Search results for "Protein kinases"

showing 10 items of 427 documents

Cardiac effects of isoliquiritigenin

1997

The effects of isoliquiritigenin on force of contraction (Fc), L-type Ca2+ current (I(Ca)) and intracellular Ca2+ concentration ([Ca2+]i) were investigated in rat ventricular heart muscle. Isoliquiritigenin increased Fc and I(Ca) and, after longer exposure times, resting tension and [Ca2+]i. The effect of isoliquiritigenin (100 microM) on I(Ca) was diminished by Rp-cAMPS (30 microM). 1H-[1,2,4]oxa- diazolo[4,3-a]quinoxalin-1-one (50 microM) did not influence the effects of isoliquiritigenin on Fc and I(Ca). The positive inotropic effects of isoprenaline and forskolin, but not of 3-isobutyl-1-methylxanthine, were potentiated by isoliquiritigenin (100 microM). In the presence of milrinone (10…

Malemedicine.medical_specialtyPatch-Clamp TechniquesFura-2In Vitro TechniquesMembrane PotentialsRats Sprague-Dawleychemistry.chemical_compoundChalconeChalconesAldehyde ReductaseInternal medicineIsoprenalinemedicineAnimalsDrug InteractionsEnzyme InhibitorsCyclic GMPPharmacologyPlants MedicinalForskolinMyocardiumPhosphodiesteraseHeartCyclic AMP-Dependent Protein KinasesMyocardial ContractionRatsElectrophysiologyEndocrinologychemistryGuanylate CyclaseMilrinoneCalciumFemalemedicine.symptomSoluble guanylyl cyclaseIsoliquiritigeninMuscle contractionmedicine.drugEuropean Journal of Pharmacology
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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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Sensing by the membrane-bound sensor kinase DcuS: exogenous versus endogenous sensing of C(4)-dicarboxylates in bacteria.

2010

Bacteria are able to grow at the expense of both common (succinate, L-malate, fumarate and aspartate) and uncommon (L-tartrate and D-malate) C4-dicarboxylates, which are components of central metabolism. Two types of sensors/regulators responding to the C4-dicarboxylates function in Escherichia coli, Bacillus, Lactobacillus and related bacteria. The first type represents membrane-integral two-component systems, while the second includes cytoplasmic LysR-type transcriptional regulators. The difference in location and substrate specificity allows the exogenous induction of metabolic genes by common C4-dicarboxylates, and endogenous induction by uncommon C4-dicarboxylates. The two-component s…

Microbiology (medical)Dicarboxylic Acid TransportersModels MolecularBacteriaEscherichia coli ProteinsCell MembraneRegulatory siteGene Expression Regulation BacterialBiologyLigand (biochemistry)MicrobiologyTransmembrane domainBiochemistryProtein kinase domainBacterial ProteinsPAS domainExtracellularEscherichia coliDicarboxylic AcidsBinding siteSignal transductionProtein KinasesSignal TransductionFuture microbiology
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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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The Escherichia coli Envelope Stress Sensor CpxA Responds to Changes in Lipid Bilayer Properties

2015

The Cpx stress response system is induced by various environmental and cellular stimuli. It is also activated in Escherichia coli strains lacking the major phospholipid, phosphatidylethanolamine (PE). However, it is not known whether CpxA directly senses changes in the lipid bilayer or the presence of misfolded proteins due to the lack of PE in their membranes. To address this question, we used an in vitro reconstitution system and vesicles with different lipid compositions to track modulations in the activity of CpxA in different lipid bilayers. Moreover, the Cpx response was validated in vivo by monitoring expression of a PcpxP-gfp reporter in lipid-engineered strains of E. coli. Our comb…

Models MolecularCardiolipinsSurface PropertiesRecombinant Fusion ProteinsGreen Fluorescent ProteinsLipid BilayersArabidopsisPhospholipidBiologymedicine.disease_causeBiochemistrychemistry.chemical_compoundBacterial ProteinsGenes ReportermedicineAcholeplasma laidlawiiPhosphorylationLipid bilayerEscherichia coliPlant ProteinsPhosphatidylethanolamineEscherichia coli ProteinsPhosphatidylethanolaminesVesicleGlycosyltransferasesMembrane ProteinsPhosphatidylglycerolsCell biologychemistryMembrane proteinlipids (amino acids peptides and proteins)Protein foldingSignal transductionProtein KinasesProtein Processing Post-TranslationalSignal TransductionBiochemistry
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Plasticity of the PAS domain and a potential role for signal transduction in the histidine kinase DcuS

2008

The mechanistic understanding of how membrane-embedded sensor kinases recognize signals and regulate kinase activity is currently limited. Here we report structure-function relationships of the multidomain membrane sensor kinase DcuS using solid-state NMR, structural modeling and mutagenesis. Experimental data of an individual cytoplasmic Per-Arnt-Sim (PAS) domain were compared to structural models generated in silico. These studies, together with previous NMR work on the periplasmic PAS domain, enabled structural investigations of a membrane-embedded 40-kDa construct by solid-state NMR, comprising both PAS segments and the membrane domain. Structural alterations are largely limited to prot…

Models MolecularCytoplasmHistidine KinaseMolecular Sequence DataHAMP domainStructural BiologyPAS domainEscherichia coliAmino Acid SequenceKinase activityProtein Structure QuaternaryNuclear Magnetic Resonance BiomolecularMolecular BiologybiologyEscherichia coli ProteinsHistidine kinaseProtein Structure TertiaryCell biologyTransmembrane domainBiochemistryProtein kinase domainCyclic nucleotide-binding domainbiology.proteinGRB2Protein KinasesSignal Transduction
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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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