Search results for "binding"

showing 10 items of 3896 documents

The gene encoding the transcriptional repressor BERF-1 maps to a region of conserved synteny on mouse chromosome 16 and human chromosome 3 and a rela…

1999

We have recently identified and characterized a Kruppel-like zinc finger protein (BERF-1), that functions as a repressor of β enolase gene transcription. By interspecific backcross analysis the gene encoding BERF-1 was localized 4.7 cM proximal to the <i>Mtv6</i> locus on mouse chromosome 16, and an isolated pseudogene was localized to mouse chromosome 8, about 5.3 cM distal to the D8Mit4 marker. Nucleotide sequence identity and chomosome location indicate that the gene encoding BERF-1 is the mouse homologue (<i>Zfp148</i>) of ZNF148 localized to human chromosome 3q21, a common translocation site in acute myeloid leukemia patients.

Genetic MarkersDNA ComplementaryTranscription GeneticKruppel-Like Transcription FactorsBiologyHybrid CellsPolymerase Chain ReactionGene Expression Regulation EnzymologicMiceChromosome 16GeneticsAnimalsHumansMolecular BiologyGenetics (clinical)Conserved SequenceSyntenyDNA PrimersGeneticsBase SequenceYY1Chromosome MappingTAF9Zinc FingersTCF4DNA-Binding ProteinsRepressor ProteinsChromosome 3GATAD2BPhosphopyruvate Hydratasecardiovascular systemChromosomes Human Pair 3Chromosome 22PseudogenesTranscription FactorsCytogenetics and cell genetics
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TET2 mutation is an independent favorable prognostic factor in myelodysplastic syndromes (MDSs).

2009

Abstract Oncogenic pathways underlying in the development of myelodysplastic syndromes (MDS) remain poorly characterized, but mutations of the ten-eleven translocation 2 (TET2) gene are frequently observed. In the present work, we evaluated the prognostic impact of TET2 mutations in MDS. Frameshift, nonsense, missense mutations, or defects in gene structure were identified in 22 (22.9%) of 96 patients (95% confidence interval [CI], 14.5-31.3 patients). Mutated and unmutated patients did not significantly differ in initial clinical or hematologic parameters. The 5-year OS was 76.9% (95% CI, 49.2%-91.3%) in mutated versus 18.3% (95% CI, 4.2%-41.1%) in unmutated patients (P = .005). The 3-year…

Genetic MarkersMalemedicine.medical_specialtyPathologyImmunologyBiochemistryGastroenterologyDisease-Free SurvivalFrameshift mutationDioxygenasesPredictive Value of TestsRisk FactorsInternal medicineProto-Oncogene ProteinsmedicineMissense mutationHumansAgedAged 80 and overUnivariate analysisProportional hazards modelbusiness.industryMyelodysplastic syndromesHazard ratioCell BiologyHematologyMiddle Agedmedicine.diseaseConfidence intervalDNA-Binding ProteinsSurvival RateInternational Prognostic Scoring SystemMyelodysplastic SyndromesMutationFemalebusinessFollow-Up StudiesBlood
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Real-Time Quantification in Plasma of Human Telomerase Reverse Transcriptase (hTERT) mRNA: A Simple Blood Test to Monitor Disease in Cancer Patients

2001

Real-Time Quantification in Plasma of Human Telomerase Reverse Transcriptase (hTERT) mRNA: A Simple Blood Test to Monitor Disease in Cancer Patients

Genetic MarkersTelomeraseDiseaseBiologyPathology and Forensic MedicineNeoplasmsBiomarkers TumormedicineHumansBlood testTelomerase reverse transcriptaseRNA MessengerLymphoma FollicularTelomeraseMolecular BiologyMessenger RNAmedicine.diagnostic_testReverse Transcriptase Polymerase Chain ReactionCancerCell BiologyPrognosismedicine.diseaseNucleotidyltransferaseMolecular biologyDNA-Binding ProteinsReverse transcription polymerase chain reactionRNAColorectal NeoplasmsLaboratory Investigation
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Comparative architectural aspects of regions of conserved synteny on human chromosome 11p15.3 and mouse chromosome 7 (including genes WEE1 and LMO1)

2001

Human chromosome 11p15.3 is associated with chromosome aberrations in the Beckwith Wiedemann Syndrome and implicated in the pathogenesis of different tumor types including lung cancer and leukemias. To date, only single tumor-relevant genes with linkage to this region (e.g. LMO1) have been found suggesting that this region may harbor additional potential disease associated genes. Although this genomic area has been studied for years, the exact order of genes/chromosome markers between D11S572 and the WEE1 gene locus remained unclear. Using the FISH technique and PAC clones of the flanking markers we determined the order of the genomic markers. Based on these clones we established a PAC cont…

Genetic Markerscongenital hereditary and neonatal diseases and abnormalitiesBeckwith–Wiedemann syndromeCell Cycle ProteinsBiologyChromosomesEvolution MolecularContig MappingMiceChromosome regionsGene OrderMetalloproteinsGeneticsmedicineAnimalsHumansCloning MolecularMolecular BiologyGeneConserved SequenceIn Situ Hybridization FluorescenceGenetics (clinical)Repetitive Sequences Nucleic AcidSyntenyOncogene ProteinsGeneticsChromosome 7 (human)Base CompositionChromosomes Human Pair 11Nuclear ProteinsChromosomeSequence Analysis DNALIM Domain ProteinsProtein-Tyrosine Kinasesmedicine.diseaseAT Rich SequenceGC Rich SequenceDNA-Binding ProteinsChromosome 3CpG IslandsChromosome 21Transcription FactorsCytogenetic and Genome Research
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Identification of sequences in the human peptide transporter subunit TAP1 required for transporter associated with antigen processing (TAP) function

2001

The heterodimeric peptide transporter associated with antigen processing (TAP) consisting of the subunits TAP1 and TAP2 mediates the transport of cytosolic peptides into the lumen of the endoplasmic reticulum (ER). In order to accurately define domains required for peptide transporter function, a molecular approach based on the construction of a panel of human TAP1 mutants and their expression in TAP1(-/-) cells was employed. The characteristics and biological activity of the various TAP1 mutants were determined, and compared to that of wild-type TAP1 and TAP1(-/-) control cells. All mutant TAP1 proteins were localized in the ER and were capable of forming complexes with the TAP2 subunit. H…

Genetic VectorsImmunologyAntigen presentationBiological Transport ActiveEpitopes T-LymphocyteTransfectionMajor histocompatibility complexMiceAntigenATP Binding Cassette Transporter Subfamily B Member 3MHC class ITumor Cells CulturedAnimalsHumansLymphocytic choriomeningitis virusImmunology and AllergyAmino Acid SequenceATP Binding Cassette Transporter Subfamily B Member 2Sequence DeletionMice KnockoutAntigen PresentationbiologyAntigen processingHistocompatibility Antigens Class IGeneral MedicineTransporter associated with antigen processingMHC restrictionCytotoxicity Tests ImmunologicMolecular biologyPeptide FragmentsCell biologyMice Inbred C57BLPeptide transportMutagenesis Site-Directedbiology.proteinATP-Binding Cassette TransportersDimerizationT-Lymphocytes CytotoxicInternational Immunology
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Baculoviral display of functional scFv and synthetic IgG-binding domains.

2000

Viral vectors displaying specific ligand binding moities such as scFv fragments or intact antibodies hold promise for the development of targeted gene therapy vectors. In this report we describe baculoviral vectors displaying either functional scFv fragments or the synthetic Z/ZZ IgG binding domain derived from protein A. Display on the baculovirus surface was achieved via fusion of the scFv fragment or Z/ZZ domain to the N-terminus of gp64, the major envelope protein of the Autographa californica nuclear polyhedrosis virus, AcNPV. As examples of scFv fragments we have used a murine scFv specific for the hapten 2-phenyloxazolone and a human scFv specific for carcinoembryonic antigen. In pri…

Genetic enhancementvirusesRecombinant Fusion ProteinsBlotting WesternBiophysicschemical and pharmacologic phenomenaEnzyme-Linked Immunosorbent AssayVectors in gene therapySpodopteraBiochemistryViral vector03 medical and health sciencesMice0302 clinical medicineAntibody SpecificityPeptide LibraryAnimalsHumansMolecular BiologyImmunoglobulin FragmentsCells Cultured030304 developmental biology0303 health sciencesbiologyOxazoloneNuclear Polyhedrosis VirusCell Biologyrespiratory systembiology.organism_classificationMolecular biology3. Good healthCarcinoembryonic AntigenAutographa californicaIgG binding030220 oncology & carcinogenesisImmunoglobulin Gbiology.proteinBinding Sites AntibodyAntibodyHaptenBaculoviridaeHaptensViral Fusion ProteinsBiochemical and biophysical research communications
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Cholesterol and Amyloid-β: Evidence for a Cross-Talk between Astrocytes and Neuronal Cells.

2011

Accumulating data supports the concept that alterations of cholesterol metabolism might influence the development of Alzheimer's disease (AD), a neurodegenerative disorder characterized by progressive accumulation of amyloid-β (Aβ) peptides in the brain. Changes in the neuronal production of Aβ have been described as a function of cholesterol levels, thus suggesting a causal link between cholesterol homeostasis dysregulation and AD pathogenesis. Under physiological conditions, cholesterol uptake in the brain is efficiently prevented by the blood-brain barrier, and mature neurons are thought to rely on glial cells for their cholesterol supply. In the present study, we tested the hypothesis t…

Genetically modified mouseBlotting WesternEnzyme-Linked Immunosorbent AssayMice TransgenicCell LinePathogenesisMicechemistry.chemical_compoundAlzheimer DiseasemedicineAnimalsHomeostasisHumansBrain ChemistryNeuronsAmyloid beta-PeptidesbiologyCholesterolGeneral NeuroscienceTransporterReceptor Cross-TalkGeneral Medicinemedicine.diseaseCoculture TechniquesPsychiatry and Mental healthClinical PsychologyCholesterolATP Binding Cassette Transporter 1chemistryAstrocytesABCA1biology.proteinATP-Binding Cassette Transporterslipids (amino acids peptides and proteins)Geriatrics and GerontologyAlzheimer's diseaseNeuroscienceHomeostasisATP Binding Cassette Transporter 1
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A Cre-inducible diphtheria toxin receptor mediates cell lineage ablation after toxin administration.

2004

A new system for lineage ablation is based on transgenic expression of a diphtheria toxin receptor (DTR) in mouse cells and application of diphtheria toxin (DT). To streamline this approach, we generated Cre-inducible DTR transgenic mice (iDTR) in which Cre-mediated excision of a STOP cassette renders cells sensitive to DT. We tested the iDTR strain by crossing to the T cell- and B cell-specific CD4-Cre and CD19-Cre strains, respectively, and observed efficient ablation of T and B cells after exposure to DT. In MOGi-Cre/iDTR double transgenic mice expressing Cre recombinase in oligodendrocytes, we observed myelin loss after intraperitoneal DT injections. Thus, DT crosses the blood-brain bar…

Genetically modified mouseCell SurvivalTransgeneT cellT-LymphocytesCellCre recombinaseApoptosisMice TransgenicReceptors Cell SurfaceBiologyBiochemistryCell LineMicemedicineAnimalsCell LineageDiphtheria ToxinReceptorMolecular BiologyDiphtheria toxinIntegrasesCell DifferentiationCell BiologyMolecular biologyRecombinant ProteinsOligodendrogliamedicine.anatomical_structureCell cultureIntercellular Signaling Peptides and ProteinsBiotechnologyHeparin-binding EGF-like Growth FactorNature methods
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Profilin1 activity in cerebellar granule neurons is required for radial migration in vivo.

2014

Neuron migration defects are an important aspect of human neuropathies. The underlying molecular mechanisms of such migration defects are largely unknown. Actin dynamics has been recognized as an important determinant of neuronal migration, and we recently found that the actin-binding protein profilin1 is relevant for radial migration of cerebellar granule neurons (CGN). As the exploited brain-specific mutants lacked profilin1 in both neurons and glial cells, it remained unknown whether profilin1 activity in CGN is relevant for CGN migration in vivo. To test this, we capitalized on a transgenic mouse line that expresses a tamoxifen-inducible Cre variant in CGN, but no other cerebellar cell …

Genetically modified mouseCerebellumNeurogenesisShort CommunicationMutantMice TransgenicBiologyCellular and Molecular NeuroscienceMiceProfilinsIn vivoCell MovementCerebellummedicineAnimalsActin-binding proteinNeuronsCell BiologyActinsCell biologyTreadmillingmedicine.anatomical_structureProfilinCerebellar cortexbiology.proteinNeurogliaCell adhesionmigration
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Glycosylation deficiency at either one of the two glycan attachment sites of cellular prion protein preserves susceptibility to bovine spongiform enc…

2004

The conversion into abnormally folded prion protein (PrP) plays a key role in prion diseases. PrP(C) carries two N-linked glycan chains at amino acid residues 180 and 196 (mouse). Previous in vitro data indicated that the conversion process may not require glycosylation of PrP. However, it is conceivable that these glycans function as intermolecular binding sites during the de novo infection of cells on susceptible organisms and/or play a role for the interaction of both PrP isoforms. Such receptor-like properties could contribute to the formation of specific prion strains. However, in earlier studies, mutations at the glycosylation sites of PrP led to intracellular trafficking abnormalitie…

Genetically modified mouseGlycanGlycosylationGlycosylationPrionsanimal diseasesBovine spongiform encephalopathyMutantBlotting WesternScrapieMice TransgenicCHO CellsCell SeparationBiologyBiochemistryCell LinePrion Diseaseschemistry.chemical_compoundMicePolysaccharidesCell Line TumorCricetinaemedicineAnimalsImmunoprecipitationProtein IsoformsBiotinylationDisulfidesTransgenesCloning MolecularMolecular BiologyBinding SitesWild typeBrainCell Biologymedicine.diseaseFlow CytometryVirologyMolecular biologyIn vitronervous system diseasesEncephalopathy Bovine SpongiformMice Inbred C57BLchemistryMutationbiology.proteinCattleScrapieThe Journal of biological chemistry
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