Search results for "Amy"

showing 10 items of 1486 documents

Inhibition of the hydrolytic and transpeptidase activities of rat kidney gamma-glutamyl transpeptidase by specific monoclonal antibodies

1999

Monoclonal antibodies (mAb) against the native form of rat kidney gamma-glutamyl transpeptidase (GGT) were isolated by screening hybridomas with rat kidney brush-border membrane vesicles. They were directed against protein rather than sugar epitopes in that each recognized all GGT isoforms. All of them inhibited partially the enzyme activity of GGT. They were specific in that they inhibited the rat enzyme, but not the mouse or human enzyme. Kinetic analyses were carried out with free GGT and GGT-mAb complexes with d-gamma-glutamyl-p-nitroanilide in the presence or absence of maleate, or in the presence or absence of alanine, cysteine, cystine or glycylglycine as gamma-glutamyl acceptors. mA…

CarbohydratesCystineKidneydigestive systemBiochemistryGlutaminase activityEpitopeMicechemistry.chemical_compoundGlutaminaseAnimalsHumansRats WistarAcivicinchemistry.chemical_classificationMice Inbred BALB CbiologyChemistryGlutaminaseHydrolysisAntibodies Monoclonalgamma-GlutamyltransferaseMolecular biologydigestive system diseasesEnzyme assayRatsIsoenzymesEnzymeBiochemistrybiology.proteinFemaleCysteineEuropean Journal of Biochemistry
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Markers of Inflammation and Infection Influence the Outcome of Patients With Baseline Asymptomatic Carotid Lesions

2005

Background and Purpose— It is still in debate whether the evaluation of markers of infection and inflammation may be of importance for cerebrovascular and cardiovascular prevention, and we aimed to investigate this field in a prospective 5-year clinical follow-up study in patients with early stages of atherosclerosis. Methods— We studied 668 subjects divided in 3 groups according to the results of carotid ultrasound examination: (1) normal subjects, if intima-media thickness (IMT) was <0.9 mm; (2) with IMT, if IMT was between 0.9 and 1.5 mm; and (3) with asymptomatic carotid plaque, if IMT was >1.5 mm. Traditional cardiovascular risk factors were investigated, and laboratory analysis…

Carotid Artery DiseasesMalePathologyTime FactorsCytomegalovirusFibrinogenCardiovascular SystematherosclerosiRisk FactorsStrokeUltrasonographyChlamydiabiologyChlamydophila pneumoniaeMiddle AgedLipidsEchocardiography DopplerStrokeC-Reactive ProteinCarotid ArteriesCardiovascular DiseasesDisease ProgressionFemalemedicine.symptomTunica MediaCardiology and Cardiovascular Medicinemedicine.drugmedicine.medical_specialtyCongenital cytomegalovirus infectionInfectionsAsymptomaticCentral nervous system diseaseSex FactorsInternal medicinemedicineHumanscarotid arterieAgedAdvanced and Specialized NursingAnalysis of VarianceHelicobacter pyloriVascular diseasebusiness.industryFibrinogenHelicobacter pyloriAtherosclerosisbiology.organism_classificationmedicine.diseaseinfectioninflammationImmunoglobulin GNeurology (clinical)Tunica IntimabusinessFollow-Up StudiesStroke
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Impact of infectious burden on progression of carotid atherosclerosis.

2002

Background and Purpose— Recent findings suggest a causative role of infections in the pathogenesis of atherosclerosis. The extent of atherosclerosis and the prognosis of patients with atherosclerosis seem to be increased by the number of infections to which an individual has been exposed. In a prospective study, we evaluated the effect of 8 pathogens and the aggregate pathogen burden on the progression of carotid atherosclerosis. Methods— In 504 patients (74.9% men; age, 62.9±10 years), we measured intima-media thickness and prevalence of carotid artery stenosis. Follow-up measurements after a mean of 2.5 years were available in 427 patients (85%). Blood samples were taken, and IgG or IgA …

Carotid Artery DiseasesMalemedicine.medical_specialtyMycoplasma pneumoniaePathologyEpstein-Barr Virus InfectionsStatinHaemophilus Infectionsmedicine.drug_classComorbiditymedicine.disease_causeAntibodies ViralInfectionsGastroenterologyVirusHelicobacter InfectionsSeroepidemiologic StudiesInternal medicineGermanymedicineOdds RatioPrevalenceHumansMycoplasma InfectionsProspective StudiesProspective cohort studyChlamydophila InfectionsUltrasonographyAdvanced and Specialized NursingChlamydiaVascular diseasebusiness.industryHerpes SimplexOdds ratioMiddle Agedmedicine.diseaseAntibodies BacterialImmunoglobulin AHerpes simplex virusCarotid ArteriesImmunoglobulin GCytomegalovirus InfectionsDisease ProgressionFemaleNeurology (clinical)Cardiology and Cardiovascular MedicinebusinessTunica IntimaTunica MediaStroke
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Characterization of fusion from without induced by herpes simplex virus

1991

The process of fusion from without (FFWO) induced by herpes simplex virus (HSV) was analyzed by using various inhibitors and compared to fusion from within (FFWI). The fate of certain elements of the cytoskeleton after FFWO was also investigated. Our experiments demonstrate FFWO as a very suitable system for study of early virus-cell interactions. Zn++ ions proved inhibitory for penetration whilst pretreatment of cells with Ca++ ions before infection enhanced FFWO activity. Dissociation of penetration from the fusion process itself was possible by use of Zn++ ions, low pH-treatment and antiserum on the one hand and N-ethylmaleimide and cytochalasin D on the other. Penetration itself needs o…

Cations DivalentCycloheximideBiologyVirusCell FusionCell membranechemistry.chemical_compoundSpecies SpecificityLectinsVirologymedicineAnimalsSimplexvirusProtease InhibitorsVero CellsCytoskeletonPolysaccharide-LyasesCytochalasin DCell fusionCell MembraneLipid bilayer fusionGeneral MedicineTunicamycinLipidsVirologymedicine.anatomical_structurechemistryEthylmaleimideVero cellReceptors VirusGlycoconjugatesArchives of Virology
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Reversible stress-induced lipid body formation in fast twitch rat myofibers

2012

We analyzed the existence of lipid bodies (LBs) in the fast twitch rat flexor digitorum brevis (FDB) myofibers and found that these structures were scarce. However, isolation procedure of the myofibers, heath shock, viral infection or the glycosylation inhibitor tunicamycin induced formation of the LBs, which were stationary structures flanking Z lines. We next infected FDB myofibers with recombinant Semliki Forest virus expressing caveolin 3-yellow fluorescent protein (cav3-YFP) since this chimeric protein was targeted to the LBs facilitating their further analysis. Photobleaching experiments showed that the LBs recovered cav 3-YFP extremely slowly, indicating that they were not continuous…

Caveolin 3Blotting WesternGolgi ApparatusBiologyEndoplasmic ReticulumSemliki Forest virusRats Sprague-Dawleychemistry.chemical_compoundSarcolemmaBacterial ProteinsAnimalsCells CulturedSarcolemmaLipogenesisEndoplasmic reticulumCell BiologyTunicamycinBrefeldin AEndoplasmic Reticulum StressLipid Metabolismmusculoskeletal systembiology.organism_classificationFusion proteinRatsCell biologyCaveolin 3Luminescent ProteinsProtein TransportSarcoplasmic ReticulumCholesterolBiochemistrychemistryMuscle Fibers Fast-TwitchVirusesUnfolded protein responseFemaleExperimental Cell Research
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Susceptibility of Pseudomonas aeruginosa isolates to ceftazidime is unrelated to the expression of the outer membrane protein OprC.

1997

Previously, it has been postulated that the porin OprC facilitates the diffusion of ceftazidime through the outer membrane of Pseudomonas aeruginosa. To further investigate this claim, the outer membrane protein (OMP) profiles of 22 ceftazidime-susceptible clinical isolates were analyzed. No correlation was found between MIC values and the level of expression of OprC. Further, OprC was either undetectable or expressed in reduced amounts in 12 isolates. In contrast, OprF and OprE were present in all isolates studied. This study suggests that OprC is dispensable for the permeation of ceftazidime through the outer membrane of P. aeruginosa.

CeftazidimePorinsmedicine.disease_causePorinaCeftazidimeMicrobiologyBacterial ProteinsDrug DiscoverymedicineHumansPharmacology (medical)Antibacterial agentPharmacologybiologyPseudomonas aeruginosaGeneral Medicinebiology.organism_classificationCephalosporinsImipenemInfectious DiseasesOncologyMembrane proteinSpainPorinPseudomonas aeruginosaThienamycinsBacterial outer membranePseudomonadaceaemedicine.drugBacterial Outer Membrane ProteinsChemotherapy
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ALS-linked FUS mutations confer loss and gain of function in the nucleus by promoting excessive formation of dysfunctional paraspeckles

2019

Mutations in the FUS gene cause amyotrophic lateral sclerosis (ALS-FUS). Mutant FUS is known to confer cytoplasmic gain of function but its effects in the nucleus are less understood. FUS is an essential component of paraspeckles, subnuclear bodies assembled on a lncRNA NEAT1. Paraspeckles may play a protective role specifically in degenerating spinal motor neurons. However it is still unknown how endogenous levels of mutant FUS would affect NEAT1/paraspeckles. Using novel cell lines with the FUS gene modified by CRISPR/Cas9 and human patient fibroblasts, we found that endogenous levels of mutant FUS cause accumulation of NEAT1 isoforms and paraspeckles. However, despite only mild cytoplasm…

Cell NucleusResearchAmyotrophic Lateral SclerosisIntranuclear Inclusion BodiesNEAT1lcsh:RC346-429Cell LineLoss of Function MutationCell Line TumorFused in sarcoma (FUS)ParaspeckleHumansProtein IsoformsRNA-Binding Protein FUSRNA Long NoncodingAmyotrophic lateral sclerosis (ALS)CRISPR-Cas Systemslcsh:Neurology. Diseases of the nervous systemActa Neuropathologica Communications
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Galantamine modulates nicotinic receptor and blocks Aβ-enhanced glutamate toxicity

2004

Galantamine is a plant alkaloid that is used in the treatment of Alzheimer's disease. We have studied the effects of galantamine on beta-amyloid-enhanced glutamate toxicity using primary rat cultured cortical neurons. Nicotine and galantamine alone, and in combination, protected neurons against this neurotoxicity. The protection was not blocked by alpha4beta2 nicotinic acetylcholine receptor (nAChR) antagonists, but was partially blocked by alpha7 nAChR antagonists. Galantamine induced phosphorylation of Akt, an effector of phosphatidylinositol 3-kinase (PI3K), while PI3K inhibitors blocked the protective effect and Akt phosphorylation. The antibody FK1, which selectively blocks the alloste…

Cell SurvivalBiophysicsGlutamic AcidReceptors NicotinicPharmacologycomplex mixturesBiochemistryNeuroprotectionmedicineGalantamineAnimalsDrug InteractionsMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayCerebral CortexNeuronsAmyloid beta-PeptidesDose-Response Relationship DrugGalantamineChemistryGlutamate receptorNeurotoxicityCell Biologymedicine.diseaseRatsNeuroprotective AgentsNicotinic agonistnervous systemPhosphorylationmedicine.drugBiochemical and Biophysical Research Communications
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Geldanamycin-induced osteosarcoma cell death is associated with hyperacetylation and loss of mitochondrial pool of heat shock protein 60 (hsp60)

2013

Osteosarcoma is one of the most malignant tumors of childhood and adolescence that is often resistant to standard chemo- and radio-therapy. Geldanamycin and geldanamycin analogs have been recently studied as potential anticancer agents for osteosarcoma treatment. Here, for the first time, we have presented novel anticancer mechanisms of geldanamycin biological activity. Moreover, we demonstrated an association between the effects of geldanamycin on the major heat shock proteins (HSPs) and the overall survival of highly metastatic human osteosarcoma 143B cells. We demonstrated that the treatment of 143B cells with geldanamycin caused a subsequent upregulation of cytoplasmic Hsp90 and Hsp70 w…

Cell SurvivalLactams Macrocycliclcsh:MedicineApoptosisBone NeoplasmsBiologyMitochondrionMitochondrial Proteinschemistry.chemical_compoundGeldanamycin Hsp60 Osteosarcoma cellHeat shock proteinCell Line Tumorpolycyclic compoundsBenzoquinonesHumansHeat shocklcsh:ScienceCell ProliferationOsteosarcomaMultidisciplinaryAntibiotics Antineoplasticlcsh:RAcetylationChaperonin 60GeldanamycinHsp90Molecular biologyMitochondriaProtein TransportchemistryCancer cellCancer researchbiology.proteinApoptotic signaling pathwayHSP60lcsh:QDrug Screening Assays AntitumorProtein Processing Post-TranslationalResearch ArticleSignal Transduction
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Inhibitors of Rho-kinase modulate amyloid-β (Aβ) secretion but lack selectivity for Aβ42

2005

Certain non-steroidal anti-inflammatory drugs (NSAIDs) preferentially inhibit production of the amyloidogenic Abeta42 peptide, presumably by direct modulation of gamma-secretase activity. A recent report indicated that NSAIDs could reduce Abeta42 by inhibition of the small GTPase Rho, and a single inhibitor of Rho kinase (ROCK) mimicked the effects of Abeta42-lowering NSAIDs. To investigate whether Abeta42 reduction is a common property of ROCK inhibitors, we tested commercially available compounds in cell lines that were previously used to demonstrate the Abeta42-lowering activity of NSAIDs. Surprisingly, we found that two ROCK inhibitors reduced total Abeta secretion in a dose-dependent m…

Cell SurvivalMutantPeptideCHO CellsProtein Serine-Threonine KinasesPharmacologyBiochemistryAmyloid beta-Protein PrecursorCellular and Molecular NeuroscienceCricetulusCricetinaeEndopeptidasesmental disordersAmyloid precursor proteinAnimalsAspartic Acid EndopeptidasesSecretionSmall GTPaseEnzyme InhibitorsRho-associated protein kinasechemistry.chemical_classificationrho-Associated KinasesAmyloid beta-PeptidesbiologyAnti-Inflammatory Agents Non-SteroidalIntracellular Signaling Peptides and ProteinsIn vitro toxicologyProtein-Tyrosine KinasesPeptide Fragmentsnervous system diseasesBiochemistrychemistrybiology.proteinAmyloid Precursor Protein SecretasesSelectivityProtein Processing Post-TranslationalJournal of Neurochemistry
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