Search results for "KINASE"

showing 10 items of 2635 documents

Alkylation at the active site of the D-3-hydroxybutyrate dehydrogenase (BDH), a membrane phospholipid-dependent enzyme, by 3-chloroacetyl pyridine ad…

1997

The structure of the rat liver's D-3-hydroxybutyrate dehydrogenase (BDH) active site has been investigated using an affinity alkylating reagent, the 3-chloroacetyl pyridine adenine dinucleotide (3-CAPAD). This NAD+ analogue reagent strongly inactivates the enzyme following a concentration- and time-dependent process with a stoichiometry of approximately 1. The reagent reacts at the coenzyme binding site as revealed by the efficient protection by NADH. The effect of 3-CAPAD is stronger with the enzyme into its natural membrane environment than with the lipid-free purified apoBDH or with the reconstituted apoBDH-mitochondrial phospholipid complex. The pH-dependent effect on the inactivation p…

AlkylationStereochemistryAffinity labelMitochondria LiverDehydrogenaseBiochemistryHydroxybutyrate DehydrogenaseMembrane LipidsAnimalsCoenzyme bindingCysteineBinding sitePhospholipidsBinding SitesAffinity labelingMolecular StructurebiologyChemistryActive siteAffinity LabelsGeneral MedicineNADRatsReagentLinear Modelsbiology.proteinNAD+ kinaseBiochimie
researchProduct

Cellular stress induces cap-independent alpha-enolase/MBP-1 translation.

2015

AbstractMyc promoter-binding protein-1 (MBP-1) is a shorter protein variant of the glycolytic enzyme alpha-enolase. Although several lines of evidence indicate that MBP-1 acts as a tumor suppressor, the cellular mechanisms and signaling pathways underlying MBP-1 expression still remain largely elusive. To dissect these pathways, we used the SkBr3 breast cancer cell line and non-tumorigenic HEK293T cells ectopically overexpressing alpha-enolase/MBP-1. Here, we demonstrate that induced cell stresses promote MBP-1 expression through the AKT/PERK/eIF2α signaling axis. Our results contribute to shedding light on the molecular mechanisms underlying MBP-1 expression in non-tumorigenic and cancer c…

Alpha-enolaseCellEukaryotic Initiation Factor-2Alternative translationBiochemistryeIF-2 KinaseBreast cancerHEK293 CellStructural BiologyProtein IsoformsbiologyMedicine (all)Translation (biology)Recombinant ProteinEndoplasmic Reticulum StressRecombinant ProteinsNeoplasm ProteinsDNA-Binding ProteinsGene Expression Regulation Neoplasticmedicine.anatomical_structureFemaleSignal transductionMyc promoter-binding protein-1Breast NeoplasmHumanSignal TransductionCell SurvivalDNA-Binding ProteinRecombinant Fusion ProteinsBiophysicsBreast NeoplasmsNeoplasm ProteinGeneticCell Line TumorEndoplasmic reticulum streGeneticsmedicineBiomarkers TumorHumansGene SilencingMolecular BiologyProtein kinase BTumor Suppressor ProteinTumor Suppressor ProteinsHEK 293 cellsProtein IsoformCell BiologySettore BIO/18 - GeneticaHEK293 CellsBiophysicGene Expression RegulationPhosphopyruvate HydrataseCancer cellbiology.proteinUnfolded protein responseCancer researchProto-Oncogene Proteins c-aktRecombinant Fusion ProteinFEBS letters
researchProduct

Irreversible Inhibition of Epidermal Growth Factor Receptor Activity by 3-Aminopropanamides

2012

Irreversible epidermal growth factor receptor (EGFR) inhibitors contain a reactive warhead which covalently interacts with a conserved cysteine residue in the kinase domain. The acrylamide fragment, a commonly employed warhead, effectively alkylates Cys797 of EGFR, but its reactivity can cause rapid metabolic deactivation or nonspecific reactions with off-targets. We describe here a new series of irreversible inhibitors containing a 3-aminopropanamide linked in position 6 to 4-anilinoquinazoline or 4-anilinoquinoline-3- carbonitrile driving portions. Some of these compounds proved to be as efficient as their acrylamide analogues in inhibiting EGFR-TK (TK = tyrosine kinase) autophosphorylati…

AmideCell SurvivalEGFR inhibitorsQuinolineAntineoplastic AgentsAntineoplastic AgentStructure-Activity RelationshipT790MGefitinibCell Line TumorDrug DiscoveryPropionatemedicineHumansStructure–activity relationshipEpidermal growth factor receptorPhosphorylationAniline CompoundsbiologyChemistryDrug Discovery3003 Pharmaceutical ScienceAutophosphorylationQuinazolineAniline CompoundAmidesSettore CHIM/08 - Chimica FarmaceuticaErbB ReceptorsBiochemistryProtein kinase domainDrug Resistance NeoplasmQuinazolinesQuinolinesbiology.proteinMolecular MedicinePhosphorylationReceptor Epidermal Growth FactorPropionatesDrug Screening Assays AntitumorTyrosine kinaseHumanmedicine.drugJournal of Medicinal Chemistry
researchProduct

Activation of classical protein kinase C decreases transport via systems y+and y+L

2007

Activation of protein kinase C (PKC) downregulates the human cationic amino acid transporters hCAT-1 (SLC7A1) and hCAT-3 (SLC7A3) (Rotmann A, Strand D, Martiné U, Closs EI. J Biol Chem 279: 54185–54192, 2004; Rotmann A, Vekony N, Gassner D, Niegisch G, Strand D, Martine U, Closs EI. Biochem J 395: 117–123, 2006). However, others found that PKC increased arginine transport in various mammalian cell types, suggesting that the expression of different arginine transporters might be responsible for the opposite PKC effects. We thus investigated the consequence of PKC activation by phorbol-12-myristate-13-acetate (PMA) in various human cell lines expressing leucine-insensitive system y+[hCAT-1, h…

Amino Acid Transport System y+ArgininePhysiologyBiological Transport ActiveBiologyArginineEnzyme activatorLeucineCell Line TumorHumansRNA MessengerCationic Amino Acid TransportersProtein Kinase CProtein kinase CRegulation of gene expressionchemistry.chemical_classificationBase SequenceAmino Acid Transport System y+LCell BiologyMolecular biologyEnzyme ActivationEnzymeGene Expression RegulationchemistryTetradecanoylphorbol AcetateTetradecanoylphorbol AcetateLeucineAmerican Journal of Physiology-Cell Physiology
researchProduct

CyaC, a redox-regulated adenylate cyclase of Sinorhizobium meliloti with a quinone responsive diheme-B membrane anchor domain.

2019

The nucleotide cyclase CyaC of Sinorhizobium meliloti is a member of class III adenylate cyclases (AC), a diverse group present in all forms of life. CyaC is membrane-integral by a hexahelical membrane domain (6TM) with the basic topology of mammalian ACs. The 6TM domain of CyaC contains a tetra-histidine signature that is universally present in the membrane anchors of bacterial diheme-B succinate-quinone oxidoreductases. Heterologous expression of cyaC imparted activity for cAMP formation from ATP to Escherichia coli, whereas guanylate cyclase activity was not detectable. Detergent solubilized and purified CyaC was a diheme-B protein and carried a binuclear iron-sulfur cluster. Single poin…

Amino Acid Transport SystemsAdenylate kinasemedicine.disease_causeMicrobiologyCyclase03 medical and health sciencesmedicineBenzoquinonesNucleotideHistidineAmino Acid SequenceMolecular BiologyEscherichia coliHistidine030304 developmental biologychemistry.chemical_classification0303 health sciencesSinorhizobium melilotibiology030306 microbiologyEscherichia coli ProteinsGuanylate cyclase activityQuinonesMembrane Proteinsbiology.organism_classificationchemistryBiochemistryGenes BacterialHeterologous expressionOxidation-ReductionAdenylyl CyclasesSinorhizobium melilotiMolecular microbiology
researchProduct

Induction of apoptosis in human retinoblastoma cells by topoisomerase inhibitors

1998

PURPOSE:To examine the apoptotic effect induced in human retinoblastoma Y79 cells by camptothecin, etoposide, and amsacrine, to examine the effect of these drugs on the expression of many apoptosis-related modulators, and to test the antiapoptotic effect exerted by insulin-like growth factor-I (IGF-I). METHODS:Morphologic features of apoptosis were demonstrated using acridine orange- ethidium bromide staining and electron microscopy. DNA fragmentation was determined by means of an in situ cell detection procedure (TdT-dUTP terminal nick-end labeling [TUNEL]) or by electrophoresis on agarose gels and was quantified by enzyme-linked immunosorbent assay. The expression of apoptosis-related mod…

AmsacrineCyclin-Dependent Kinase Inhibitor p21topoisomeraseCell SurvivalRetinal NeoplasmsRetinoblastomaApoptosisDNA NeoplasmInsulin-Like Growth Factor Binding Protein 3DNA Topoisomerases Type IProto-Oncogene Proteins c-bcl-2CyclinsProto-Oncogene ProteinsDactinomycinTumor Cells CulturedHumansCamptothecinCycloheximideEnzyme InhibitorsTopoisomerase I InhibitorsTumor Suppressor Protein p53DNA DamageEtoposidebcl-2-Associated X Protein
researchProduct

Application of C1-Esterase Inhibitor During Reperfusion of Ischemic Myocardium

2001

Background—Complement activation during reperfusion of ischemic myocardium augments myocardial injury, and complement inhibition with C1-esterase inhibitor (C1-INH) at the time of reperfusion exerts marked cardioprotective effects in experimental studies. Application of C1-INH in newborns, however, was recently reported to have dangerous and even lethal side effects. This study addresses the essential role of dosage in studies using C1-INH.Methods and Results—Cardioprotection by C1-INH was examined in a pig model with 60 minutes of coronary occlusion followed by 120 minutes of reperfusion. C1-INH was administered intravenously 5 to 10 minutes before coronary reperfusion without heparin at a…

Anaphylatoxinsmedicine.medical_specialtyNecrosisSwineHeart VentriclesPartial PressureMyocardial IschemiaIschemiaComplement C1 Inactivator ProteinsPharmacologyNecrosisTroponin TCoronary CirculationPhysiology (medical)Internal medicineAnimalsMedicineLactic AcidMyocardial infarctionCardiac OutputCreatine KinaseCardioprotectionDose-Response Relationship Drugbiologybusiness.industryMyocardiumHemodynamicsHeparinmedicine.diseaseComplement systemOxygenMicroscopy ElectronEndocrinologyCoronary occlusionEnzyme inhibitorReperfusion Injurybiology.proteinBlood Gas Analysismedicine.symptomCardiology and Cardiovascular Medicinebusinessmedicine.drugCirculation
researchProduct

Inhibition of Histone Deacetylase Activity in Human Endometrial Stromal Cells Promotes Extracellular Matrix Remodelling and Limits Embryo Invasion

2011

Invasion of the trophoblast into the maternal decidua is regulated by both the trophoectoderm and the endometrial stroma, and entails the action of tissue remodeling enzymes. Trophoblast invasion requires the action of metalloproteinases (MMPs) to degrade extracellular matrix (ECM) proteins and in turn, decidual cells express tissue inhibitors of MMPs (TIMPs). The balance between these promoting and restraining factors is a key event for the successful outcome of pregnancy. Gene expression is post-transcriptionally regulated by histone deacetylases (HDACs) that unpacks condensed chromatin activating gene expression. In this study we analyze the effect of histone acetylation on the expressio…

Anatomy and PhysiologyGene ExpressionHydroxamic AcidsEndometriumEndocrinologyPregnancyMolecular Cell BiologyCells Culturedreproductive and urinary physiologyRegulation of gene expressionMultidisciplinarybiologyQRObstetrics and GynecologyExtracellular MatrixChromatinCell biologyHistonemedicine.anatomical_structureMatrix Metalloproteinase 9embryonic structuresMatrix Metalloproteinase 2MedicineFemaleHistone deacetylase activityResearch Articlemedicine.drugAdultStromal cellScienceDown-RegulationGene Expression Regulation EnzymologicYoung AdultmedicineHumansEmbryo ImplantationBiologyTissue Inhibitor of Metalloproteinase-3Tissue Inhibitor of Metalloproteinase-1Reproductive SystemTrophoblastUrokinase-Type Plasminogen ActivatorMolecular biologyHistone Deacetylase InhibitorsTrichostatin AAcetylationbiology.proteinStromal CellsDevelopmental Biology
researchProduct

Endothelial Leptin Receptor Deletion Promotes Cardiac Autophagy and Angiogenesis Following Pressure Overload by Suppressing Akt/mTOR Signaling.

2019

Background: Cardiac remodeling is modulated by overnutrition or starvation. The adipokine leptin mediates energy balance between adipose tissue and brain. Leptin and its receptors are expressed in the heart. Methods and Results: To examine the importance of endothelial leptin signaling in cardiac hypertrophy, transverse aortic constriction was used in mice with inducible endothelium-specific deletion of leptin receptors (End.LepR-KO) or littermate controls (End.LepR-WT). End.LepR-KO was associated with improved left ventricular function (fractional shortening, 28.4% versus 18.8%; P =0.0114), reduced left ventricular dilation (end-systolic inner left ventricular diameter, 3.59 versus 4.08 m…

AngiogenesisAdipose tissueAdipokineCardiomegaly030204 cardiovascular system & hematologyVentricular Function Left03 medical and health sciences0302 clinical medicineAutophagyMedicineAnimalsHumansGenetic Predisposition to Disease030212 general & internal medicineProtein kinase BCells Cultured2. Zero hungerPressure overloadHeart FailureMice KnockoutLeptin receptorNeovascularization Pathologicbusiness.industryLeptinMyocardiumTOR Serine-Threonine KinasesAutophagyEndothelial CellsFibrosisCell biologyDisease Models AnimalPhenotypeReceptors LeptinFemaleCardiology and Cardiovascular MedicinebusinessProto-Oncogene Proteins c-aktGene DeletionSignal TransductionCirculation. Heart failure
researchProduct

Novel 3-Azaindolyl-4-arylmaleimides Exhibiting Potent Antiangiogenic Efficacy, Protein Kinase Inhibition, and Antiproliferative Activity

2012

Tumor growth and metastasis are highly associated with the overexpression of protein kinases (PKs) regulating cell growth, apoptosis resistance, and prolonged cell survival. This study describes novel azaindolyl-maleimides with significant inhibition of PKs, such as VEGFR, FLT-3, and GSK-3β which are related to carcinogenesis. Furthermore, these compounds exhibit high kinase selectivity and potent inhibition of angiogenesis and cell proliferation, offering versatile options in cancer treatment strategies.

AngiogenesisAngiogenesis InhibitorsApoptosisChick EmbryoPharmacologymedicine.disease_causeMetastasisMaleimidesNeovascularizationGlycogen Synthase Kinase 3Structure-Activity RelationshipNeoplasmsDrug DiscoveryHuman Umbilical Vein Endothelial Cellspolycyclic compoundsmedicineAnimalsHumansProtein kinase AProtein Kinase InhibitorsGSK3BCells CulturedCell ProliferationGlycogen Synthase Kinase 3 betaMolecular StructureNeovascularization PathologicKinaseChemistryCell growthCell CycleVascular Endothelial Growth Factor Receptor-3medicine.diseaseVascular Endothelial Growth Factor Receptor-2Growth Inhibitorsfms-Like Tyrosine Kinase 3Molecular Medicinemedicine.symptomCarcinogenesisJournal of Medicinal Chemistry
researchProduct