Search results for "BLAST"

showing 10 items of 2136 documents

Cytoglobin is a respiratory protein in connective tissue and neurons, which is up-regulated by hypoxia.

2004

Cytoglobin is a recently discovered vertebrate globin distantly related to myoglobin, and its function is unknown. Here we present the first detailed analysis of the distribution and expression of cytoglobin. Northern and Western blotting experiments show the presence of cytoglobin mRNA and protein in a broad range of tissues. Quantitative PCR demonstrates an up-regulation of cytoglobin mRNA levels in rat heart and liver under hypoxic conditions (22 and 44 h of 9% oxygen). Immunofluorescence studies with three antibodies directed against different epitopes of the protein consistently show cytoglobin in connective tissue fibroblasts as well as in hepatic stellate cells. Cytoglobin is also pr…

CytoplasmRespiratory SystemFluorescent Antibody TechniqueBiochemistryMiceAntibody SpecificityChlorocebus aethiopsRespiratory functionHypoxiaNeuronsMice Inbred BALB CReverse Transcriptase Polymerase Chain ReactionCytoglobinNuclear ProteinsImmunohistochemistryGlobinsRespiratory proteinTracheamedicine.anatomical_structureLiverConnective TissueNeuroglobinRecombinant Fusion ProteinsGreen Fluorescent ProteinsMolecular Sequence DataConnective tissueBiologyTransfectionAntibodiesBone and BonesmedicineAnimalsHumansGlobinAmino Acid SequenceRNA MessengerMolecular BiologyVero CellsCell NucleusMessenger RNAMyocardiumCytoglobinCell BiologyFibroblastsMolecular biologyPeptide FragmentsRatsOxygenLuminescent ProteinsGene Expression RegulationHepatic stellate cellHeLa CellsThe Journal of biological chemistry
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Neuraminidase deficiency presenting as non-immune hydrops fetalis

1984

A newborn infant with oedema, ascites and hepatosplenomegaly is described. In ascites fluid foamy macrophages were found, in a liver biopsy cytoplasmic inclusions and membrane-bound vacuoles were seen. Furthermore the child excreted excessive amounts of sialic acid-rich oligosaccharides in the urine, and therefore a neurovisceral degenerative disorder was assumed. The diagnosis of sialidosis was confirmed by enzymatic assay in cultured fibroblasts, in which a complete deficiency of the lysosomal enzyme neuraminidase could be demonstrated. After recurrent septicaemias the child became dystrophic and died at the age of 6 months. Our case is compared with sialidosis observed by other authors, …

Cytoplasmic inclusionHepatosplenomegalyNeuraminidaseOligosaccharidesMucolipidosesalpha-MannosidaseHydrops fetalisMannosidasesAscitesLeukocytesmedicineLysosomal storage diseaseEdemaHumansSialidosisalpha-L-Fucosidasemedicine.diagnostic_testbiologybusiness.industryInfant NewbornFibroblastsbeta-Galactosidasemedicine.diseasebeta-N-AcetylhexosaminidasesHexosaminidasesLiverLiver biopsyPediatrics Perinatology and Child HealthImmunologybiology.proteinFemalemedicine.symptomLysosomesbusinessNeuraminidaseEuropean Journal of Pediatrics
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Cytotoxic effects of antibodies to proteinase 3 (C-ANCA) on human endothelial cells.

1994

SUMMARY Autoantibodies directed against cytoplasmic antigens of neutrophils (ANCA), especially those with specificity for proteinase 3 (PR-3) and myeloperoxidase, are valuable markers for differential diagnosis and monitoring of disease activity in Wegener's granulomatosis (WG) and other vasculitides. Till now, several concepts concerning a direct role of antibodies against PR-3 in the pathogenesis of WG have been discussed. Recently we were able to show that these antibodies recognize PR-3 translocated into the membrane of human endothelial cells. The aim of this study was to investigate putative cytotoxic effects of antibodies to PR-3 on human endothelial cells. Antibodies were obtained b…

Cytotoxicity ImmunologicC-ANCAEndotheliumMyeloblastinImmunologyAutoantigensChromatography AffinityAntibodies Antineutrophil CytoplasmicAntigenProteinase 3medicineImmunology and AllergyCytotoxic T cellHumansLupus Erythematosus SystemicCells CulturedAutoantibodiesMixed Connective Tissue DiseasebiologySerine EndopeptidasesAntibody-Dependent Cell CytotoxicityGranulomatosis with PolyangiitisEndothelial stem cellmedicine.anatomical_structureSjogren's SyndromeMyeloperoxidaseImmunologybiology.proteinEndothelium VascularAntibodyResearch ArticleClinical and experimental immunology
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Therapeutic afucosylated monoclonal antibody and bispecific T-cell engagers for T-cell acute lymphoblastic leukemia

2021

BackgroundT-cell acute lymphoblastic leukemia (T-ALL) is an aggressive disease with a poor cure rate for relapsed/resistant patients. Due to the lack of T-cell restricted targetable antigens, effective immune-therapeutics are not presently available and the treatment of chemo-refractory T-ALL is still an unmet clinical need. To develop novel immune-therapy for T-ALL, we generated an afucosylated monoclonal antibody (mAb) (ahuUMG1) and two different bispecific T-cell engagers (BTCEs) against UMG1, a unique CD43-epitope highly and selectively expressed by T-ALL cells from pediatric and adult patients.MethodsUMG1 expression was assessed by immunohistochemistry (IHC) on a wide panel of normal t…

Cytotoxicity ImmunologicCancer Research2434T-LymphocytesMice SCIDafucosylated monoclonal antibodyLymphocyte ActivationPrecursor T-Cell Lymphoblastic Leukemia-LymphomaEpitopesJurkat CellsAntineoplastic Agents ImmunologicalAntibody SpecificityMice Inbred NODantigensAntibodies BispecificTumor MicroenvironmentImmunology and Allergyantibodieshematologic neoplasms1506RC254-282Antibody-dependent cell-mediated cytotoxicityLeukosialinbispecific T-cell engagersmedicine.diagnostic_testbiologyhematological malignancieNeoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.anatomical_structureantibodieOncologytranslational medical researchMolecular MedicineImmunohistochemistryFemaleimmunotherapyAntibodyT-ALLT-cell engagersT-cell acute lymphoblastic leukemiamedicine.drug_classT cellImmunologySettore MED/08 - Anatomia PatologicaMonoclonal antibodyAntibodies Monoclonal HumanizedFlow cytometryT Acute Lymphoblastic LeukemiaantigenAntigenPhagocytosismedicineAnimalsHumanshematological malignanciesCell ProliferationPharmacologyT-cell engagerbusiness.industryhematological malignancies; antibodies; antigens; hematologic neoplasms; immunotherapy; neoplasm; T-ALL; T-cell engagers; translational medical research; translational researchBasic Tumor ImmunologyXenograft Model Antitumor Assaystranslational researchCancer researchbiology.proteinneoplasmbusinesshematologic neoplasmneoplasm
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Both mature KIR+ and immature KIR- NK cells control pediatric acute B-cell precursor leukemia in NOD.Cg-Prkdcscid IL2rgtmWjl/Sz mice.

2014

Therapeutic natural killer (NK)-cell-mediated alloreactivity toward acute myeloid leukemia has largely been attributed to mismatches between killer immunoglobulin-like receptors (KIRs) on NK cells and their ligands, HLA class I molecules, on target cells. While adult acute B-cell precursor leukemia (BCP-ALL) appears to be resistant to NK-cell-mediated lysis, recent data indicate that pediatric BCP-ALL might yet be a target of NK cells. In this study, we demonstrate in a donor-patient-specific NOD.Cg-Prkdc(scid) IL2rg(tmWjl)/Sz (NSG) xenotransplantation model that NK cells mediate considerable alloreactivity toward pediatric BCP-ALL in vivo. Notably, both adoptively transferred mature KIR(+)…

Cytotoxicity ImmunologicGenotypeXenotransplantationmedicine.medical_treatmentImmunologyTransplantation HeterologousAntineoplastic AgentsGraft vs Leukemia EffectHuman leukocyte antigenBiochemistryMiceImmune systemReceptors KIRMice Inbred NODPrecursor B-Cell Lymphoblastic Leukemia-LymphomamedicineAnimalsHumansChildB cellSevere combined immunodeficiencybusiness.industryHematopoietic Stem Cell TransplantationMyeloid leukemiaCell BiologyHematologyDNA Methylationmedicine.diseasePrognosisTransplantationKiller Cells NaturalLeukemiaDisease Models Animalmedicine.anatomical_structureImmunologyAzacitidineCytokinesInterleukin-2businessBlood
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Aneuploid IMR90 cells induced by depletion of pRB, DNMT1 and MAD2 show a common gene expression signature

2019

Chromosome segregation defects lead to aneuploidy which is a major feature of solid tumors. How diploid cells face chromosome mis-segregation and how aneuploidy is tolerated in tumor cells are not completely defined yet. Thus, an important goal of cancer genetics is to identify gene networks that underlie aneuploidy and are involved in its tolerance. To this aim, we induced aneuploidy in IMR90 human primary cells by depleting pRB, DNMT1 and MAD2 and analyzed their gene expression profiles by microarray analysis. Bioinformatic analysis revealed a common gene expression profile of IMR90 cells that became aneuploid. Gene Set Enrichment Analysis (GSEA) also revealed gene-sets/pathways that are …

DNA (Cytosine-5-)-Methyltransferase 1AneuploidyBiologyMicroarrayReal-Time Polymerase Chain ReactionRetinoblastoma ProteinCell LineRNA interferenceGene expressionProtein Interaction MappingGeneticsmedicineHumansGeneOligonucleotide Array Sequence AnalysisMicroarray analysis techniquesGene Expression ProfilingBioinformatics analysiChromosomeFibroblastsmedicine.diseaseAneuploidyGene Expression RegulationRNAiMad2 ProteinsDNMT1Cancer researchKIF4ARNA InterferenceTranscriptomeIMR90 human fibroblast
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Dysregulation of DNA methylation induced by past arsenic treatment causes persistent genomic instability in mammalian cells

2015

The mechanisms by which arsenic-induced genomic instability is initiated and maintained are poorly understood. To investigate potential epigenetic mechanisms, in this study we evaluated global DNA methylation levels in V79 cells and human HaCaT keratinocytes at several time points during expanded growth of cell cultures following removal of arsenite exposures. We have found altered genomic methylation patterns that persisted up to 40 cell generations in HaCaT cells after the treatments were withdrawn. Moreover, mRNA expression levels were evaluated by RT-PCR for DNMT1, DNMT3A, DNMT3B, HMLH1, and HMSH2 genes, demonstrating that the down regulation of DNMT3A and DNMT3B genes, but not DNMT1, o…

DNA (Cytosine-5-)-Methyltransferase 1KeratinocytesDNA methylationArsenitesarsenicNuclear ProteinsFibroblastsgenomic instabilityArticleDNA Methyltransferase 3ASettore BIO/18 - GeneticaCricetulusLong Interspersed Nucleotide ElementsMutS Homolog 2 Protein5-MethylcytosineAnimalsDNA (Cytosine-5-)-MethyltransferasesMutL Protein Homolog 1Promoter Regions GeneticCells CulturedAdaptor Proteins Signal Transducing
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Antitumor Effects of a Combined 5-Aza-2′Deoxycytidine and Valproic Acid Treatment on Rhabdomyosarcoma and Medulloblastoma in Ptch Mutant Mice

2009

Abstract Patched (Ptch) heterozygous mice develop medulloblastoma (MB) and rhabdomyosarcoma (RMS) resembling the corresponding human tumors. We have previously shown that epigenetic silencing of the intact Ptch allele contributes to tumor formation in this model. Here, we investigated whether targeting of epigenetic silencing mechanisms could be useful in the treatment of Ptch-associated cancers. A reduction of endogenous DNA methyltransferase1 (Dnmt1) activity significantly reduced tumor incidence in heterozygous Ptch knockout mice. A combined treatment with the Dnmt inhibitor 5-aza-2′deoxycytidine (5-aza-dC) and the histone deacetlyase (HDAC) inhibitor valproic acid (VPA) efficiently prev…

DNA (Cytosine-5-)-Methyltransferase 1Patched ReceptorsPatchedCancer Researchmedicine.drug_classGene ExpressionDecitabineReceptors Cell SurfaceBiologyDecitabineHistone DeacetylasesHistonesMice03 medical and health sciences0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsRhabdomyosarcomamedicineAnimalsDNA (Cytosine-5-)-MethyltransferasesGene SilencingMuscle SkeletalRhabdomyosarcoma030304 developmental biologyMedulloblastomaMice Inbred BALB C0303 health sciencesValproic AcidHistone deacetylase inhibitorCancerAcetylationDNA Methylationmedicine.disease3. Good healthHistone Deacetylase InhibitorsMice Inbred C57BLPatched-1 Receptorstomatognathic diseasesOncology030220 oncology & carcinogenesisAzacitidineCancer researchDNMT1Epigenetic therapyMedulloblastomamedicine.drugCancer Research
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Compromised repair of radiation-induced DNA double-strand breaks in Fanconi anemia fibroblasts in G2

2020

Fanconi anemia (FA) is a rare chromosomal instability syndrome with various clinical features and high cancer incidence. Despite being a DNA repair disorder syndrome and a frequently observed clinical hypersensitivity of FA patients towards ionizing radiation, the experimental evidence regarding the efficiency of radiation-induced DNA double-strand break (DSB) repair in FA is very controversial. Here, we performed a thorough analysis of the repair of radiation-induced DSBs in G1 and G2 in FA fibroblasts of complementation groups A, C, D1 (BRCA2), D2, E, F, G and P (SLX4) in comparison to normal human lung and skin fibroblasts. γH2AX, 53BP1, or RPA foci quantification after X-irradiation was…

DNA End-Joining RepairBiologyBiochemistryFanconi Anemia Complementation Group F ProteinHistonesRecombinases03 medical and health scienceschemistry.chemical_compound0302 clinical medicineFanconi anemiaChromosome instabilitymedicineHumansDNA Breaks Double-StrandedFanconi Anemia Complementation Group G ProteinMolecular BiologyCells Cultured030304 developmental biologyBRCA2 ProteinChromosome Aberrations0303 health sciencesFanconi Anemia Complementation Group A ProteinFanconi Anemia Complementation Group D2 ProteinX-RaysCell CycleFanconi Anemia Complementation Group C ProteinRecombinational DNA RepairChromosomeDNACell BiologyFibroblastsCell cyclemedicine.diseaseFanconi Anemia Complementation Group E ProteinComplementationKineticsenzymes and coenzymes (carbohydrates)Fanconi Anemiachemistry030220 oncology & carcinogenesisPremature chromosome condensationMutationCancer researchChromatidTumor Suppressor p53-Binding Protein 1DNADNA Repair
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Poly(ADP-ribosyl)ation accelerates DNA repair in a pathway dependent on Cockayne syndrome B protein

2003

Activation of poly(ADP-ribose)polymerases 1 and 2 (PARP-1 and PARP-2) is one of the earliest responses of mammalian cells to DNA damage by numerous genotoxic agents. We have analysed the influence of PARP inhibition, either achieved by over-expression of the DNA binding domain of PARP-1 or by treatment with 3,4-dihydro-5-[4-(1-piperidinyl)butoxyl]-1(2H)-isoquinolinone, on the repair of single-strand breaks (SSB), pyrimidine dimers and oxidative base modifications sensitive to Fpg protein (mostly 8-hydroxyguanine) in mammalian cells at very low, non-cytotoxic levels of DNA damage. The data show that the repair rates of all three types of DNA damage are significantly lower in PARP-inhibited c…

DNA RepairDNA damageDNA repairPoly ADP ribose polymerase[SDV]Life Sciences [q-bio]Pyrimidine dimerBiologyPoly(ADP-ribose) Polymerase InhibitorsPoly (ADP-Ribose) Polymerase InhibitorCockayne syndromeDexamethasone03 medical and health sciencesMice0302 clinical medicinePiperidinesCricetinaeGeneticsmedicineAnimalsPoly-ADP-Ribose Binding ProteinsComputingMilieux_MISCELLANEOUS030304 developmental biologyCell Line TransformedMice Knockout0303 health sciencesDNA HelicasesArticlesDNADNA repair protein XRCC4Fibroblastsmedicine.diseaseIsoquinolinesMolecular biology3. Good healthDNA Repair Enzymes030220 oncology & carcinogenesisPoly(ADP-ribose) PolymerasesNucleotide excision repairDNA DamageSignal Transduction
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