Search results for "Adenosine Diphosphate Ribose"

showing 10 items of 15 documents

Nitric oxide: comparative synthesis and signaling in animal and plant cells.

2001

Since its identification as an endothelium-derived relaxing factor in the 1980s, nitric oxide has become the source of intensive and exciting research in animals. Nitric oxide is now considered to be a widespread signaling molecule involved in the regulation of an impressive spectrum of mammalian cellular functions. Its diverse effects have been attributed to an ability to chemically react with dioxygen and its redox forms and with specific iron- and thiol-containing proteins. Moreover, the effects of nitric oxide are dependent on the dynamic regulation of its biosynthetic enzyme nitric oxide synthase. Recently, the role of nitric oxide in plants has received much attention. Plants not only…

0106 biological sciencesPlant ScienceNitric Oxide01 natural sciencesAconitaseRedoxNitric oxide03 medical and health scienceschemistry.chemical_compound[SDV.BV]Life Sciences [q-bio]/Vegetal BiologyAnimals[SDV.BV] Life Sciences [q-bio]/Vegetal BiologyCyclic GMP030304 developmental biologyAconitate HydrataseMammals0303 health sciencesAdenosine Diphosphate RibosebiologyPlantsPlant cellBiosynthetic enzymeNitric oxide synthasechemistryBiochemistrybiology.proteinSignal transductionNitric Oxide SynthaseReactive Oxygen SpeciesSalicylic AcidSalicylic acid010606 plant biology & botanySignal TransductionTrends in plant science
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In vitro model for DNA double‐strand break repair analysis in breast cancer reveals cell type–specific associations with age and prognosis

2016

Dysfunction of homologous recombination is a common denominator of changes associated with breast cancer-predisposing mutations. In our previous work, we identified a functional signature in peripheral blood lymphocytes from women who were predisposed that indicated a shift from homologous recombination to alternative, error-prone DNA double-strand break (DSB) repair pathways. To capture both hereditary and nonhereditary factors, we newly established a protocol for isolation and ex vivo analysis of epithelial cells, epithelial-mesenchymal transition cells (EMTs), and fibroblasts from breast cancer specimens (147 patients). By applying a fluorescence-based test system, we analyzed the error-…

Adult0301 basic medicinePathologymedicine.medical_specialtyEpithelial-Mesenchymal TransitionDNA RepairDNA repairCellBreast NeoplasmsBiologymedicine.disease_causeBiochemistry03 medical and health sciences0302 clinical medicineBreast cancerCell Line TumorGeneticsmedicineHumansDNA Breaks Double-StrandedGenetic Predisposition to DiseaseBreastEpithelial–mesenchymal transitionHomologous RecombinationMolecular BiologyAgedAged 80 and overAdenosine Diphosphate RiboseMutationAge FactorsMiddle AgedDNA repair protein XRCC4Prognosismedicine.diseaseDouble Strand Break Repair030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisMutationCancer researchFemaleHomologous recombinationBiotechnologyThe FASEB Journal
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A comparative biochemical, pharmacological and immunological study of Clostridium novyi alpha-toxin, C. difficile toxin B and C. sordellii lethal tox…

1991

The three clostridial cytotoxins, i.e. alpha-toxin of C. novyi (Tox alpha-nov), toxin B of C. difficile (ToxB-dif) and lethal toxin of C. sordellii (LT-sor) consist of single peptide chains of about 200,000 (Tox alpha-nov), 250,000 (LT-sor) and 275,000 (ToxB-dif) mol. wts. ToxB-dif and LT-sor but not Tox alpha-nov cross-reacted with rabbit polyclonal antibodies. Toxicity upon i.v. injection in mice was similar (LD50, 100 hr, 50-200 ng/kg) and was characterized by a slowly developing fluid loss into the interstitial space. When injected into the rat paw the toxins caused a delayed local edema lasting for days. In vitro the three toxins provoked a persistent retraction of endothelial cells cu…

Bacterial ToxinsClostridium sordelliiClostridium difficile toxin BChick EmbryoBiologyPulmonary ArteryToxicologymedicine.disease_causeMedian lethal doseMicrobiologyLethal Dose 50chemistry.chemical_compoundMiceBacterial ProteinsmedicineAnimalsMicroscopy Phase-ContrastUridineCells CulturedClostridiumAdenosine Diphosphate RiboseToxinClostridioides difficileCytotoxinsRats Inbred Strainsbiology.organism_classificationClostridium novyiUridineRatsEndothelial stem cellchemistryADP-ribosylationPotassiumFemaleEndothelium VascularToxicon : official journal of the International Society on Toxinology
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Differentiative pathway activated by 3-aminobenzamide, an inhibitor of PARP, in human osteosarcoma MG-63 cells

2004

AbstractThis study describes the molecular mechanism by which treatment with 3-AB, a potent inhibitor of PARP, allows human osteosarcoma MG-63 cells to restrict growth and enter differentiation. Our findings show that in MG-63 cells, aberrant gene expression keeps Rb protein constitutively inactivated through hyperphosphorylation and this promotes uncontrolled proliferation of the cells. After 3-AB-treatment, the poly(ADP-ribosyl)ation of nuclear proteins markedly decreases and this results in an increase in both the hypophosphorylated active form of Rb and pRb/E2F complexes. These effects are accompanied by G1 arrest, downregulation of gene products required for proliferation (cyclin D1, β…

Blotting WesternBiophysicsHyperphosphorylationCell Cycle ProteinsPoly(ADP-ribose) Polymerase InhibitorsCell cycleRetinoblastoma ProteinBiochemistryPARPRb proteinCyclin D1Downregulation and upregulationStructural BiologyCell Line TumorGene expressionGeneticsHumansImmunoprecipitationOsteopontinEnzyme InhibitorsPhosphorylationE2FMolecular BiologyDNA PrimersAdenosine Diphosphate RiboseOsteosarcomaBase SequencebiologyReverse Transcriptase Polymerase Chain ReactionG1 PhaseCell DifferentiationCell BiologyCell cycleFlow Cytometry3-ABE2F Transcription FactorsChromatinDNA-Binding ProteinsGene Expression RegulationDifferentiationBenzamidesbiology.proteinCancer researchTranscription FactorsFEBS Letters
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Dynamics of complement activation in aHUS and how to monitor eculizumab therapy.

2014

Atypical hemolytic-uremic syndrome (aHUS) is associated with genetic complement abnormalities/anti–complement factor H antibodies, which paved the way to treatment with eculizumab. We studied 44 aHUS patients and their relatives to (1) test new assays of complement activation, (2) verify whether such abnormality occurs also in unaffected mutation carriers, and (3) search for a tool for eculizumab titration. An abnormal circulating complement profile (low C3, high C5a, or SC5b-9) was found in 47% to 64% of patients, irrespective of disease phase. Acute aHUS serum, but not serum from remission, caused wider C3 and C5b-9 deposits than control serum on unstimulated human microvascular endotheli…

MaleTime FactorsClinical Trials and ObservationsComplement Membrane Attack Complexurologic and male genital diseasesBiochemistryGlomerulonephritisInside BLOOD Commentaryhemic and lymphatic diseasesMembranoproliferative glomerulonephritisMonoclonalHumanizedComplement ActivationAtypical Hemolytic Uremic SyndromeEndothelial CellHematologyRemission Inductionfood and beveragesHematologyComplement C3Eculizumabmedicine.anatomical_structureFactor HFemalecomplementaHUS eculizumabmedicine.drugMembranoproliferativeHumanmedicine.medical_specialtyEndotheliumMonitoringTime FactorGlomerulonephritis MembranoproliferativeImmunologyBiologyAntibodies Monoclonal HumanizedAntibodiesInternal medicineAtypical hemolytic uremic syndromemedicineHumansPhysiologicMonitoring PhysiologicAdenosine Diphosphate RiboseEndothelial CellsCell Biologymedicine.diseaseComplement systemImmunologyAdenosine Diphosphate Ribose; Antibodies Monoclonal Humanized; Atypical Hemolytic Uremic Syndrome; Complement Activation; Complement C3; Complement Membrane Attack Complex; Endothelial Cells; Female; Glomerulonephritis Membranoproliferative; Hemolytic-Uremic Syndrome; Humans; Male; Remission Induction; Time Factors; Monitoring Physiologic; Hematology; Biochemistry; Cell Biology; ImmunologyHemolytic-Uremic SyndromeComplement membrane attack complexBlood
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Presence of phosphorylatedO-ribosyl-adenosine In T-ψ-stem of yeast methlonine initiator tRNA

1989

We report in this paper on isolation and characterization of two unknown nucleosides G* and [A*] located in the T-psi-stem of yeast methionine initiator tRNA, using the combined means of HPLC protocols, real time UV-absorption spectrum, and post-run mass spectrometry by electron impact or fast atom bombardment. The G* nucleoside in position 65 was identified as unmodified guanosine. The structure of the unknown [A*] in position 64 was characterized as an isomeric form of O-ribosyl-adenosine by comparison of its chromatographic, UV-spectral and mass spectrometric properties with those of authentic O-alpha-ribofuranosyl-(1"----2')-adenosine isolated from biosynthetic poly(adenosine diphosphat…

Poly Adenosine Diphosphate RiboseAdenosineRNA Transfer MetIon chromatographySaccharomyces cerevisiaeGuanosineSaccharomyces cerevisiaeBiologyChromatography DEAE-CelluloseGas Chromatography-Mass Spectrometrychemistry.chemical_compoundMethionineGeneticsmedicinePhosphorylationChromatography High Pressure LiquidGuanosineAdenosine diphosphate riboseNucleosidesRNA Transfer Amino Acid-SpecificFast atom bombardmentbiology.organism_classificationAdenosineYeastchemistryBiochemistryNucleic Acid ConformationNucleosidemedicine.drugNucleic Acids Research
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Poly-ADP-Ribose (PAR) as an epigenetic flag

2009

Epigenetics is the study of hereditable chromatin modifications, such as DNA methylation, histone modifications, and nucleosome-remodelling, which occur without alterations to the DNA sequence. The establishment of different epigenetic states in eukaryotes depends on regulatory mechanisms that induce structural changes in chromatin in response to environmental and cellular cues. Two classes of enzymes modulate chromatin accessibility: chromatin-covalent modifiers and ATP-dependent chromatin remodelling complexes. The first class of enzymes catalyzes covalent modifications of DNA as well as the amino- and carboxy-terminal tails of histones, while the second uses the energy of ATP hydrolysis …

Poly Adenosine Diphosphate RiboseCancer ResearchHistone-modifying enzymesEpigenetic regulation of neurogenesisDNA MethylationBiologyChromatin Assembly and DisassemblyChromatin remodelingEpigenesis GeneticChromatinHistonesEpigenetics of physical exerciseBiochemistryHistone methylationAnimalsHumansHistone codePARP epigeneticsPoly(ADP-ribose) PolymerasesMolecular BiologyEpigenomicsEpigenetics
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The nucleosome-remodeling ATPase ISWI is regulated by poly-ADP-ribosylation.

2008

ATP-dependent nucleosome-remodeling enzymes and covalent modifiers of chromatin set the functional state of chromatin. However, how these enzymatic activities are coordinated in the nucleus is largely unknown. We found that the evolutionary conserved nucleosome-remodeling ATPase ISWI and the poly-ADP-ribose polymerase PARP genetically interact. We present evidence showing that ISWI is target of poly-ADP-ribosylation. Poly-ADP-ribosylation counteracts ISWI function in vitro and in vivo. Our work suggests that ISWI is a physiological target of PARP and that poly-ADP-ribosylation can be a new, important post-translational modification regulating the activity of ATP-dependent nucleosome remodel…

Poly Adenosine Diphosphate RiboseImmunoprecipitationQH301-705.5Poly ADP ribose polymeraseATPaseBlotting WesternBiochemistryChromosomesGeneral Biochemistry Genetics and Molecular BiologySettore BIO/10 - BiochimicaAnimalsDrosophila ProteinsImmunoprecipitationNucleosomeBiology (General)Transcription factorIn Situ Hybridization FluorescencePolymeraseAdenosine TriphosphatasesGeneral Immunology and MicrobiologybiologyGeneral NeuroscienceGenetics and GenomicsPARP ISWI Poly(ADP)ribosylation Chromatin remodellingCell BiologyChromatinISWI PARPNucleosomesChromatinSettore BIO/18 - GeneticaDrosophila melanogasterBiochemistrybiology.proteinPoly(ADP-ribose) PolymerasesGeneral Agricultural and Biological SciencesFunction (biology)Transcription FactorsResearch ArticlePLoS Biology
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Alteration of poly (ADP-Rib) synthesis during progesterone- caused gene expression in oviducts of quails.

1976

Summary The biological model of the selective induction of RNA synthesis in oviducts of estrogen stimulated immature quails by progesterone has been used to clarify whether poly (ADP-Rib) is involved in DNA transcription. The chromatin-bound as well as the soluble poly (ADP-Rib) polymerase has been isolated from oviducts and the optimal reaction conditions have been determined. The activities, as measured by the incorporation rates of NAD + into poly (ADP-Rib), of both, chromatin-bound « endogenouspolymerase (in the absence of « exogenousDNA and histones) and soluble enzyme (native DNA - lysine-rich histone ratio: 4.3) from progesterone treated quail oviducts, have been determined to be onl…

Poly Adenosine Diphosphate Riboseanimal structuresTime FactorsMuscle ProteinsCoturnixOviductsBiochemistryHistoneschemistry.chemical_compoundNAD+ NucleosidaseGene expressionAnimalsDiethylstilbestrolPolymeraseProgesteronechemistry.chemical_classificationCell NucleusbiologyNucleoside Diphosphate SugarsGeneral MedicineAvidinMolecular biologyEnzyme assayKineticsEnzymeHistonechemistrybiology.proteinOviductFemaleNAD+ kinaseDNABiochimie
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Rho protein inactivation induced apoptosis of cultured human endothelial cells.

2002

Small GTP-binding Rho GTPases regulate important signaling pathways in endothelial cells, but little is known about their role in endothelial cell apoptosis. Clostridial cytotoxins specifically inactivate GTPases by glucosylation [ Clostridium difficile toxin B-10463 (TcdB-10463), C. difficile toxin B-1470 (TcdB-1470)] or ADP ribosylation ( C. botulinum C3 toxin). Exposure of human umbilical cord vein endothelial cells (HUVEC) to TcdB-10463, which inhibits RhoA/Rac1/Cdc42, or to C3 toxin, which inhibits RhoA, -B, -C, resulted in apoptosis, whereas inactivation of Rac1/Cdc42 with TcdB-1470 was without effect, suggesting that Rho inhibition was responsible for endothelial apoptosis. Disruptio…

Pulmonary and Respiratory Medicinerac1 GTP-Binding Proteinrho GTP-Binding ProteinsProgrammed cell deathUmbilical VeinsEndotheliumPhysiologyBacterial ToxinsCASP8 and FADD-Like Apoptosis Regulating ProteinApoptosisBcl-2-associated X proteinBacterial ProteinsPhysiology (medical)Proto-Oncogene ProteinsmedicineCyclic AMPIn Situ Nick-End LabelingHumanscdc42 GTP-Binding ProteinCells Culturedbcl-2-Associated X ProteinAdenosine Diphosphate RibosebiologyCaspase 3Intracellular Signaling Peptides and ProteinsCell BiologyCaspase 9Cell biologyNeoplasm ProteinsEndothelial stem cellmedicine.anatomical_structureCdc42 GTP-Binding ProteinProto-Oncogene Proteins c-bcl-2Cell cultureApoptosisCaspasesbiology.proteinMyeloid Cell Leukemia Sequence 1 ProteinEndothelium VascularSignal transductionCarrier ProteinsrhoA GTP-Binding ProteinBH3 Interacting Domain Death Agonist ProteinSignal TransductionAmerican journal of physiology. Lung cellular and molecular physiology
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