Search results for "3b"

showing 10 items of 143 documents

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
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Activation of the alternative pathway of complement: efficient fluid-phase amplification by blockade of the regulatory complement protein β1H through…

1981

Current concepts of activation of the alternative pathway of complement (APC) focus on the central role of an amplification mechanism triggered by C3b which is covalently bound to the surfact of activating substances. Using sulfated polyanions as model substances, an efficient fluid-phase activation of complement is demonstrated in contrast to solid-phase activation. It is shown that particulate high-molecular weight sulfated polyanions are capable of reversible binding the guinea pig and human regulatory protein beta1H. This fixation leads to an extensive activation of C3 and factor B because the regulatory function of beta1H is blocked in the fluid-phase C3b-dependent amplification system…

AnionsChemical PhenomenaComplement Pathway AlternativeGuinea PigsImmunologyBiologyComplement factor BAbsorptionGuinea pigSulfationComplement C3b Inactivator ProteinsAnimalsHumansImmunology and AllergyComplement ActivationRegulation of gene expressionChemistry PhysicalSulfatesGoatsImmune SeraComplement C3Complement systemCell biologyKineticsBiochemistryCovalent bondComplement Factor HComplement C3bAlternative complement pathwayFunction (biology)European Journal of Immunology
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Factors influencing the interaction of herpes simplex virus glycoprotein C with the third component of complement.

1992

The factors influencing the interaction of herpes simplex virus (HSV) glycoprotein C (gC) with the third component of complement (C3) were investigated in this study. The ability of gC of HSV type 1 (gC-1) to bind to the C3b fragment of C3 was found to be influenced by cell specific processing of gC-1 in a different manner, binding being remarkably enhanced in some cell lines following removal of sialic acid residues. Testing several intertypic recombinants of HSV we found that only strains expressing gC-1 exhibited binding to C3b, even though their genome consisted mainly of HSV-2 sequences in some recombinants. Expression of type-2 glycoproteins gB, gD, gE, gG, gH, and gI did not alter th…

AnionsRosette FormationMolecular Sequence DataBiologyIn Vitro Techniquesmedicine.disease_causeViruschemistry.chemical_compoundStructure-Activity RelationshipViral Envelope ProteinsVirologymedicineTumor Cells CulturedAnimalsHumansSimplexvirusAmino Acid SequenceVero Cellschemistry.chemical_classificationHeparinTemperatureGeneral MedicineNeomycinHerpesvirus glycoprotein BVirologySialic acidHerpes simplex viruschemistryComplement C3bVero cellbiology.proteinAntibodyGlycoproteinmedicine.drugProtein BindingArchives of virology
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Role of the Non-Canonical RNAi Pathway in the Antifungal Resistance and Virulence of Mucorales

2021

Mucorales are the causal agents for the lethal disease known as mucormycosis. Mortality rates of mucormycosis can reach up to 90%, due to the mucoralean antifungal drug resistance and the lack of effective therapies. A concerning urgency among the medical and scientific community claims to find targets for the development of new treatments. Here, we reviewed different studies describing the role and machinery of a novel non-canonical RNAi pathway (NCRIP) only conserved in Mucorales. Its non-canonical features are the independence of Dicer and Argonaute proteins. Conversely, NCRIP relies on RNA-dependent RNA Polymerases (RdRP) and an atypical ribonuclease III (RNase III). NCRIP regulates the…

AntifungalTransposable element0301 basic medicineMucoralesAntifungal Agentstransposonmedicine.drug_classRNA Stability030106 microbiologyAntifungal drugVirulenceReviewQH426-470mucormycosis03 medical and health sciencesDrug Resistance FungalRNA interferenceFongsmedicineGeneticsbiochemistryRNA MessengerRibonuclease IIIepimutantGenetics (clinical)Genome stabilityGeneticsRdRPR3B2biologyMucormycosisnon-canonical RNAiRNA FungalArgonauteantifungal resistancemedicine.diseasebiology.organism_classificationvirulenceRNA silencing030104 developmental biologyNon canonicalbiology.proteinInfeccióMucoralesRNA Interferencegenome stabilitySignal TransductionDicerGenes
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The apolipoprotein(a) moiety of lipoprotein(a) interacts with the complement activation fragment iC3b but does not functionally affect C3 activation …

1992

A previous study has shown that complement component C3 binds to recombinant apolipoprotein(a) (r-apo(a)). In the present report we have investigated the interactions between lipoprotein(a) (Lp(a)), r-apo(a) and C3 in relation to complement activation and degradation. Neither Lp(a) nor r-apo(a) affected complement activation as indicated by sheep and rabbit red blood cell hemolytic assays, and by assessment of the amount of C3a generated in zymosan-activated human serum in the presence or absence of Lp(a). Crossed immunoelectrophoretic analyses indicated that Lp(a) retarded the migration of iC3b in complement-activated serum but had no effects on C3, C3b, C3c or C3dg. Recombinant apo(a) exh…

Apolipoprotein BLipoproteinsApoprotein(a)chemistry.chemical_compoundHumansComplement ActivationbiologyComplement C3Lipoprotein(a)N-Acetylneuraminic AcidComplement systemSialic acidApolipoproteinsBiochemistrychemistryLow-density lipoproteinComplement C3bSialic Acidsbiology.proteiniC3bElectrophoresis Polyacrylamide Gellipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineImmunoelectrophoresis Two-DimensionalN-Acetylneuraminic acidLipoprotein(a)LipoproteinAtherosclerosis
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Amyloid-β toxicity and tau hyperphosphorylation are linked via RCAN1 in Alzheimer's disease.

2011

Amyloid-β peptide (Aβ) toxicity and tau hyperphosphorylation are hallmarks of Alzheimer’s disease (AD). How their molecular relationships may affect the etiology, progression, and severity of the disease, however, has not been elucidated. We now report that incubation of foetal rat cortical neurons with Aβ up-regulates expression of the Regulator of Calcineurin gene RCAN1, and this is mediated by Aβ-induced oxidative stress. Calcineurin (PPP3CA) is a serine-threonine phosphatase that dephosphorylates tau. RCAN1 proteins inhibit this phosphatase activity of calcineurin. Increased expression of RCAN1 also causes up-regulation of glycogen synthase kinase-3beta (GSK3β), a tau kinase. Thus, incr…

Apolipoprotein EAdultMuscle Proteinstau ProteinsBiologymedicine.disease_causeTransfectionArticleDephosphorylationGlycogen Synthase Kinase 3GSK-3Alzheimer DiseasemedicineAnimalsHumansLymphocytesPhosphorylationRNA Small InterferingGSK3BCells CulturedChromatography High Pressure LiquidRegulation of gene expressionCerebral CortexNeuronsAmyloid beta-PeptidesGlycogen Synthase Kinase 3 betaGeneral NeuroscienceCalcineurinIntracellular Signaling Peptides and ProteinsGeneral MedicineMiddle Agedmedicine.diseaseEmbryo MammalianMolecular biologyGlutathionePeptide FragmentsCell biologyRatsCalcineurinDNA-Binding ProteinsPsychiatry and Mental healthClinical PsychologyOxidative StressGene Expression RegulationFemaleGeriatrics and GerontologyAlzheimer's diseaseOxidative stressJournal of Alzheimer's disease : JAD
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GSK-3? Can Regulate the Sensitivity of MIA-PaCa-2 Pancreatic and MCF-7 Breast Cancer Cells to Chemotherapeutic Drugs, Targeted Therapeutics and Nutra…

2021

Glycogen synthase kinase-3 (GSK-3) is a regulator of signaling pathways. KRas is frequently mutated in pancreatic cancers. The growth of certain pancreatic cancers is KRas-dependent and can be suppressed by GSK-3 inhibitors, documenting a link between KRas and GSK-3. To further elucidate the roles of GSK-3β in drug-resistance, we transfected KRas-dependent MIA-PaCa-2 pancreatic cells with wild-type (WT) and kinase-dead (KD) forms of GSK-3β. Transfection of MIA-PaCa-2 cells with WT-GSK-3β increased their resistance to various chemotherapeutic drugs and certain small molecule inhibitors. Transfection of cells with KD-GSK-3β often increased therapeutic sensitivity. An exception was observed wi…

Berberineendocrine system diseasesmedicine.medical_treatmentRegulatormedicine.disease_causeDeoxycytidinePiperazinesTargeted therapychemotherapeutic drugsTargeted therapyNitrophenolsBreast cancerGSK-3BGlycolysisMolecular Targeted TherapyNeoplasm Metastasistargeted therapy;lcsh:QH301-705.5Tumor Stem Cell AssaySulfonamidesTumorbiologyChemistryGeneral MedicineTransfectionMetforminDisease ProgressionMCF-7 CellsFemaleKRASNutraceuticalsFluorouracilSignal transductionGlycolysisSignal TransductionBCL2bcl-X ProteinAntineoplastic AgentsBreast Neoplasmsmacromolecular substancesAdenocarcinomaArticleCell LineInhibitory Concentration 50Cell Line TumorThiadiazolesmedicineDiabetes MellitusKRasHumansGlycogen synthaseProtein Kinase InhibitorsCell ProliferationChemotherapeu-tic drugsGlycogen Synthase Kinase 3 betaGSK-3βAdenylate KinaseBiphenyl Compoundsnutraceuticals;PDACβ-cateninGemcitabine?-cateninMalariaPancreatic Neoplasmslcsh:Biology (General)MCF-7DoxorubicinDietary SupplementsCancer researchbiology.protein
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Turán type inequalities for generalized inverse trigonometric functions

2013

In this paper we study the inverse of the eigenfunction $\sin_p$ of the one-dimensional $p$-Laplace operator and its dependence on the parameter $p$, and we present a Tur\'an type inequality for this function. Similar inequalities are given also for other generalized inverse trigonometric and hyperbolic functions. In particular, we deduce a Tur\'an type inequality for a series considered by Ramanujan, involving the digamma function.

Bernstein functionsPure mathematicsTurán-type inequalitiesGeneralized inverseSeries (mathematics)General Mathematics33C99 33B99ta111Hyperbolic functionMathematics::Classical Analysis and ODEsInverseEigenfunctions of p-LaplacianEigenfunctionRamanujan's sumGeneralized trigonometric functionsymbols.namesakeDigamma functionMathematics - Classical Analysis and ODEsCompletely monotone functionsLog-convexitysymbolsTrigonometric functionsLog-concavityMathematicsFilomat
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Cyclic AMP-mediated upregulation of the expression of neuronal NO synthase in human A673 neuroepithelioma cells results in a decrease in the level of…

2004

The expression level of neuronal nitric oxide synthase (nNOS) can vary depending on the (patho)physiological conditions. Here we document a marked induction of nNOS mRNA, protein, and total NO production in response to dibutyryl cyclic AMP (db-cAMP) in human A673 neuroepithelial cells. However, the upregulation of nNOS was associated with a decreased level of production of bioactive NO and by an increase in the level of generation of reactive oxygen species (ROS). ROS production could be prevented by the NOS inhibitor L-NAME, suggesting nNOS itself is involved in ROS generation. Sepiapterin supplementation of db-cAMP-treated A673 cells could restore full bioactive NO production, most likely…

CAMP-Responsive Element ModulatorNitric Oxide Synthase Type IBiologyCREBNitric OxideBiochemistryAdenylyl cyclaseCyclic AMP Response Element Modulatorchemistry.chemical_compoundMiceNeuroblastomaCoactivatorComplement C3b Inactivator ProteinsCyclic AMPAnimalsHumansNeuroectodermal Tumors Primitive PeripheralCREB-binding proteinEnzyme InhibitorsProtein kinase AeducationCyclic AMP Response Element-Binding ProteinGTP CyclohydrolaseCAMP response element bindingHomeodomain ProteinsNeuronseducation.field_of_studyForskolinPhosphoric Diester HydrolasesIntracellular Signaling Peptides and ProteinsBlood ProteinsLIM Domain ProteinsMolecular biologyCyclic AMP-Dependent Protein KinasesPterinsUp-RegulationDNA-Binding ProteinsRepressor ProteinsAntisense Elements (Genetics)NG-Nitroarginine Methyl EsterchemistryBucladesineGene Expression RegulationComplement Factor Hbiology.proteinNitric Oxide SynthaseReactive Oxygen SpeciesSignal TransductionBiochemistry
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GSK3β as a novel promising target to overcome chemoresistance in pancreatic cancer

2021

Pancreatic cancer is an aggressive malignancy with increasing incidence and poor prognosis due to its late diagnosis and intrinsic chemoresistance. Most pancreatic cancer patients present with locally advanced or metastatic disease characterized by inherent resistance to chemotherapy. These features pose a series of therapeutic challenges and new targets are urgently needed. Glycogen synthase kinase 3 beta (GSK3β) is a conserved serine/threonine kinase, which regulates key cellular processes including cell proliferation, DNA repair, cell cycle progression, signaling and metabolic pathways. GSK3β is implicated in non-malignant and malignant diseases including inflammation, neurodegenerative …

Cancer ResearchDNA repairDruggabilityDiseaseMalignancyPancreatic cancerHumansMedicinePharmacology (medical)GSK3BCell ProliferationPharmacologyGlycogen Synthase Kinase 3 betabusiness.industryKinaseGSK3βCancerTumor chromatin profilingOncogenesPancreatic cancermedicine.diseaseAnticancer drug combinationsPancreatic NeoplasmsInfectious DiseasesOncologyDrug Resistance NeoplasmCancer researchbusinessChemoresistanceDrug Resistance Updates
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