Search results for "Pathway"

showing 10 items of 1685 documents

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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Genomic portrait of a sporadic amyotrophic lateral sclerosis case in a large spinocerebellar ataxia type 1 family

2020

Background: Repeat expansions in the spinocerebellar ataxia type 1 (SCA1) gene ATXN1 increases the risk for amyotrophic lateral sclerosis (ALS), supporting a relationship between these disorders. We recently reported the co-existence, in a large SCA1 family, of a clinically definite ALS individual bearing an intermediate ATXN1 expansion and SCA1 patients with a full expansion, some of which manifested signs of lower motor neuron involvement. Methods: In this study, we employed a systems biology approach that integrated multiple genomic analyses of the ALS patient and some SCA1 family members. Results: Our analysis identified common and distinctive candidate genes/variants and related biolog…

Candidate geneSpinocerebellar Ataxia Type 1Medicine (miscellaneous)lcsh:MedicineNetworkBiologyArticle03 medical and health sciences0302 clinical medicinemulti-omics; networkC9orf72medicineCustomized aCGHAmyotrophic lateral sclerosisGene030304 developmental biologyTAF15Genetics0303 health sciencesMulti-omicslcsh:Rmedicine.diseaseAmyotrophic lateral sclerosisPhenotypeSCA1-MNNGSSpinocerebellar ataxiaSpinocerebellar ataxia030217 neurology & neurosurgeryPathway
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Cannabinoid receptor 1 modulates the autophagic flux independent of mTOR- and BECLIN1-complex

2013

Cannabinoid Receptor 1 (CB1) has been initially described as the receptor for Delta-9-Tetrahydrocannabinol in the central nervous system (CNS), mediating retrograde synaptic signaling of the endocannabinoid system. Beside its expression in various CNS regions, CB1 is ubiquituous in peripheral tissues, where it mediates, among other activities, the cell's energy homeostasis. We sought to examine the role of CB1 in the context of the evolutionarily conserved autophagic machinery, a main constituent of the regulation of the intracellular energy status. Manipulating CB1 by siRNA knockdown in mammalian cells caused an elevated autophagic flux, while the expression of autophagy-related genes rema…

Cannabinoid receptorMorpholinesGreen Fluorescent ProteinsDown-RegulationmTORC1NaphthalenesBiochemistryMiceCellular and Molecular NeurosciencePiperidinesReceptor Cannabinoid CB1RimonabantAutophagymedicineAnimalsHumansEnzyme InhibitorsCannabinoid Receptor AntagonistsCells CulturedPI3K/AKT/mTOR pathwayAdenine NucleotidesChemistryTOR Serine-Threonine KinasesAutophagyMembrane ProteinsCalcium Channel BlockersEmbryo MammalianEndocannabinoid systemBenzoxazinesCell biologyMice Inbred C57BLnervous systemAstrocytesPyrazolesBeclin-1lipids (amino acids peptides and proteins)MacrolidesSynaptic signalingRimonabantApoptosis Regulatory ProteinsFlux (metabolism)medicine.drugJournal of Neurochemistry
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Comparative biochemistry of CO2 fixation and the evolution of autotrophy

1999

Carbon dioxide fixation is a polyphyletic trait that has evolved in widely separated prokaryotic branches. The three principal CO2-assimilation pathways are (i) the reductive pentose-phosphate cycle, i. e. the Calvin-Benson cycle; (ii) the reductive citric acid (or Arnon) cycle; and (iii) the net synthesis of acetyl-CoA from CO/CO2, or Wood pathway. Sequence analysis and the comparative biochemistry of these routes suggest that all of them were shaped to a considerable extent by the evolutionary recruitment of enzymes. Molecular phylogenetic trees show that the Calvin-Benson cycle was a relatively late development in the (eu)bacterial branch, suggesting that some form(s) of carbon assimilat…

Carbon dioxide assimilationArnon cycleCalvin-Benson cycle; Arnon cycle; Wood pathway; Semi-enzymatic synthesis; Carbon dioxide assimilationCalvin-Benson cycle:CIENCIAS DE LA VIDA::Microbiología [UNESCO]Wood pathwaySemi-enzymatic synthesisUNESCO::CIENCIAS DE LA VIDA::Microbiología
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Phylostratic Shift of Whole-Genome Duplications in Normal Mammalian Tissues towards Unicellularity Is Driven by Developmental Bivalent Genes and Reve…

2020

Tumours were recently revealed to undergo a phylostratic and phenotypic shift to unicellularity. As well, aggressive tumours are characterized by an increased proportion of polyploid cells. In order to investigate a possible shared causation of these two features, we performed a comparative phylostratigraphic analysis of ploidy-related genes, obtained from transcriptomic data for polyploid and diploid human and mouse tissues using pairwise cross-species transcriptome comparison and principal component analysis. Our results indicate that polyploidy shifts the evolutionary age balance of the expressed genes from the late metazoan phylostrata towards the upregulation of unicellular and early m…

CarcinogenesisCircadian clockAntineoplastic AgentsBiologyGenomeArticleCatalysisBivalent (genetics)Epigenesis Geneticlcsh:ChemistryProto-Oncogene Proteins c-mycInorganic ChemistryTranscriptomeMicePolyploidGene DuplicationNeoplasmsProtein Interaction MappingAnimalsHumanscancerEpigeneticsPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologyGenepolyploidybivalent genesSpectroscopyGeneticsGenomePloidiesCircadian Rhythm Signaling Peptides and ProteinsOrganic Chemistryearly multicellularityviral-origin oncogenesOncogenesGeneral MedicineembryonalityPhenotypeNeoplasm ProteinsunicellularityComputer Science ApplicationsGene Expression Regulation Neoplasticlcsh:Biology (General)lcsh:QD1-999Drug Resistance NeoplasmMetabolic Networks and PathwaysInternational Journal of Molecular Sciences
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Aspidin PB, a phloroglucinol derivative, induces apoptosis in human hepatocarcinoma HepG2 cells by modulating PI3K/Akt/GSK3β pathway.

2012

Aspidin PB, a phloroglucinol derivative isolated from Dryopteris fragrans (L.) Schott, has been previously reported to exert high biological activities. In the present study, we analyzed the apoptotic mechanisms of aspidin PB on human hepatoma cell line, HepG2. Initially, aspidin PB was shown to inhibit the growth of HepG2 cells in a time and dose-dependent manner. After treatment with aspidin PB for 72 h, 48 h and 24 h using MTT assay, the IC(50) values were 10.59 μM, 20.86 μM and 46.59 μM, respectively. Aspidin PB was capable to induce apoptosis, as measured by mitochondrial membrane potential (ΔΨm), acridine orange (AO) staining and propidium iodide (PI)/annexin V-FITC double staining. T…

Carcinoma HepatocellularApoptosisBiologyPhloroglucinolToxicologyWortmanninchemistry.chemical_compoundGlycogen Synthase Kinase 3Phosphatidylinositol 3-KinasesAnnexinHumansMTT assayPropidium iodideProtein kinase BProtein Kinase InhibitorsPI3K/AKT/mTOR pathwayCell ProliferationPhosphoinositide-3 Kinase InhibitorsMembrane Potential MitochondrialGlycogen Synthase Kinase 3 betaMicroscopy ConfocalAcridine orangeLiver NeoplasmsGeneral MedicineHep G2 CellsFlow CytometryMolecular biologyAndrostadieneschemistryApoptosisWortmanninProto-Oncogene Proteins c-aktSignal TransductionChemico-biological interactions
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Expression of WISPs and of their novel alternative variants in human hepatocellular carcinoma cells

2005

WISPs (Wnt-induced secreted proteins) are members of the CCN (CTGF/Cyr61/Nov) family involved in fibrotic disorders and tumorigenesis. They have a typical structure composed of four conserved cysteine-rich modular domains, but variants of CCN members lacking one or more modules, generated by alternative splicing or gene mutations, have been described in various pathological conditions. WISP genes were first described as downstream targets of the Wnt signaling pathway, which is frequently altered in human hepatocellular carcinoma (HCC). In the present study, WISP mRNA expression was analyzed by RT-PCR in four human HCC cell lines (HepG2, HuH-6, HuH-7, HA22T/VGH). Our results show for the fir…

Carcinoma HepatocellularWISPHepatocellular carcinomaApoptosisGene mutationBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyCCN Intercellular Signaling ProteinsWntalternative splicingHistory and Philosophy of ScienceCell Line TumorProto-Oncogene ProteinsCCN Intercellular Signaling ProteinsmedicineHumansRNA MessengerGeneDNA PrimersOncogene ProteinsGeneticsCCNModels GeneticReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceLiver NeoplasmsAlternative splicingIntracellular Signaling Peptides and ProteinsWnt signaling pathwaydigestive system diseasesNeoplasm ProteinsInsulin-Like Growth Factor Binding ProteinsRepressor ProteinsCTGFCYR61Cancer researchIntercellular Signaling Peptides and ProteinsRNACarcinogenesisWISPWntTranscription Factors
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Segmental dyskinesia in Wolff–Parkinson–White syndrome: A possible cause of dilatative cardiomyopathy

2006

Wolff-Parkinson-White (WPW) is a syndrome characterized by the presence of an accessory pathway that skipping A-V node may lead the electrical stimulus from the atrium directly to the ventricle. Some studies reported the finding of myocardial dyskinesia in the segments precociously activated by the accessory pathway, at echocardiogram and at nuclear cardiac study. Soria et al. reported, in 1985, an increased incidence of dilative cardiomyopathy in patients with WPW. The pathophysiological pathway that leads to ventricular dilation may be due to the increase of end-diastolic pressure secondary to a tachycardia-induced cardiomyopathy. Tachycardia-induced cardiomyopathy is usually secondary to…

Cardiomyopathy DilatedTachycardiamedicine.medical_specialtyCardiomyopathyHemodynamicsAccessory pathwayAneurysmInternal medicinemedicineHumanscardiovascular diseasesChildbusiness.industryInfantArrhythmias Cardiacmedicine.diseasePathophysiologymedicine.anatomical_structureDyskinesiaVentriclecardiovascular systemCardiologyWolff-Parkinson-White Syndromemedicine.symptomCardiology and Cardiovascular MedicinebusinessFollow-Up StudiesInternational Journal of Cardiology
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Nitroglycerin-induced cardioprotection is endothelial nitric oxide synthase- dependent

2015

Purpose We sought to evaluate the contribution of the endogenous NO pathway to the cardioprotective action of nitroglycerin (NTG). Methods and Results Anesthetized rabbits were subjected to 30-min myocardial ischemia (isc) and 3-h reperfusion (rep) and randomized into: Control group (no further intervention); PostC group (application of 8 cycles 30-sec isc/rep) and NTG treated group (2 μg/kg-1/min-1 IV bolus) for 65 min starting 10 min prior to rep. In additional groups, pharmacological inhibitors of NOS, nNOS, iNOS, PI3K, adenosine receptors and PKG were administrated with or without NTG. The infarcted (I) to risk (R) ratio was estimated. In a second experimental series tissue samples were…

Cardioprotectiongenetic structuresbiologybusiness.industryNitrotyrosineEndogenyPharmacologybiology.organism_classificationBiochemistryAdenosine receptoreye diseaseschemistry.chemical_compoundBolus (medicine)chemistryEnosPhysiology (medical)AnesthesiaMedicinebusinessProtein kinase BPI3K/AKT/mTOR pathwayFree Radical Biology and Medicine
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