Search results for "Ligases"

showing 10 items of 72 documents

Correlative gene expression pattern linking RNF123 to cellular stress–senescence genes in patients with depressive disorder: Implication of DRD1 in t…

2013

Abstract Background The expression level of the RNF1213 gene in blood cells has been identified as a disease risk marker, more than ten years before the diagnosis of depression ( Glahn et al., 2012 ). To explore the status of this gene in the acute depressive state we have quantified the expression of RNF123 in the blood leukocytes ( N =17), dorsolateral prefrontal and cingulate cortex ( N =24) of patients with diagnosed depression and of matched controls. We have measured the expression of the DRD1 gene as a “neuronal probe”. We have also quantified the mRNA of six genes previously identified as markers of the biopsychological stress associated with major depression: FOS, DUSP1, OGG1, STMN…

AdultCingulate cortexSenescencemedicine.medical_specialtyPsychosisUbiquitin-Protein LigasesPsychotic depressionYoung AdultDopamineInternal medicineGene expressionLeukocytesmedicineHumansRNA MessengerDepression (differential diagnoses)Cerebral CortexDepressive Disorder MajorReceptors Dopamine D1Middle Agedmedicine.diseasePsychiatry and Mental healthClinical PsychologyEndocrinologymedicine.anatomical_structureCerebral cortexFemaleTranscriptomePsychologyNeuroscienceStress Psychologicalmedicine.drugJournal of Affective Disorders
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Immune escape of AKT overexpressing ovarian cancer cells

2012

Platinum-resistance is the most crucial problem for treatment of ovarian cancer. There is a clinical need for new treatment strategies which overcome platinum resistance. As survival is strongly influenced by immunological parameters, immunotherapeutic strategies appear promising. Therefore a better understanding of the interaction between ovarian tumour cells and cells of the immune system is a necessary prerequisite. In the present study we aimed to enlighten the interactions between platinum resistant and platinum sensitive ovarian cancer cells and natural-killer (NK)-cells. Modified FATAL assay was used for determining the killing efficiency of NK-cells for the parental A2780 cells and …

Cancer Researchendocrine system diseasesUbiquitin-Protein LigasesCellApoptosisBiologymedicine.disease_causeInhibitor of Apoptosis ProteinsImmune systemCell Line TumormedicineHumansPlatinumOvarian NeoplasmsCancerCell cyclemedicine.diseaseBaculoviral IAP Repeat-Containing 3 Proteinfemale genital diseases and pregnancy complicationsGene Expression Regulation NeoplasticKiller Cells Naturalmedicine.anatomical_structureOncologyDrug Resistance NeoplasmCell cultureApoptosisCancer researchFemaleOvarian cancerCarcinogenesisProto-Oncogene Proteins c-aktInternational Journal of Oncology
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Novel deletion of the E3A ubiquitin protein ligase gene detected by multiplex ligation-dependent probe amplification in a patient with Angelman syndr…

2010

Angelman syndrome (AS) is a severe neurobehavioural disorder caused by failure of expression of the maternal copy of the imprinted domain located on 15q11-q13. There are different mechanisms leading to AS: maternal microdeletion, uniparental disomy, defects in a putative imprinting centre, mutations of the E3 ubiquitin protein ligase (UBE3A) gene. However, some of suspected cases of AS are still scored negative to all the latter mutations. Recently, it has been shown that a proportion of negative cases bear large deletions overlapping one or more exons of the UBE3A gene. These deletions are difficult to detect by conventional gene-scanning methods due to the masking effect by the non-delete…

Malecongenital hereditary and neonatal diseases and abnormalitiesClinical Biochemistrygene dosageBiochemistryGene dosageExonSettore BIO/13 - Biologia ApplicataAngelman syndromemedicineUBE3AHumansMultiplexGenetic TestingMultiplex ligation-dependent probe amplificationChildMolecular BiologyGeneticsbiologyubiquitin-protein ligasesgenetic association studiemedicine.diseaseMolecular biologyUniparental disomyUbiquitin ligaseAngelman syndromebiology.proteinMolecular MedicineOriginal ArticleFemaleGene Deletion
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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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Association of CYP2R1 rs10766197 with MS risk and disease progression

2017

Background MS is a neurodegenerative autoimmune disease resulting from a complex interaction of genetic and environmental factors. Among these, vitamin D and genetic variants associated with vitamin D-metabolism gain great attention. The aim of our study was to assess five SNPs in NADSYN1 and CYP2R1 genes in relation to serum 25-OH-vitamin D3 levels in MS patients and controls. Methods 25-OH-vitamin D3 levels and genotyping of CYP2R1- and NADSYN1-SNPs were investigated both in MS patients and in healthy controls. Results The analysis revealed lower 25-OH-vitamin D3 concentrations in MS patients than in controls and an association of rs10766197 CYP2R1 SNP with MS risk. After stratifying MS p…

AdultMale0301 basic medicineOncologymedicine.medical_specialtyPathologyMultiple SclerosisGenotypeSingle-nucleotide polymorphismPolymorphism Single NucleotideSeverity of Illness IndexpolymorphismDisability Evaluation03 medical and health sciencesCellular and Molecular NeuroscienceSex Factors0302 clinical medicineInternal medicinegendermedicineVitamin D and neurologyHumansSNPGenetic Predisposition to DiseaseNADSYN1AlleleCytochrome P450 Family 2GenotypingRetrospective Studiesbusiness.industryMultiple sclerosisCase-control studyvitamin dMiddle Agedmedicine.diseaseMinor allele frequency030104 developmental biologyCase-Control Studiesmultiple sclerosiDisease ProgressionCYP2R1Cholestanetriol 26-MonooxygenaseFemaleCarbon-Nitrogen Ligases with Glutamine as Amide-N-Donorgeneticbusiness030217 neurology & neurosurgeryJournal of Neuroscience Research
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Proteome-Wide Characterization of the RNA-Binding Protein RALY-Interactome Using the in Vivo-Biotinylation-Pulldown-Quant (iBioPQ) Approach

2013

RALY is a member of the heterogeneous nuclear ribonucleoproteins, a family of RNA-binding proteins generally involved in many processes of mRNA metabolism. No quantitative proteomic analysis of RALY-containing ribonucleoparticles (RNPs) has been performed so far, and the biological role of RALY remains elusive. Here, we present a workflow for the characterization of RALY's interaction partners, termed iBioPQ, that involves in vivo biotinylation of biotin acceptor peptide (BAP)-fused protein in the presence of the prokaryotic biotin holoenzyme synthetase of BirA so that it can be purified using streptavidin-coated magnetic beads, circumventing the need for specific antibodies and providing e…

ProteomeRecombinant Fusion ProteinsMolecular Sequence DataBiotinRNA-binding proteinBiologyHeterogeneous ribonucleoprotein particleProteomicsPoly(A)-Binding Protein IBiochemistryInteractomeELAV-Like Protein 103 medical and health scienceschemistry.chemical_compound0302 clinical medicineNuclear Matrix-Associated ProteinsBiotinProtein Interaction MappingHumansCarbon-Nitrogen LigasesAmino Acid SequenceProtein Interaction MapsPeptide sequence030304 developmental biology0303 health sciencesEscherichia coli ProteinsHeterogeneous-Nuclear Ribonucleoprotein Group CRNA-Binding ProteinsGeneral ChemistryRepressor ProteinsHEK293 CellsELAV ProteinsGene Expression RegulationBiochemistrychemistryProtein Biosynthesis030220 oncology & carcinogenesisBiotinylationProteomeBiological AssayStreptavidinHeLa CellsProtein BindingJournal of Proteome Research
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NOSIP, a novel modulator of endothelial nitric oxide synthase activity.

2001

Production of nitric oxide (NO) in endothelial cells is regulated by direct interactions of endothelial nitric oxide synthase (eNOS) with effector proteins such as Ca2+-calmodulin, by posttranslational modifications such as phosphorylation via protein kinase B, and by translocation of the enzyme from the plasma membrane caveolae to intracellular compartments. Reversible acylation of eNOS is thought to contribute to the intracellular trafficking of the enzyme; however, protein factor(s) that govern the translocation of the enzyme are still unknown. Here we have used the yeast two-hybrid system and identified a novel 34 kDa protein, termed NOSIP (eNOS interacting protein), which avidly binds …

Ubiquitin-Protein LigasesMolecular Sequence DataCHO CellsCaveolaeBiochemistryNitric oxideSubstrate Specificitychemistry.chemical_compoundEnosCaveolaeCricetinaeTwo-Hybrid System TechniquesGeneticsAnimalsHumansAmino Acid SequenceRNA MessengerMolecular BiologyProtein kinase BCalcimycinBinding SitesbiologyAkt/PKB signaling pathwayGene Expression Profilingbiology.organism_classificationImmunohistochemistryPrecipitin TestsTransport proteinCell biologyNitric oxide synthaseProtein TransportchemistryBiochemistrybiology.proteinEndothelium VascularNitric Oxide SynthaseCarrier ProteinsSequence AlignmentIntracellularBiotechnologyProtein BindingFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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Translation of HTT mRNA with expanded CAG repeats is regulated by the MID1-PP2A protein complex.

2012

Expansion of CAG repeats is a common feature of various neurodegenerative disorders, including Huntington's disease. Here we show that expanded CAG repeats bind to a translation regulatory protein complex containing MID1, protein phosphatase 2A and 40S ribosomal S6 kinase. Binding of the MID1-protein phosphatase 2A protein complex increases with CAG repeat size and stimulates translation of the CAG repeat expansion containing messenger RNA in a MID1-, protein phosphatase 2A- and mammalian target of rapamycin-dependent manner. Our data indicate that pathological CAG repeat expansions upregulate protein translation leading to an overproduction of aberrant protein and suggest that the MID1-com…

metabolism [Microtubule Proteins]General Physics and AstronomyHTT protein humanRibosomal s6 kinaseMice0302 clinical medicinemetabolism [Transcription Factors]Protein Phosphatase 2Luciferasesgenetics [Nerve Tissue Proteins]genetics [Protein Biosynthesis]0303 health sciencesHuntingtin ProteinMultidisciplinarybiologyTOR Serine-Threonine KinasesNuclear ProteinsTranslation (biology)3. Good healthmetabolism [Luciferases]Microtubule Proteinsddc:500metabolism [Nuclear Proteins]genetics [Trinucleotide Repeat Expansion]Protein Bindingcongenital hereditary and neonatal diseases and abnormalitiesMTOR protein humanUbiquitin-Protein LigasesBlotting WesternNerve Tissue Proteinsmetabolism [TOR Serine-Threonine Kinases]metabolism [RNA Messenger]General Biochemistry Genetics and Molecular Biology03 medical and health sciencesgenetics [RNA Messenger]mental disordersHuntingtin ProteinAnimalsHumansEukaryotic Small Ribosomal SubunitRNA MessengerNucleotide Motifs030304 developmental biologyMessenger RNAmetabolism [Nerve Tissue Proteins]RNAmetabolism [Protein Phosphatase 2]General ChemistryProtein phosphatase 2Molecular biologynervous system diseasesProtein Biosynthesisbiology.proteinTrinucleotide repeat expansionTrinucleotide Repeat Expansion030217 neurology & neurosurgeryMid1 protein humanHeLa CellsTranscription FactorsNature communications
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Ligase Chain Reaction (LCR®) assay for semi-quantitative detection of HBV DNA in mononuclear leukocytes of patients with chronic hepatitis B

1996

Summary. A ligase chain reaction (LCR®)-based approach to detect hepatitis B virus (HBV) DNA in peripheral blood mononuclear cells (PBMC) is described. Using this new amplification technique, we determined semi-quantitatively the amount of a short HBV S-gene fragment in PBMC lysates of 25 patients with different forms of chronic hepatitis (group A (n= 8), hepatitis B s antigen (HBsAg)+/hepatitis B e antigen (HBeAg)+; group B (n= 9), HBsAg+/HBeAg-; group C (n= 8), HBsAg-/HBeAg-). The LCR results were compared with the findings obtained with polymerase chain reaction (PCR) amplification of three distinct HBV gene regions (preS1/2, S and C) and related to the serological profiles of the patien…

Hepatitis B virusHBsAgHepatitis B virus DNA polymerasemedicine.disease_causePolymerase Chain ReactionSensitivity and Specificitylaw.inventionLigaseslawVirologymedicineHumansHepatitis B e AntigensLigase chain reactionPolymerase chain reactionHepatitis B virusHepatitis B Surface AntigensHepatologyClinical Laboratory Techniquesbusiness.industryvirus diseasesHepatitis BHepatitis Bmedicine.diseaseVirologyMolecular biologydigestive system diseasesInfectious DiseasesHBeAgDNA ViralLeukocytes MononuclearPrimer (molecular biology)business
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Inverse regulation of vascular endothelial growth factor and VHL tumor suppressor gene in sporadic renal cell carcinomas is correlated with vascular …

1999

Tumors associated with the VHL (von Hippel-Lindau) disease, such as hemangioblastomas and renal carcinomas and their sporadic counterparts, are cystic and well vascularized. Mutations of the VHL tumor-suppressor gene and elevated levels of vascular endothelial growth factor (VEGF) have been described in these tumors. The upregulation of VEGF has been shown in vitro as a consequence of alteration of the VHL gene. No comprehensive in vivo analysis has yet been carried out of the factors affecting tumor growth, vascularization, VEGF, and VHL expression. We performed immunohistochemistry and mRNA studies on primary sporadic renal carcinomas and matching normal renal tissue. We semiquantitativel…

AdultMaleVascular Endothelial Growth Factor APathologymedicine.medical_specialtyendocrine system diseasesTumor suppressor geneAngiogenesisUbiquitin-Protein LigasesEndothelial Growth FactorsBiologyurologic and male genital diseasesmedicine.disease_causeLigaseschemistry.chemical_compoundDrug DiscoverymedicineHumansGenes Tumor SuppressorCarcinoma Renal CellGenetics (clinical)AgedLymphokinesKidneyNeovascularization PathologicVascular Endothelial Growth FactorsTumor Suppressor ProteinsProteinsMiddle Agedmedicine.diseaseKidney Neoplasmsfemale genital diseases and pregnancy complicationsGene Expression Regulation NeoplasticVascular endothelial growth factorVascular endothelial growth factor AClear cell renal cell carcinomamedicine.anatomical_structurechemistryVon Hippel-Lindau Tumor Suppressor ProteinMolecular MedicineFemaleCarcinogenesisClear cellJournal of Molecular Medicine
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