Search results for "Transferase"

showing 10 items of 1030 documents

Catechol-O-Methyltransferase (COMT) Val158Met Polymorphism and Eating Disorders: Data From a New Biobank and Meta-Analysis of Previously Published St…

2017

Objectives: We investigated whether catechol-O-methyltransferase (COMT) Val158Met polymorphism is associated with eating disorders (EDs). Methods: We conducted a systematic literature search of studies published until 15 January 2017 and added data from the Italian ‘Biobanca Veneta per i Disturbi Alimentari’ biobank, performing a meta-analysis comparing COMT Val158Met genotype and allele frequencies in EDs and anorexia nervosa (AN) or bulimia nervosa (BN) patients versus controls. Results: Ten studies plus Biobanca Veneta per i Disturbi Alimentari (ED: n = 920, controls: n = 261 controls) with 3541 ED patients (AN = 2388; BN = 233) and 3684 controls were included. There were no significant …

Anorexia NervosaGenotypeVal158MetCatechol O-MethyltransferasePolymorphism Single Nucleotidecatechol-O-methyltransferase (COMT)polymorphismFeeding and Eating DisordersGene FrequencyCase-Control Studiesmental disordersJournal ArticleHumansBulimia NervosaVal158Met; anorexia nervosa; bulimia nervosa; catechol-O-methyltransferase (COMT); polymorphismBiological Specimen BanksEuropean eating disorders review : the journal of the Eating Disorders Association
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Isolation and characterization of Saccharomyces cerevisiae mutants resistant to aculeacin A

1991

Aculeacin A is a lipopeptide that inhibits beta-glucan synthesis in yeasts. A number of Saccharomyces cerevisiae mutants resistant to this antibiotic were isolated, and four loci (ACR1, ACR2, ACR3, and ACR4) whose products are involved in the sensitivity to aculeacin A of yeast cells were defined. Mutants containing mutations in the four loci were also resistant to echinocandin B, another member of this lipopeptide family of antibiotics. In contrast, acr1, acr3, and acr4 mutants were resistant to papulacandin B (an antibiotic containing a disaccharide linked to two fatty acid chains that also inhibits beta-glucan synthesis), but acr2 mutants were susceptible to this antibiotic. This result …

Antifungal AgentsLlevat de cervesaGenotypeMutantSaccharomyces cerevisiaePapulacandin BSaccharomyces cerevisiaemedicine.disease_causePeptides CyclicMicrobiologyFungal ProteinsEchinocandinschemistry.chemical_compoundCell WallEchinocandin BmedicinePharmacology (medical)PharmacologyFungal proteinMutationbiologyMutagenicity TestsMembrane ProteinsLipopeptideAminoglicòsidbiology.organism_classificationYeastAnti-Bacterial AgentsAminoglucòsidsAminoglycosidesInfectious DiseaseschemistryBiochemistryGlucosyltransferasesMutationSchizosaccharomyces pombe ProteinsPeptidesResearch Article
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The DNA methylation inhibitor 5-azacytidine modulates 6-thioguanine toxicity in mammalian cells

2003

In order to assess the effects of combining two antimetabolites used separately to treat human leukemias, we carried out an experimental study by exposing V79 Chinese hamster cells, a 6-thioguanine (6-tG)-sensitive cell line, to sequential and concurrent treatments with 5-azacytidine (5-azaC) and 6-tG. In this paper, we demonstrate that there is a clear dependency for the way in which this combination was tested. Pre-treatment with 5-azaC made V79 cells more resistant to 6-tG by a substantial reduction in 6-tG incorporation into DNA; this effect could still be detected for several cell divisions after the removal of 5-azaC, and was achieved neither by reduced cell growth nor by the inductio…

Antimetabolites AntineoplasticHypoxanthine Phosphoribosyltransferasemedicine.drug_classCell SurvivalCellHamsterToxicologyAntimetaboliteChinese hamster6-thioguanineCricetulus5-azacytidineCricetinaeAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsThioguanineCells CulturedbiologyCell growthtoxicityDrug SynergismGeneral MedicineDNAProdrugDNA Methylationbiology.organism_classificationMolecular biologySettore BIO/18 - Geneticamedicine.anatomical_structureBiochemistryCell cultureToxicityAzacitidineSister Chromatid ExchangeCell Division
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Glutathione metabolism in skeletal muscle derived cells of the L6 line

1993

Skeletal muscle derived L6 myoblasts possess a considerably high resting total glutathione (TGSH) pool. Exposure to L-buthionine-[S,R]-sulphoximine resulted in a 90% depletion of the intracellular TGSH pool. All the key enzymes of glutathione metabolism, especially glutathione S-transferase, were observed to be considerably active in the undifferentiated cells. Se-dependent glutathione peroxidase activity appeared to account for most of the total GSH peroxidase activity of the cells. A significant contribution of gamma-glutamyl transpeptidase-independent (5 mM acivicin insensitive) mechanism to the extracellular GSH uptake capacity of the muscle cells was evident. Efflux of oxidized glutath…

AntioxidantGPX3AntimetabolitesPhysiologymedicine.medical_treatmentGlutathione reductaseBiologyCell Linechemistry.chemical_compoundtert-ButylhydroperoxideMethionine SulfoximinemedicineAnimalsMyocyteInhibinsButhionine SulfoximineAcivicinGlutathione TransferaseMusclesSkeletal muscleGlutathioneMetabolismGlutathioneActivinsPeroxidesRatsmedicine.anatomical_structureBiochemistrychemistryEnergy MetabolismActa Physiologica Scandinavica
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Antioxidant and glutathione-related enzymatic activities in rat sciatic nerve

1990

Abstract The present work tries to establish the antioxidant capacity of the peripheral nervous tissue of the rat, in terms of the enzymatic activities present in this tissue that either prevent the formation of activated species as the semiquinone radical (DT-diaphorase), protect against activated oxygen species (superoxide dismutase, glutathione peroxidase), conjugate natural toxic products or xenobiotics (glutathione S-transferases, especially the activity conjugating 4-hydroxy-nonenal), or complete the glutathione system metabolism (glutathione disulfide reductase, γ-glutamyl transpeptidase). All the activities studied are lower in this tissue than they are in liver, except for γ-glutam…

AntioxidantGPX3medicine.medical_treatmentGlutathione reductaseToxicologyAntioxidantsSuperoxide dismutaseCellular and Molecular Neurosciencechemistry.chemical_compoundDevelopmental NeurosciencemedicineAnimalsQuinone ReductasesGlutathione Transferasechemistry.chemical_classificationGlutathione PeroxidasebiologySuperoxide DismutaseChemistryGlutathione peroxidaseNervous tissuegamma-GlutamyltransferaseGlutathioneGlutathioneSciatic NerveRatsGlutathione S-transferasemedicine.anatomical_structureBiochemistrybiology.proteinNeurotoxicology and Teratology
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Bacterial sensor kinases using Fe–S cluster binding PAS or GAF domains for O2sensing

2012

[4Fe-4S](2+) clusters are used by very diverse types of bacterial sensors for response to oxygen, including DNA-binding proteins of the CRP/FNR family and sensor kinases like NreB. In NreB the cluster is bound by an input domain of the PAS type. The [4Fe-4S](2+) cluster of NreB responds to O(2) by degradation to a [2Fe-2S](2+) cluster which is labile and decomposes. NreB constitutes together with AirS the NreB/AirS family of bacterial sensor kinases that contain PAS or GAF domains for binding of [4Fe-4S](2+) or [2Fe-2S](2+) clusters and oxygen sensing. The NreB/AirS family is related to the FixL sensor kinases that use hemeB binding PAS domains for oxygen sensing.

BacteriaKinaseStereochemistryChemistryIronOxygen metabolismMolecular Sequence DataPhosphotransferasesO2 sensingBioinformaticsProtein Structure TertiaryOxygenInorganic ChemistryProtein structureCluster (physics)Amino Acid SequencePeptide sequenceOxygen sensingSulfurDalton Trans.
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Clostridium difficile Toxins Disrupt Epithelial Barrier Function by Altering Membrane Microdomain Localization of Tight Junction Proteins

2001

ABSTRACT The anaerobic bacterium Clostridium difficile is the etiologic agent of pseudomembranous colitis. C. difficile toxins TcdA and TcdB are UDP-glucosyltransferases that monoglucosylate and thereby inactivate the Rho family of GTPases (W. P. Ciesla, Jr., and D. A. Bobak, J. Biol. Chem. 273:16021–16026, 1998). We utilized purified reference toxins of C. difficile , TcdA-10463 (TcdA) and TcdB-10463 (TcdB), and a model intestinal epithelial cell line to characterize their influence on tight-junction (TJ) organization and hence to analyze the mechanisms by which they contribute to the enhanced paracellular permeability and disease pathophysiology of pseudomembranous colitis. The increase i…

Bacterial ToxinsImmunologyClostridium difficile toxin ABiologyZonula Occludens-2 ProteinOccludinMicrobiologyCell junctionPermeabilityTight JunctionsMicrobiologyAdherens junctionEnterotoxinsMembrane MicrodomainsBacterial ProteinsIntestinal MucosaClostridioides difficileCell PolarityMembrane ProteinsPseudomembranous colitisClostridium difficilePhosphoproteinsMolecular PathogenesisActinsCell biologyInfectious DiseasesMembrane proteinGlucosyltransferasesParacellular transportZonula Occludens-1 ProteinParasitologyInfection and Immunity
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Delineation of the catalytic domain of Clostridium difficile toxin B-10463 to an enzymatically active N-terminal 467 amino acid fragment.

2006

Abstract In an attempt to directly approach the postulated toxic domain of Clostridium difficile 's TcdB-10463, eight subclones of different size and locations in the N-terminal third of the toxin were generated. Expression of these toxin fragments was checked in Western blots and the enzymatic activity of the expressed proteins was analyzed by glucosylating Ras related small GTP-binding proteins. Two polypeptides of 875 aa (TcdBc1–3) and 557 aa (TcdBc1-H) glucosylated their targets Rho, Rac and Cdc42 with the same activity and specificity as the holotoxin. In comparison 516 aa (TcdBc1-N) and 467 aa (TcdBc1-A) protein fragments exhibited highly reduced activity, while Tcdc1 and TcdB2–3 (aa …

Bacterial ToxinsMolecular Sequence DataClostridium difficile toxin Bmedicine.disease_causeMicrobiologyStructure-Activity RelationshipGTP-binding protein regulatorsClostridiumBacterial ProteinsGeneticsmedicineMolecular Biologychemistry.chemical_classificationBinding SitesbiologyBase SequenceToxinbiology.organism_classificationMolecular biologyPeptide FragmentsRecombinant ProteinsAmino acidEnzymechemistryCdc42 GTP-Binding ProteinBiochemistryGlucosyltransferasesbiology.proteinGlucosyltransferaseFEMS microbiology letters
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Evidence for a modular structure of the homologous repetitive C-terminal carbohydrate-binding sites of Clostridium difficile toxins and Streptococcus…

1992

The homologous C-terminal repeats of Clostridium difficile toxins (ToxA and ToxB) and streptococcal glucosyltransferases appear to mediate protein-carbohydrate interactions at cellular binding sites with sugar moieties as substrates. A consensus sequence of 134 repeating units from gram-positive bacteria indicates that these repeats have a modular design with (i) a stretch of aromatic amino acids proposed to be involved in the primary carbohydrate-protein interaction, (ii) an amplification of this interaction by repetition of the respective sequences, and (iii) a second domain, not characterized, that is responsible for carbohydrate specificity.

Bacterial ToxinsMolecular Sequence DataEnterotoxinMicrobiologyMicrobiologyStreptococcus mutanschemistry.chemical_compoundEnterotoxinsGlucosyltransferasesBacterial ProteinsGlycosyltransferaseConsensus SequenceConsensus sequenceAromatic amino acidsAmino Acid SequenceBinding siteMolecular BiologyPeptide sequenceBinding SitesbiologySequence Homology Amino AcidClostridioides difficileCytotoxinsClostridium difficilechemistryBiochemistryGlucosyltransferasesbiology.proteinCarbohydrate MetabolismResearch ArticleJournal of bacteriology
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The integrity of cholinergic basal forebrain neurons depends on expression of Nkx2-1

2011

The transcription factor Nkx2-1 belongs to the homeobox-encoding family of proteins that have essential functions in prenatal brain development. Nkx2-1 is required for the specification of cortical interneurons and several neuronal subtypes of the ventral forebrain. Moreover, this transcription factor is involved in migratory processes by regulating the expression of guidance molecules. Interestingly, Nkx2-1 expression was recently detected in the mouse brain at postnatal stages. Using two transgenic mouse lines that allow prenatal or postnatal cell type-specific deletion of Nkx2-1, we show that continuous expression of the transcription factor is essential for the maturation and maintenanc…

Basal forebrainNerve growth factornervous systemGeneral NeuroscienceForebrainCholinergicGABAergicCholinergic neuronBiologyCholine acetyltransferaseNeuroscienceTranscription factorEuropean Journal of Neuroscience
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