reproducible and Consistent Quantification of the Saccharomyces cerevisiae Proteome by SWATH-mass spectrometry *

2015

Targeted mass spectrometry by selected reaction monitoring (S/MRM) has proven to be a suitable technique for the consistent and reproducible quantification of proteins across multiple biological samples and a wide dynamic range. This performance profile is an important prerequisite for systems biology and biomedical research. However, the method is limited to the measurements of a few hundred peptides per LC-MS analysis. Recently, we introduced SWATH-MS, a combination of data independent acquisition and targeted data analysis that vastly extends the number of peptides/proteins quantified per sample, while maintaining the favorable performance profile of S/MRM. Here we applied the SWATH-MS t…

ProteomicsOsmosisSaccharomyces cerevisiae Proteins1303 BiochemistryOsmotic shockSaccharomyces cerevisiae610 Medicine & health10071 Functional Genomics Center ZurichSaccharomyces cerevisiaeOsmosisMass spectrometryBiochemistryMass SpectrometryAnalytical Chemistry1312 Molecular BiologyData-independent acquisitionMolecular Biology1602 Analytical ChemistryChromatographybiologySelected reaction monitoringTechnological Innovation and ResourcesReproducibility of Resultsbiology.organism_classificationTargeted mass spectrometryProteomeCarbohydrate Metabolism570 Life sciences; biologyPeptidesMolecular & Cellular Proteomics
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The substrate degradome of meprin metalloproteases reveals an unexpected proteolytic link between meprin β and ADAM10

2012

The in vivo roles of meprin metalloproteases in pathophysiological conditions remain elusive. Substrates define protease roles. Therefore, to identify natural substrates for human meprin α and β we employed TAILS (terminal amine isotopic labeling of substrates), a proteomics approach that enriches for N-terminal peptides of proteins and cleavage fragments. Of the 151 new extracellular substrates we identified, it was notable that ADAM10 (a disintegrin and metalloprotease domain-containing protein 10)—the constitutive α-secretase—is activated by meprin β through cleavage of the propeptide. To validate this cleavage event, we expressed recombinant proADAM10 and after preincubation with meprin…

Proteomicsalpha-2-HS-Glycoproteinmedicine.medical_treatmentADAM10ADAM10 ProteinMice0302 clinical medicine610 Medicine & healthMice KnockoutExtracellular Matrix Proteins0303 health sciencesMetalloproteinaseDegradomeMetalloendopeptidasesMeprinADAM10Terminal amine isotopic labeling of substratesADAM ProteinsElafinBiochemistryTAILSCytokinesMolecular MedicineElafinResearch Article610 Medicine & healthBiologyCell Line03 medical and health sciencesCellular and Molecular NeurosciencemedicineDisintegrinAnimalsHumansAmino Acid SequenceCystatin CMolecular Biology030304 developmental biologyPharmacologyProteaseMeprin; ADAM10; Metalloproteases; Proteomics; TAILS; DegradomeMembrane ProteinsCell BiologyADAM ProteinsHEK293 CellsMembrane proteinbiology.proteinMetalloproteases570 Life sciences; biologyAmyloid Precursor Protein SecretasesCaco-2 Cells030217 neurology & neurosurgery
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