Search results for "Mitogen-Activated Protein Kinases"

showing 10 items of 246 documents

Effect of dietary supplementation with a mixture of Vitamins C and E on fertilization of tertiary butyl hydroperoxide-treated oocytes and parthenogen…

2002

The present study aims to analyze the effect of dietary supplementation with a mixture of Vitamins C and E on fertilization and later development of tertiary butyl hydroperoxide (tBH)-treated mouse oocytes and on parthenogenetic activation of freshly ovulated mouse oocytes. We fed hybrid mice a standard diet supplemented or not supplemented with Vitamins C and E from the first day of weaning until the age of 12 weeks. We noted no significant effect of diet on fertilization rate, percentage of total and hatching blastocysts, total number of cells, mitotic index and percentage of apoptotic nuclei at 120 h post-insemination of oocytes incubated for 15 min in the presence of 0, 1, 5 and 10 micr…

Malemedicine.medical_specialtyMitotic indexAntioxidantmedicine.medical_treatmentMaturation-Promoting FactorParthenogenesisAscorbic AcidFertilization in VitroWeaningBiologychemistry.chemical_compoundEmbryonic and Fetal DevelopmentMiceHuman fertilizationFood Animalstert-ButylhydroperoxideOral administrationInternal medicineCulture TechniquesmedicineWeaningAnimalsVitamin ESmall AnimalsProtein kinase AEthanolEquineHatchingMice Inbred C57BLEndocrinologychemistryFertilizationMesothelinDietary SupplementsMice Inbred CBAOocytesAnimal Science and ZoologyFemaleMitogen-Activated Protein KinasesTheriogenology
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Sildenafil reduces neuroinflammation and restores spatial learning in rats with hepatic encephalopathy: underlying mechanisms

2015

Background: There are no specific treatments for the neurological alterations of cirrhotic patients with minimal hepatic encephalopathy (MHE). Rats with MHE due to portacaval shunt (PCS) show impaired spatial learning. The underlying mechanisms remain unknown. The aims of this work were to assess: (a) whether PCS rats show neuroinflammation in hippocampus, (b) whether treatment with sildenafil reduces neuroinflammation and restores spatial learning in PCS rats, and (c) analyze the underlying mechanisms. Methods: Neuroinflammation was assessed by determining inflammatory markers by Western blot. Phosphorylation of MAP-kinase p38 was assessed by immunohistochemistry. Membrane expression of GA…

Malemedicine.medical_specialtyNeurologySildenafilVasodilator AgentsInterleukin-1betaImmunologyHippocampusInflammationPortacaval shuntHippocampusp38 Mitogen-Activated Protein KinasesSildenafil Citratechemistry.chemical_compoundCellular and Molecular NeuroscienceReceptors GABANeuroinflammationmedicineAnimalsRats WistarMaze LearningHepatic encephalopathyNeuroinflammationHepatic encephalopathyInflammationMicrogliaPortacaval Shunt SurgicalTumor Necrosis Factor-alphabusiness.industryResearchGeneral NeuroscienceMacrophage Activationmedicine.diseasehumanitiesSildenafil treatmentRatscGMPmedicine.anatomical_structureCognitive impairmentReceptors Glutamatechemistrynervous systemNeurologyHepatic EncephalopathyMicrogliamedicine.symptombusinesshuman activitiesNeuroscience
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Overlapping phenotypes between SHORT and Noonan syndromes in patients with PTPN11 pathogenic variants

2020

Overlapping syndromes such as Noonan, Cardio-Facio-Cutaneous, Noonan syndrome (NS) with multiple lentigines and Costello syndromes are genetically heterogeneous conditions sharing a dysregulation of the RAS/mitogen-activated protein kinase (MAPK) pathway and are known collectively as the RASopathies. PTPN11 was the first disease-causing gene identified in NS and remains the more prevalent. We report seven patients from three families presenting heterozygous missense variants in PTPN11 probably responsible for a disease phenotype distinct from the classical Noonan syndrome. The clinical presentation and common features of these seven cases overlap with the SHORT syndrome. The latter is the c…

Malemusculoskeletal diseases0301 basic medicineMAPK/ERK pathwaycongenital hereditary and neonatal diseases and abnormalitiesMAP Kinase Signaling SystemProtein Tyrosine Phosphatase Non-Receptor Type 11030105 genetics & heredityBiologyGene productPhosphatidylinositol 3-Kinases03 medical and health sciencesMetabolic DiseasesGeneticsmedicineHumansMissense mutationskin and connective tissue diseasesProtein kinase BGrowth DisordersGenetics (clinical)GeneticsGenetic heterogeneityNoonan SyndromeGenetic Variationmedicine.diseasePTPN11NephrocalcinosisPhenotype030104 developmental biologySHORT syndromeHypercalcemiaNoonan syndromeFemaleMitogen-Activated Protein KinasesSignal TransductionClinical Genetics
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Rac1 GTPase, a multifunctional player in the regulation of genotoxic stress response

2013

The Ras-related C3 botulinum toxin substrate 1 (Rac1) belongs to the Ras-homologous (Rho) family of small GTPases, which transduce signals from the outside to the inside of a cell. Rac1 becomes activated upon ligand binding of a variety of receptors, including receptor tyrosine kinases and heterotrimeric G-protein-coupled receptors. After GTP loading by guanine exchange factors (GEFs), GTP-bound Rac1 engages numerous effector proteins, thereby eventually regulating cell motility and adhesion, cell cycle progression through G1, mitosis and meiosis, as well as cell death and metastasis.1 Besides, Rac1 adjusts cellular responses to genotoxic agents, such as UV light and alkylating agents, by r…

Malerac1 GTP-Binding Proteintopoisomerase IIAgingRHOADNA repairDNA damagep38 mitogen-activated protein kinasesApoptosisRAC1Editorials: Cell Cycle FeaturesDNA damage responseReceptor tyrosine kinasechemical carcinogenesisHistonesMiceTransforming Growth Factor betaRho GTPasesAnimalsMolecular BiologyTranscription factoranthracyclinesMice KnockoutbiologyKinaseNeuropeptidesConnective Tissue Growth FactorHMG-CoA reductase inhibitors (statins)Cell BiologyFibrosisgenotoxic stressActinsrac GTP-Binding ProteinsCell biologyOxidative Stressnormal tissue damageGene Expression RegulationLiverBiochemistryDoxorubicinGamma Raysbiology.proteinFemaleDNA DamageMutagensSignal TransductionDevelopmental BiologyCell Cycle
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Pharmacologic therapies in endometriosis: a systematic review

2012

To assess the literature on preclinical and clinical efficacy and safety data of pharmacologic groups proposed in the treatment of endometriosis, we performed a systematic review of publications from March 2002 to January 2012 via PubMed search. Additional relevant articles were identified from citations within these publications. A high number of medications were tested in preclinical models of endometriosis due to their theoretic capacity of disrupting important pathophysiologic pathways of the disease, such as inflammatory response, angiogenesis and cell survival, proliferation, migration, adhesion, and invasion. Tumor necrosis factor α-blockers, nuclear factor κB inhibitors, antiangioge…

Matrix metalloproteinase inhibitorAngiogenesisAnti-Inflammatory AgentsEndometriosisEndometriosisAngiogenesis InhibitorsPharmacologyp38 Mitogen-Activated Protein KinasesAntioxidantsEtanerceptmedicineAnimalsHumansHyaluronic AcidAdverse effectMelatoninTumor Necrosis Factor-alphabusiness.industryNF-kappa BObstetrics and Gynecologymedicine.diseaseMetforminReproductive MedicineEstrogen inhibitorFemaleHydroxymethylglutaryl-CoA Reductase InhibitorsEndostatinbusinessmedicine.drugFertility and Sterility
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Fas signaling-mediated T

2018

Fas induces apoptosis in activated T cell to maintain immune homeostasis, but the effects of non-apoptotic Fas signaling on T cells remain unclear. Here we show that Fas promotes TH9 cell differentiation by activating NF-κB via Ca2+-dependent PKC-β activation. In addition, PKC-β also phosphorylates p38 to inactivate NFAT1 and reduce NFAT1-NF-κB synergy to promote the Fas-induced TH9 transcription program. Fas ligation exacerbates inflammatory bowel disease by increasing TH9 cell differentiation, and promotes antitumor activity in p38 inhibitor-treated TH9 cells. Furthermore, low-dose p38 inhibitor suppresses tumor growth without inducing systemic adverse effects. In patients with tumor, rel…

Mice Inbred BALB CNFATC Transcription FactorsNF-kappa BMice NudeCell DifferentiationCancer immunotherapySignal transductionInflammatory Bowel DiseasesT-Lymphocytes Regulatoryp38 Mitogen-Activated Protein KinasesArticleMice Inbred C57BLMiceLymphocyte differentiationNeoplasmsProtein Kinase C betaAnimalsCytokinesHumansFemalefas ReceptorCD4-positive T cellsNature communications
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From Five- to Six-Membered Rings:  3,4-Diarylquinolinone as Lead for Novel p38MAP Kinase Inhibitors

2007

In this study we describe the design, synthesis, and biological evaluation of 3-(4-fluorophenyl)-4-pyridin-4-ylquinoline-2(1H)-one (5) as a new inhibitor of MAPK with a p38alphaMAPK IC50 of 1.8 muM. By keeping the common vicinal pyridine/4-F-phenyl pharmacophore, such as in prototypical imidazole 20 or isoxazole 13 but in 5 connected to the six-membered quinoline core, we were particularly interested in comparing biological activity, details of molecular geometry, and different binding modes of these compounds. Compounds 20 and 13 were active both in the p38alpha- and JNK3-assay, whereas 5 was selective for p38alpha, with no JNK3 inhibition. By comparing the X-ray structures of the compound…

Models MolecularBinding SitesMolecular modelStereochemistryQuinolineBiological activityQuinolonesCrystallography X-RayHeterocyclic Compounds 4 or More Ringsp38 Mitogen-Activated Protein KinasesStructure-Activity Relationshipchemistry.chemical_compoundchemistryMitogen-Activated Protein Kinase 10Drug DiscoveryPyridineMolecular MedicineImidazoleMoietyIsoxazolePharmacophoreJournal of Medicinal Chemistry
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Signaling pathways of the TREM-1- and TLR4-mediated neutrophil oxidative burst.

2008

The triggering receptor expressed on myeloid cells 1 (TREM-1) is involved in the innate inflammatory response to microbial infections. Activation and expression of TREM-1 by polymorphonuclear neutrophils (PMN) occurs in concert with Toll-like receptors (TLR) such as TLR4 for bacterial lipopolysaccharide. However, it is currently unclear how this is mediated on a molecular level. Using pharmacological inhibitors and Western blot analysis we demonstrate that phosphatidyl inositide 3-kinase, phospholipase C and the mitogen-activated kinase p38MAPK are essential for the TREM-1- and TLR4-induced oxidative burst of human PMN. The activation of protein kinase B and extracellular signal-related kin…

Models MolecularLipopolysaccharideNeutrophilsBlotting WesternCell Separationp38 Mitogen-Activated Protein Kinaseschemistry.chemical_compoundPhosphatidylinositol 3-KinasesImmunology and AllergyHumansReceptors ImmunologicReceptorProtein kinase BRespiratory BurstMembrane GlycoproteinsPhospholipase CKinaseFlow CytometryTriggering Receptor Expressed on Myeloid Cells-1Respiratory burstCell biologyEnzyme ActivationToll-Like Receptor 4chemistryTLR4Signal transductionProto-Oncogene Proteins c-aktSignal TransductionJournal of innate immunity
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Molecular mechanism of α2β1 integrin interaction with human echovirus 1

2009

Conformational activation increases the affinity of integrins to their ligands. On ligand binding, further changes in integrin conformation elicit cellular signalling. Unlike any of the natural ligands of alpha2beta1 integrin, human echovirus 1 (EV1) seemed to bind more avidly a 'closed' than an activated 'open' form of the alpha2I domain. Furthermore, a mutation E336A in the alpha2 subunit, which inactivated alpha2beta1 as a collagen receptor, enhanced alpha2beta1 binding to EV1. Thus, EV1 seems to recognize an inactive integrin, and not even the virus binding could trigger the conformational activation of alpha2beta1. This was supported by the fact that the integrin clustering by EV1 did …

Models MolecularProtein Conformationmedia_common.quotation_subjectIntegrinCHO CellsIn Vitro TechniquesBiologyp38 Mitogen-Activated Protein KinasesCD49cArticleGeneral Biochemistry Genetics and Molecular BiologyCell LineCollagen receptorCricetulusCricetinaeChlorocebus aethiopsAnimalsHumansBinding siteInternalizationMolecular Biologymedia_commonBinding SitesGeneral Immunology and MicrobiologyGeneral NeuroscienceRecombinant ProteinsEnterovirus B HumanProtein Structure TertiaryCell biologyAmino Acid SubstitutionIntegrin alpha MBiochemistryMutagenesis Site-Directedbiology.proteinReceptors VirusIntegrin beta 6Integrin alpha2beta1Signal transductionSignal TransductionThe EMBO Journal
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Design, synthesis, and biological evaluation of novel disubstituted dibenzosuberones as highly potent and selective inhibitors of p38 mitogen activat…

2012

Synthesis, biological testing, structure-activity relationships (SARs), and selectivity of novel disubstituted dibenzosuberone derivatives as p38 MAP kinase inhibitors are described. Hydrophilic moieties were introduced at the 7-, 8-, and 9-position of the 2-phenylamino-dibenzosuberones, improving physicochemical properties as well as potency. Extremely potent inhibitors were obtained, with half-maximal inhibitory concentration (IC(50)) values in the low nM range in a whole blood assay measuring the inhibition of cytokine release. The high potency of the target compounds together with the outstanding selectivity of this novel class of compounds toward p38 mitogen activated protein (MAP) kin…

Models MolecularProtein Conformationp38 mitogen-activated protein kinasesmedicine.medical_treatmentChemistry Techniques SyntheticDibenzocycloheptenesp38 Mitogen-Activated Protein KinasesSubstrate SpecificityInhibitory Concentration 50Structure-Activity RelationshipProtein structureDrug DiscoverymedicinePotencyStructure–activity relationshipHumansProtein Kinase InhibitorsbiologyKinaseChemistryCombinatorial chemistryKineticsCytokineBiochemistryMitogen-activated protein kinaseDrug Designbiology.proteinMolecular MedicineSelectivityHydrophobic and Hydrophilic InteractionsJournal of medicinal chemistry
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