Search results for " enzymes"

showing 10 items of 240 documents

MGMT activity, promoter methylation and immunohistochemistry of pretreatment and recurrent malignant gliomas: a comparative study on astrocytoma and …

2010

The DNA repair protein O(6)-methylguanine-DNA methyltransferase (MGMT) is a key player in tumor cell resistance. Promoter methylation, MGMT activity and immunohistochemistry are used for determining the MGMT status. However, it is unclear whether MGMT promoter methylation correlates with MGMT activity and whether MGMT promoter methylation of the pretreatment tumor predicts the MGMT status of recurrences. To address these questions, we determined MGMT activity promoter methylation and immunoreactivity in pretreatment and recurrent glioblastomas (GB, WHO Grade IV), and in astrocytomas (WHO Grade III). We show that GB that were promoter methylated display a range of 0-62 fmol/mg MGMT and tumor…

Cancer Researchmedicine.medical_specialtyPathologyMethyltransferaseDNA repairAstrocytomaBiologyRecurrenceCell Line TumormedicineHumansPromoter Regions GeneticDNA Modification MethylasesneoplasmsBrain NeoplasmsTumor Suppressor ProteinsAstrocytomaCancerAnatomical pathologyBiological activityMethylationDNA Methylationmedicine.diseaseImmunohistochemistrydigestive system diseasesDNA Repair EnzymesOncologyCancer researchImmunohistochemistryGlioblastomaInternational Journal of Cancer
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Novel Approaches for Glioblastoma Treatment: Focus on Tumor Heterogeneity, Treatment Resistance, and Computational Tools

2019

BACKGROUND: Glioblastoma (GBM) is a highly aggressive primary brain tumor. Currently, the suggested line of action is the surgical resection followed by radiotherapy and treatment with the adjuvant temozolomide (TMZ), a DNA alkylating agent. However, the ability of tumor cells to deeply infiltrate the surrounding tissue makes complete resection quite impossible, and in consequence, the probability of tumor recurrence is high, and the prognosis is not positive. GBM is highly heterogeneous and adapts to treatment in most individuals. Nevertheless, these mechanisms of adaption are unknown. RECENT FINDINGS: In this review, we will discuss the recent discoveries in molecular and cellular heterog…

Cancer Researchmedicine.medical_treatmentDNA Mutational AnalysisBrain tumorBioinformaticsComplete resectionTumor heterogeneityCancer VaccinesMicrotubulesArticleClonal EvolutionMachine LearningGenetic HeterogeneityCancer stem cellAntineoplastic Combined Chemotherapy ProtocolsTumor MicroenvironmentMedicineHumansTreatment resistancePrecision MedicineDNA Modification MethylasesImmune Checkpoint InhibitorsTemozolomideModels Geneticbusiness.industryBrain NeoplasmsTumor Suppressor ProteinsBrainComputational BiologyChemoradiotherapy Adjuvantmedicine.diseasePrognosisRadiation therapyDNA Repair EnzymesOncologyDrug Resistance NeoplasmMutationTumor Suppressor Protein p53businessGlioblastomaGlioblastomamedicine.drug
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Fetuin-A and Cystatin C Are Endogenous Inhibitors of Human Meprin Metalloproteases

2010

Meprin α and β, zinc metalloproteinases, play significant roles in inflammation, including inflammatory bowel disease (IBD), possibly by activating cytokines, like interleukin 1β, interleukin 18, or tumor growth factor α. Although a number of potential activators for meprins are known, no endogenous inhibitors have been identified. In this work, we analyzed the inhibitory potential of human plasma and identified bovine fetuin-A as an endogenous meprin inhibitor with a K(i) (inhibition constant) of 4.2 × 10(-5) M for meprin α and a K(i) of 1.1 × 10(-6) M meprin β. This correlated with data obtained for a fetuin-A homologue from carp (nephrosin inhibitor) that revealed a potent meprin α and β…

Carpsalpha-2-HS-GlycoproteinMolecular Sequence DataMatrix metalloproteinaseBiochemistryPlasma03 medical and health sciencesmedicineAnimalsHumansAmino Acid SequenceCystatin C030304 developmental biology0303 health sciencesMetalloproteinasebiology030302 biochemistry & molecular biologyProteolytic enzymesMetalloendopeptidasesBlood ProteinsTrypsinFetuinProtease inhibitor (biology)3. Good healthBiochemistryCystatin Cbiology.proteinCattleCystatinSequence Alignmentmedicine.drugBiochemistry
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Shed membrane vesicles and clustering of membrane-bound proteolytic enzymes

2003

Publisher Summary Eukaryotic cells appear to release into the extracellular medium several populations of exovesicles, which are suggested to have different origins and functions and are identified by different names. This chapter deals with vesicles believed to originate from the cell membrane and named membrane vesicles. These are structures in which membrane-bound proteolytic enzymes are clustered and they play important roles in matrix remodeling. Relatively large membrane vesicles (diameters ranging from 100 nm to 1 μm) are shed from plasma membranes through unidentified budding mechanisms. These membrane structures are enriched in selected plasma-membrane components including integrin…

Cell membraneCell signalingmedicine.anatomical_structureVesicleCellIntegrinExtracellularmedicinebiology.proteinProteolytic enzymesBiologyMicrovesiclesCell biology
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Exercise and antioxidant supplements in the elderly

2013

Abstract Both exercise and aging increase reactive oxygen species (ROS), which can result in damage to cells. Aging is the result of damage caused by ROS to the mitochondrial genome in post mitotic cells and numerous studies have demonstrated an increase in ROS or their byproducts with exercise. ROS can cause oxidative stress as they overwhelm the antioxidant cellular defenses. Therefore interventions aimed at limiting or inhibiting ROS production, such as supplementation with antioxidant vitamins, should be able to reduce fatigue during muscle contraction and the rate of formation of aging changes with a consequent reduction of the aging rate and disease pathogenesis. However, it has been …

Cell signalingAgingAntioxidantmedicine.medical_treatmentmedia_common.quotation_subjectPopulationPGC-1αSkeletal musclePhysical Therapy Sports Therapy and RehabilitationPharmacologyBiologymedicine.disease_causeNF-κBchemistry.chemical_compoundmedicineOrthopedics and Sports Medicineeducationmedia_commonchemistry.chemical_classificationeducation.field_of_studyReactive oxygen speciesAdaptationsLongevitySkeletal muscleNF-κBmedicine.anatomical_structurechemistryBiochemistryOxidative stressAntioxidant enzymesOxidative stressJournal of Sport and Health Science
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Lafora disease fibroblasts exemplify the molecular interdependence between thioredoxin 1 and the proteasome in mammalian cells

2013

13 páginas, 8 figuras (que no aparecen en este documento, se pueden consultar en: http://www.sciencedirect.com/science/article/pii/S0891584913003274#ec0005)

Cell signalingProteasome Endopeptidase ComplexBlotting WesternFree radicalsBiologyBiochemistryLafora diseaseThioredoxin 1MiceThioredoxinsPhysiology (medical)medicineAnimalsHumansImmunoprecipitationLafora diseaseEndoplasmic Reticulum Chaperone BiPCell proliferationMicroscopy ConfocalProteasomeReverse Transcriptase Polymerase Chain ReactionEndoplasmic reticulumCell cycleFibroblastsSubcellular localizationmedicine.diseaseFlow CytometryCell biologyRare diseasesCytosolOxidative StressBiochemistryProteasomeLafora DiseaseUnfolded protein responseNIH 3T3 CellsAntioxidant enzymesOxidation-Reduction
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Pyridinedicarboxylates, the first mechanism-derived inhibitors for prolyl 4-hydroxylase, selectively suppress cellular hydroxyprolyl biosynthesis. De…

1987

Two pyridinedicarboxylates, predicted [Hanauske-Abel (1983) M.D.-Ph.D. Thesis, Philipps Universität Marburg] and later found to be potent reversible inhibitors of purified prolyl 4-hydroxylase [Majaama, Hanauske-Abel, Günzler & Kivirikko (1984) Eur. J. Biochem. 138, 239-245] were investigated with respect to their effect on hydroxyprolyl biosynthesis in the fibroblast/collagen and the macrophage/Clq systems, and the effect was compared with that of the iron chelator 2,2′-dipyridyl, the compound usually employed to inhibit cellular hydroxyprolyl formation. Only the enzyme-mechanism-derived pyridinedicarboxylates were highly selective inhibitors, and only they lacked overt cytotoxicity. M…

Cell typeCell SurvivalComplement Activating EnzymesGuinea PigsProcollagen-Proline DioxygenaseBiologyBiochemistrychemistry.chemical_compoundBiosynthesisComplement C1In vivomedicineAnimalsHumansSecretionPicolinic AcidsFibroblastCytotoxicityMolecular BiologyCells CulturedDose-Response Relationship DrugComplement C1qEndoplasmic reticulumCell BiologyFibroblastsHydroxyprolineMicroscopy Electronmedicine.anatomical_structureBiochemistrychemistryLipophilicityCollagenResearch ArticleBiochemical Journal
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Design of enzyme-mediated controlled release systems based on silica mesoporous supports capped with ester-glycol groups

2012

[EN] An ethylene glycol-capped hybrid material for the controlled release of molecules in the presence of esterase enzyme has been prepared. The final organic-inorganic hybrid solid S1 was synthesized by a two-step procedure. In the first step, the pores of an inorganic MCM-41 support (in the form of nanoparticles) were loaded with [Ru(bipy) 3]Cl 2 complex, and then, in the second step, the pore outlets were functionalized with ester glycol moieties that acted as molecular caps. In the absence of an enzyme, release of the complex from aqueous suspensions of S1 at pH 8.0 is inhibited due to the steric hindrance imposed by the bulky ester glycol moieties. Upon addition of esterase enzyme, del…

Cell viabilityINGENIERIA DE LA CONSTRUCCIONEthyleneRuthenium complexesMCM-41 supportsCytotoxicityGlycol derivativesEsteraseFunctionalizedOrganic-inorganic hybrid solidsGlycolschemistry.chemical_compoundQUIMICA ORGANICATumor Cells CulturedElectrochemistryControlled release systemsOrganic chemistryControlled releaseGeneral Materials ScienceSteric hindrancesMCF-7 cellsSpectroscopyHydrolysisEsterasesSilicaEstersSurfaces and InterfacesSilicon DioxideCondensed Matter PhysicsControlled releaseChlorine compoundsEster bondsBody fluidsHybrid materialsHybrid materialPorosityCell deathCell SurvivalSurface PropertiesCytotoxic drugsRutheniumHydrolysisEnzymatic hydrolysisEsterase enzymesPolymer chemistryHumansCamptothecin (CPT)Molecular capSize reductionsTherapeutic ApplicationEthylene glycolTwo-step procedureEsterificationSuspensions (fluids)Ruthenium compoundsQUIMICA INORGANICAMesoporous supportOligo(ethylene glycol)Cell internalizationMolecular gatesConfocal microscopychemistryEnzymatic hydrolysisEnzyme-mediated hydrolysisNanoparticlesCamptothecinCell cultureMesoporous materialAqueous suspensionsEthylene glycolHeLa Cells
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Autolysis of Yeasts

2011

Autolysis of yeast cells occurs after they have completed their life cycle and entered the death phase. It is characterized by a loss of cell membrane permeability, alteration of cell wall porosity, hydrolysis of cellular macromolecules by endogenous enzymes, and subsequent leakage of the breakdown products into the extracellular environment. Although a naturally occurring event, autolysis can be induced by exposing yeasts to elevated temperatures (40–60 °C), organic solvents, or detergents. Yeast autolysis occurs in many foods and beverages, where it may affect their sensory quality and commercial acceptability.

Cell wallHydrolysisAutolysis (biology)Cell membrane permeabilitymedicine.diagnostic_testBiochemistryProteolysisEndogenous enzymesmedicineExtracellularFood scienceBiologyYeast
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Effect of EDTA and citrate on the functional activity of the first component of complement, C1, and the C1q subcomponent.

1985

The first component of complement, C1, is a calcium-dependent complex of the three distinct subcomponents, C1q, C1r, and C1s. Earlier observations revealed that treatment of C1 with EDTA led to a loss of hemolytic C1 activity even after recalcification. Therefore, it was of interest to study whether EDTA has an additional effect on C1 and its subcomponents, beside its chelating capacity. The chelating effect of EDTA was compared to that of citrate. It was found that treatment of C1 or C1 with EDTA followed by addition of Ca++ led to a loss of hemolytic activity up to 90%, depending on EDTA concentration. Even pretreatment of EDTA with varying amounts of Ca++ did not prevent the inactivation…

Chemical PhenomenaComplement Activating EnzymesMacromolecular SubstancesImmunologyKineticschemistry.chemical_elementCalciumHemolysisDissociation (chemistry)Structure-Activity RelationshipComplement C1medicineImmunology and AllergyStructure–activity relationshipHumansChelationCitratesComplement C1qEdetic AcidComplement C1qHematologymedicine.diseaseHemolysisChemistryKineticsBiochemistrychemistryEdetic AcidCalciumImmunobiology
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