Search results for "Ubiquitin-Protein Ligases"

showing 10 items of 48 documents

Sleep disturbances in Angelman syndrome: a questionnaire study.

2003

Only few studies are available on sleep disorders in Angelman syndrome (AS), a neurodevelopmental disorder with several behavior disturbances. The aim of this study was to determine the prevalence of sleep disorders in a relatively large group of AS subjects, compared to that of age-matched controls. Forty-nine consecutive parents of patients with AS (26 males and 23 females aged 2.3-26.2 years) were interviewed and filled out a comprehensive sleep questionnaire. Based on their genetic etiology, four groups were defined: deletion of chromosome 15q11-13 (25 subjects); methylation imprinting mutation (six subjects), UBE3A mutations (seven subjects) and paternal uniparental disomy (five subjec…

AdultMaleSleep Wake DisordersPediatricsmedicine.medical_specialtyAdolescentUbiquitin-Protein LigasesComorbidityNeurodevelopmental disorderDevelopmental NeuroscienceReference ValuesAngelman syndromeSurveys and QuestionnairesmedicineUBE3APrevalenceHumansWakefulnessPsychiatryChildangelman syndrome; questionnaire study; sleep disordersSleep disorderChromosomes Human Pair 15questionnaire studySleep terrorAge FactorsGeneral MedicineSomnambulismDNA MethylationUniparental Disomymedicine.diseaseSleep in non-human animalsItalyChild PreschoolPediatrics Perinatology and Child HealthMutationsleep disordersFemaleNeurology (clinical)Sleep onsetAngelman SyndromePsychologySleepBraindevelopment
researchProduct

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
researchProduct

Myocardial 123metaiodobenzylguanidine uptake in genetic Parkinson's disease.

2008

Myocardial (123)Metaiodobenzylguanidine (MIBG) enables the assessment of postganglionic sympathetic cardiac innervation. MIBG uptake is decreased in nearly all patients with Parkinson's disease (PD). Our objective was to evaluate MIBG uptake in patients with genetic PD. We investigated MIBG uptake in 14 patients with PD associated with mutations in different genes (Parkin, DJ-1, PINK], and leucine-rich repeat kinase 2 -LRRK2), in 15 patients with idiopathic PD, and 10 control subjects. The myocardial MIGB uptake was preserved in 3 of the 4 Parkin-associated Parkinsonisms, in I of the 2 patients with DJ-1 mutations, in 1 of the 2 brothers with PINK] mutations, in 3 of the 6 unrelated patient…

AdultMalemedicine.medical_specialtyParkinson's diseaseGenotypeUbiquitin-Protein LigasesDNA Mutational AnalysisProtein Deglycase DJ-1PINK1Gene mutationProtein Serine-Threonine Kinasesmedicine.disease_causeLeucine-Rich Repeat Serine-Threonine Protein Kinase-2Severity of Illness IndexParkinCentral nervous system diseaseDiagnosis DifferentialDegenerative diseaseParkinsonian DisordersInternal medicineSurveys and QuestionnairesmedicineHumansPoint MutationPromoter Regions GeneticGenetic PD Myocardial scintigraphyOncogene ProteinsTomography Emission-Computed Single-PhotonMutationMovement Disordersbusiness.industryMyocardiumIntracellular Signaling Peptides and ProteinsParkinson DiseaseGalvanic Skin ResponseMiddle Agedmedicine.diseaseLRRK2nervous system diseases3-IodobenzylguanidineEndocrinologyNeurologySettore MED/26 - NeurologiaFemaleNeurology (clinical)RadiopharmaceuticalsbusinessProtein KinasesMovement disorders : official journal of the Movement Disorder Society
researchProduct

Reduced VLDL clearance in ApoeNpc1 mice is associated with increased Pcsk9 and Idol expression and decreased hepatic LDL-receptor levels

2010

Niemann-Pick type C1 (NPC1) promotes the transport of LDL receptor (LDL-R)-derived cholesterol from late endosomes/lysosomes to other cellular compartments. NPC1-deficient cells showed impaired regulation of liver_X receptor (LXR) and sterol regulatory element-binding protein (SREBP) target genes. We observed that Apoe(-/-)Npc1(-/-) mice displayed a marked increase in total plasma cholesterol mainly due to increased VLDL, reflecting decreased clearance. Although nuclear SREBP-2 and Ldlr mRNA levels were increased in Apoe(-/-)Npc1(-/-) liver, LDL-R protein levels were decreased in association with marked induction of proprotein convertase subtilisin/kexin type 9 (Pcsk9) and inducible degrade…

Apolipoprotein EreceptorCholesterol VLDLLDL/metabolismMacrophages Peritoneal/cytologyBiochemistryMiceEndocrinologyhemic and lymphatic diseasesReceptorsOrphan Nuclear Receptors/geneticspolycyclic compoundsnuclear receptorCells CulturedResearch ArticlesLiver X ReceptorsMice KnockoutCulturedSterol Regulatory Element Binding Protein 2/geneticslipoproteinSerine EndopeptidasesIntracellular Signaling Peptides and ProteinsLamin Type AOrphan Nuclear ReceptorsTriglycerides/bloodCholesterolLiverProteins/geneticsKexinlipids (amino acids peptides and proteins)Proprotein ConvertasesProprotein Convertase 9Sterol Regulatory Element Binding Protein 1Niemann-Pick diseaseSterol Regulatory Element Binding Protein 2medicine.medical_specialtyCellsKnockoutUbiquitin-Protein LigasesReceptors LDL/metabolismSerine Endopeptidases/geneticsQD415-436BiologyCholesterol/blooddigestive systemApolipoproteins ELiver/physiologySterol Regulatory Element Binding Protein 1/geneticsNiemann-Pick C1 ProteinInternal medicinemedicineAnimalsPeritoneal/cytologyCholesterol VLDL/metabolismUbiquitin-Protein Ligases/geneticsLiver X receptorTriglyceridesMacrophagesPCSK9Proteinsnutritional and metabolic diseasesVLDL/metabolismLamin Type A/metabolismCell BiologySterol regulatory element-binding proteinEndocrinologyReceptors LDLLDL receptorMacrophages PeritonealSterol regulatory element-binding protein 2atherosclerosisApolipoproteins E/geneticsLipoproteinJournal of Lipid Research
researchProduct

Tracheal development and the von Hippel-Lindau tumor suppressor homolog in Drosophila.

2000

von Hippel-Lindau disease is a hereditary cancer syndrome. Mutations in the VHL tumor suppressor gene predispose individuals to highly vascularized tumors. However, VHL-deficient mice die in utero due to a lack of vascularization in the placenta. To resolve the contradiction, we cloned the Drosophila VHL homologue (d-VHL) and studied its function. It showed an overall 50% similarity to the human counterpart and 76% similarity in the crucial functional domain: the elongin C binding site. The putative d-VHL protein can bind Drosophila elongin C in vitro. During embryogenesis, d-VHL is expressed in the developing tracheal regions where tube outgrowth no longer occurs. Reduced d-VHL activity (u…

Cancer Researchendocrine system diseasesTumor suppressor geneUbiquitin-Protein LigasesMolecular Sequence Dataurologic and male genital diseasesTube fusionLigasesRNA interferenceVon Hippel–Lindau tumor suppressorGeneticsmedicineAnimalsHumansGenes Tumor SuppressorAmino Acid SequenceVon Hippel–Lindau diseaseCloning MolecularneoplasmsMolecular BiologyGeneticsbiologyTumor Suppressor ProteinsProteinsCell migrationEmbryomedicine.diseasePhenotypefemale genital diseases and pregnancy complicationsCell biologyTracheaPhenotypeVon Hippel-Lindau Tumor Suppressor Proteinbiology.proteinDrosophilaOncogene
researchProduct

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
researchProduct

NFAT transcription factors in control of peripheral T cell tolerance.

2006

The Ca++-regulated calcineurin/NFAT cascade is one of the crucial signalling pathways that controls adaptive immunity. However, a number of novel experimental data suggest that, in addition to their role in T cell activation, NFATc transcription factors play also a decisive role in the generation of peripheral tolerance against self-antigens. This function of NFATc factors is mediated by controlling activation-induced cell death and clonal anergy of T helper cells and the activity of regulatory T cells. The multi-functional role of NFATc proteins characterize these transcription factors as key regulators of immunological tolerance and, if dysregulated, of development of autoimmune diseases.

Clonal AnergyClonal anergyNFATC Transcription FactorsT cellT-LymphocytesUbiquitin-Protein LigasesImmunologyPeripheral toleranceNFATForkhead Transcription FactorsBiologyNFATC Transcription FactorsAcquired immune systemCell biologyAutoimmune DiseasesCalcineurinMicemedicine.anatomical_structuremedicineImmune ToleranceImmunology and AllergyAnimalsHumansTranscription factorEuropean journal of immunology
researchProduct

A variant of Smurf2 protects mice against colitis-associated colon cancer by inducing transforming growth factor β signaling.

2011

Background & Aims Transforming growth factor (TGF)-β signaling, which is down-regulated by the E3 ubiquitin ligase Smad ubiquitin regulating factor 2 (Smurf2), promotes development of cancer. We identified a splice variant of Smurf2 (ΔE2Smurf2) and investigated its role in colon carcinogenesis in mice. Methods Colitis-associated colon cancer was induced in mice by administration of azoxymethane, followed by 3 cycles of oral administration of dextran sodium sulfate. Messenger RNA levels of Smurf2 in colon tumors and control tissue were measured by quantitative polymerase chain reaction; lymphocyte and cytokine levels were measured in tumor and tissue samples. Results Tumor-infiltrating CD4 +…

Colorectal cancermedicine.medical_treatmentLymphocyteUbiquitin-Protein LigasesSMADBiologyProinflammatory cytokineReceptors G-Protein-Coupledchemistry.chemical_compoundMiceTransforming Growth Factor betamedicineAnimalsCells CulturedHepatologyAzoxymethaneGene Expression ProfilingGastroenterologymedicine.diseaseColitisMolecular biologyUbiquitin ligaseMice Inbred C57BLProto-Oncogene Proteins c-kitCytokinemedicine.anatomical_structureHyaluronan ReceptorschemistryColonic Neoplasmsbiology.proteinCancer researchTransforming growth factorSignal TransductionGastroenterology
researchProduct

Comparative genomics and protein domain graph analyses link ubiquitination and RNA metabolism.

2006

The human gene parkin, known to cause familial Parkinson disease, as well as several other genes, likely involved in other neurodegenerative diseases or in cancer, encode proteins of the RBR family of ubiquitin ligases. Here, we describe the structural diversity of the RBR family in order to infer their functional roles. Of particular interest is a relationship detected between RBR-mediated ubiquitination and RNA metabolism: a few RBR proteins contain RNA binding domains and DEAH-box RNA helicase domains. Global protein domain graph analyses demonstrate that this connection is not RBR-specific, but instead many other proteins contain both ubiquitination and RNA-related domains. These protei…

Comparative genomicsGeneticsbiologyProtein ConformationUbiquitinUbiquitin-Protein LigasesProtein domainMolecular Sequence DataRNAGenomicsF-box proteinRNA Helicase AParkinUbiquitin ligaseProtein Structure TertiaryStructural Biologybiology.proteinAnimalsCluster AnalysisHumansRNAMolecular BiologyGeneAlgorithmsJournal of molecular biology
researchProduct

Deinococcus radiodurans' SRA-HNH domain containing protein Shp (Dr1533) is involved in faithful genome inheritance maintenance following DNA damage

2018

WOS:000452343100012; International audience; Background: Deinococcus radiodurans R1 (DR) survives conditions of extreme desiccation, irradiation and exposure to genotoxic chemicals, due to efficient DNA breaks repair, also through Mn2+ protection of DNA repair enzymes. Methods: Possible annotated domains of the DR1533 locus protein (Shp) were searched by bioinformatic analysis. The gene was cloned and expressed as fusion protein. Band-shift assays of Shp or the SRA and HNH domains were performed on oligonucleotides, genomic DNA from E. coif and DR. slip knock-out mutant was generated by homologous recombination with a kanamycin resistance cassette. Results: DR1533 contains an N-terminal SRA…

DNA RepairDNA cytosine-methylation; DNA damage; DR1533 locus; Genotoxic agents; Mn2+; SRA domain; Biophysics; Biochemistry; Molecular BiologyGenotoxic agents[SDV]Life Sciences [q-bio]DNA cytosine-methylationperspectiveSettore BIO/19 - Microbiologia GeneraleBiochemistrychemistry.chemical_compound0302 clinical medicineKanamycinCloning Molecularcytosine0303 health sciencesDR1533 locusbiologyChemistryGenotoxic agentuhrf1Mn(2+)Mn2+SRA domainDeinococcusrecognitionmanganese(ii)DNA BacterialDNA damageDNA repairoxidationUbiquitin-Protein LigasesBiophysicsSettore BIO/11 - Biologia Molecolareresistance03 medical and health sciencesBacterial ProteinsProtein DomainsDR1533 locuDrug Resistance BacterialEscherichia coliHumansfeaturesAmino Acid SequenceGeneMolecular Biology030304 developmental biologyOligonucleotideComputational BiologyDeinococcus radioduransDNA Methylationbiology.organism_classificationMolecular biologygenomic DNArepairMutationCCAAT-Enhancer-Binding ProteinsDNA damageHomologous recombination030217 neurology & neurosurgeryDNAGenome BacterialMutagens
researchProduct