Search results for "n 3"

showing 10 items of 304 documents

Caveolin 3, flotillin 1 and influenza virus hemagglutinin reside in distinct domains on the sarcolemma of skeletal myofibers.

2011

We examined the distribution of selected raft proteins on the sarcolemma of skeletal myofibers and the role of cholesterol environment in the distribution. Immunofluorescence staining showed that flotillin-1 and influenza hemagglutinin exhibited rafts that located in the domains deficient of the dystrophin glycoprotein complex, but the distribution patterns of the two proteins were different. Cholesterol depletion from the sarcolemma by means of methyl-β-cyclodextrin resulted in distorted caveolar morphology and redistribution of the caveolin 3 protein. Concomitantly, the water permeability of the sarcolemma increased significantly. However, cholesterol depletion did not reshuffle flotillin…

Flotillin-1SarcolemmaArticle SubjectCholesterolSimilar distributionRaftImmunofluorescence stainingBiologyBiochemistryVirusCell biologyCaveolin 3lcsh:Biochemistrychemistry.chemical_compoundchemistryBiochemistrylcsh:QD415-436lipids (amino acids peptides and proteins)Research ArticleBiochemistry research international
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RAB3GAP1 and RAB3GAP2 modulate basal and rapamycin-induced autophagy

2014

Macroautophagy is a degradative pathway that sequesters and transports cytosolic cargo in autophagosomes to lysosomes, and its deterioration affects intracellular proteostasis. Membrane dynamics accompanying autophagy are mostly elusive and depend on trafficking processes. RAB GTPase activating proteins (RABGAPs) are important factors for the coordination of cellular vesicle transport systems, and several TBC (TRE2-BUB2-CDC16) domain-containing RABGAPs are associated with autophagy. Employing C. elegans and human primary fibroblasts, we show that RAB3GAP1 and RAB3GAP2, which are components of the TBC domain-free RAB3GAP complex, influence protein aggregation and affect autophagy at basal an…

GTPase-activating proteinlipid dropletsrab3 GTP-Binding ProteinsATG16L1DMSO dimethyl sulfoxideFEZ20302 clinical medicineATG autophagy-relatedPhagosomesDAPI 4’ 6-diamidino-2-phenylindoleSQSTM1 sequestosome 1ATG16L1MAP1LC3 microtubule-associated protein 1 light chain 3GFP green fluorescent protein0303 health sciencesGABARAP GABA(A) receptor-associated proteinGTPase-Activating ProteinsCell biologyRAB3GAP1RAB3GAP2RABGAP RAB GTPase activating proteinATG3autophagyCALCOCO2 calcium binding and coiled-coil domain 2Basic Research PaperseV empty vectorATG8ATG5PBS phosphate-buffered salineBiologyPE phosphatidylethanolamineTBC domain TRE2-BUB2-CDC16 domainBAG3GEF guanine nucleotide exchange factor03 medical and health sciencesC. elegans Caenorhabditis elegansAnimalsHumansCaenorhabditis elegansMolecular Biology030304 developmental biologySirolimusDPH 1 6-diphenyl-1 3 5-hexatrieneproteostasisAutophagyBiological TransportCell BiologyFEZ1Bafi bafilomycin A1FEZ fasciculation and elongation protein zetaNBR1 neighbor of BRCA1 gene 1ProteostasissiRNA small interfering RNABSA bovine serum albuminRabLysosomes030217 neurology & neurosurgeryAutophagy
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Galectin-3 Impairment of MYCN-Dependent Apoptosis-Sensitive Phenotype Is Antagonized by Nutlin-3 in Neuroblastoma Cells

2012

MYCN amplification occurs in about 20-25% of human neuroblastomas and characterizes the majority of the high-risk cases, which display less than 50% prolonged survival rate despite intense multimodal treatment. Somehow paradoxically, MYCN also sensitizes neuroblastoma cells to apoptosis, understanding the molecular mechanisms of which might be relevant for the therapy of MYCN amplified neuroblastoma. We recently reported that the apoptosis-sensitive phenotype induced by MYCN is linked to stabilization of p53 and its proapoptotic kinase HIPK2. In MYCN primed neuroblastoma cells, further activation of both HIPK2 and p53 by Nutlin-3 leads to massive apoptosis in vitro and to tumor shrinkage an…

Galectin 3Cancer TreatmentGene Dosagelcsh:MedicineApoptosisProtein-Serine-Threonine KinaseBiochemistryPiperazineschemistry.chemical_compoundNeuroblastoma0302 clinical medicineMolecular Cell BiologyBasic Cancer ResearchSignaling in Cellular Processeslcsh:ScienceEnergy-Producing OrganellesApoptotic SignalingNuclear ProteinOncogene Proteins0303 health sciencesN-Myc Proto-Oncogene ProteinMultidisciplinaryCell DeathImidazolesOncogene ProteinNuclear ProteinsTransfectionNutlin3. Good healthGene Expression Regulation NeoplasticProtein TransportCell killingPhenotypeOncologyGalectin-3030220 oncology & carcinogenesisGene Knockdown TechniquesMedicineResearch ArticleSignal TransductionHumanBiologyBioenergeticsProtein Serine-Threonine KinasesN-Myc Proto-Oncogene ProteinModels Biological03 medical and health sciencesNeuroblastomaCell Line TumormedicineHumansBiologyImidazolePiperazineneoplasms030304 developmental biologylcsh:RGene AmplificationChemotherapy and Drug Treatmentmedicine.diseasechemistryCell cultureApoptosisPediatric OncologyCytoprotectionGene Knockdown TechniqueCancer researchlcsh:QTumor Suppressor Protein p53Carrier ProteinsCarrier ProteinDNA Damage
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Proliferation of gastrointestinal carcinoma cells by T lymphocyte factors interleukin-3 and granulocyte-macrophage colony-stimulating factor

1991

Hematopoietic growth factors have been well characterized by cDNA cloning in recent years. In order to determine the influence of rhGM-CSF and rhIL-3 on epithelial cells of the gastrointestinal tract, their influence on in vitro cultured gastric and pancreas cancer cells was determined. A more than two-fold enhancement of proliferation was observed by IL-3 and GM-CSF in Mz-Sto-1 gastric and 818-4 pancreas carcinoma cells, applying a sensitive microculture system which allows precise quantification. The highest growth rates were obtained adding 1-10 ng/ml of the growth factors, but even picogram amounts were effective. Expression of mRNA for GM-CSF and IL-3 remained undetectable in the cell …

Gastrointestinal tractT-LymphocytesImmunologyGranulocyte-Macrophage Colony-Stimulating FactorBiologyLymphocyte ActivationMolecular biologyIn vitroPancreatic NeoplasmsHaematopoiesisGranulocyte macrophage colony-stimulating factorStomach NeoplasmsCell cultureCancer cellTumor Cells CulturedmedicineHumansInterleukin-3ReceptorCell DivisionInterleukin 3medicine.drugImmunologic Research
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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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From interleukin-9 to T helper 9 cells

2012

Abstract Interleukin-9 (IL-9), cloned more than 20 years ago, was initially thought to be a Th2-specific cytokine. This assumption was initially confirmed by functional analyses showing that both IL-9 and Th2 cells play an important role in the pathogenesis of asthma, IgE class switch recombination, and resolution of parasitic infections. However, recently it was shown that IL-9-producing CD4(+) T cells represent the discrete T helper subset Th9 cells. Herein, we will review the cytokines and transcription factors known to promote the development of Th9 cells and their potential functional properties in relation to the biological activities of IL-9. In addition, we will discuss how Th9 cell…

General NeuroscienceZAP70T helper cellBiologyGeneral Biochemistry Genetics and Molecular BiologyInterleukin 21medicine.anatomical_structureHistory and Philosophy of ScienceImmunologymedicineCytotoxic T cellInterleukin 9IL-2 receptorAntigen-presenting cellInterleukin 3Annals of the New York Academy of Sciences
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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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Meta-analysis of genome-wide linkage scans of attention deficit hyperactivity disorder

2008

Contains fulltext : 69243.pdf (Publisher’s version ) (Closed access) Genetic contribution to the development of attention deficit hyperactivity disorder (ADHD) is well established. Seven independent genome-wide linkage scans have been performed to map loci that increase the risk for ADHD. Although significant linkage signals were identified in some of the studies, there has been limited replications between the various independent datasets. The current study gathered the results from all seven of the ADHD linkage scans and performed a Genome Scan Meta Analysis (GSMA) to identify the genomic region with most consistent linkage evidence across the studies. Genome-wide significant linkage (P(S…

Genetics and epigenetic pathways of disease [NCMLS 6]Genetic LinkageEuropean Continental Ancestry GroupMedizinGenome ScanBiologyNeuroinformatics [DCN 3]Mental health [NCEBP 9]Genetic determinismWhite PeopleArticleChromosomesGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineGene mappingCognitive neurosciences [UMCN 3.2]Genetic linkageGenetic predispositionmedicinePerception and Action [DCN 1]Attention deficit hyperactivity disorderHumansddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und JugendaltersGenetics (clinical)030304 developmental biologyProbabilityLinkage (software)Genetics0303 health sciencesGenomeGenome HumanPair 16Chromosome Mappingmedicine.diseasePsychiatry and Mental healthGenetic defects of metabolism [UMCN 5.1]Attention Deficit Disorder with HyperactivityMeta-analysisLod ScoreFunctional Neurogenomics [DCN 2]030217 neurology & neurosurgeryChromosomes Human Pair 16HumanAmerican Journal of Medical Genetics. Part B: Neuropsychiatric Genetics
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No association between two polymorphisms of the serotonin transporter gene and combined type attention deficit hyperactivity disorder.

2008

Contains fulltext : 71091.pdf (Publisher’s version ) (Closed access) Several independent studies have reported association between serotonin transporter gene (SLC6A4) polymorphisms and attention deficit hyperactivity disorder (ADHD). Five studies found evidence for association between the long-allele of a 44-bp insertion/deletion polymorphism (5-HTTLPR) and ADHD. Another two studies corroborated this finding while a further six studies did not find such an association. For a second polymorphism within the gene, a variable number tandem repeat (VNTR) within intron 2, one study demonstrated that the 12/12 genotype was significantly less frequent in ADHD cases compared to controls, while a sec…

Genetics and epigenetic pathways of disease [NCMLS 6]MedizinNeuroinformatics [DCN 3]0302 clinical medicinePolymorphism (computer science)GenotypePerception and Action [DCN 1]Childhealth care economics and organizationsSerotonin transporterGenetics (clinical)GeneticsSerotonin Plasma Membrane Transport Proteins0303 health sciencesDepression030305 genetics & heredityTransmission disequilibrium testhumanitiesVariable number tandem repeatPsychiatry and Mental healthChild Preschool/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingFunctional Neurogenomics [DCN 2]medicine.medical_specialtyAdolescenteducationBiologybehavioral disciplines and activitiesMental health [NCEBP 9]Genomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesCellular and Molecular NeuroscienceSDG 3 - Good Health and Well-beingCognitive neurosciences [UMCN 3.2]Internal medicinemental disordersmedicineAttention deficit hyperactivity disorderHumansGenetic Predisposition to Diseaseddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und JugendaltersAssociation (psychology)Gene030304 developmental biologyFamily HealthPolymorphism Geneticbusiness.industryMood Disordersmedicine.diseaseMoodEndocrinologyMood disordersGenetic defects of metabolism [UMCN 5.1]Attention Deficit Disorder with Hyperactivitybiology.proteinbusiness030217 neurology & neurosurgery
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Usher syndrome: molecular links of pathogenesis, proteins and pathways.

2006

Contains fulltext : 50437.pdf (Publisher’s version ) (Closed access) Usher syndrome is the most common form of deaf-blindness. The syndrome is both clinically and genetically heterogeneous, and to date, eight causative genes have been identified. The proteins encoded by these genes are part of a dynamic protein complex that is present in hair cells of the inner ear and in photoreceptor cells of the retina. The localization of the Usher proteins and the phenotype in animal models indicate that the Usher protein complex is essential in the morphogenesis of the stereocilia bundle in hair cells and in the calycal processes of photoreceptor cells. In addition, the Usher proteins are important in…

Genetics and epigenetic pathways of disease [NCMLS 6]Usher syndromeCell Cycle ProteinsNerve Tissue ProteinsBiologyRetinaAdherens junctionMiceHair Cells AuditoryCell polarityGeneticsmedicineotorhinolaryngologic diseasesNeurosensory disorders [UMCN 3.3]AnimalsHumansProtein IsoformsCell Cycle ProteinMolecular BiologyGenetics (clinical)Renal disorder [IGMD 9]Adaptor Proteins Signal TransducingStereociliumMembrane ProteinsSignal transducing adaptor proteinGeneral MedicineActin cytoskeletonmedicine.diseaseeye diseasesCell biologyCytoskeletal ProteinsGenetic defects of metabolism [UMCN 5.1]Ear InnerMultiprotein ComplexesCateninSynapsessense organsUsher SyndromesPhotoreceptor Cells Vertebrate
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