Search results for " Mitogen"

showing 10 items of 202 documents

Design and synthesis of 1-aryl-5-anilinoindazoles as c-Jun N-terminal kinase inhibitors.

2012

Starting from pyrazole HTS hit (1), a series of 1-aryl-1H-indazoles have been synthesized as JNK3 inhibitors with moderate selectivity against JNK1. SAR studies led to the synthesis of 5r as double digital nanomolar JNK3 inhibitor with good in vivo exposure.

IndazolesStereochemistryClinical BiochemistryPharmaceutical SciencePlasma protein bindingPyrazoleBiochemistrychemistry.chemical_compoundStructure-Activity RelationshipIn vivoMitogen-Activated Protein Kinase 10Drug DiscoveryStructure–activity relationshipAnimalsMitogen-Activated Protein Kinase 8Molecular BiologyProtein Kinase InhibitorsAniline CompoundsChemistryKinaseArylOrganic Chemistryc-junJNK Mitogen-Activated Protein KinasesBrainCombinatorial chemistryRatsDrug DesignMolecular MedicineSelectivityHalf-LifeProtein BindingBioorganicmedicinal chemistry letters
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Updated insights into the mechanism of action and clinical profile of the immunoadjuvant QS-21: A review

2019

Background Vaccine adjuvants are compounds that significantly enhance/prolong the immune response to a co-administered antigen. The limitations of the use of aluminium salts that are unable to elicite cell responses against intracellular pathogens such as those causing malaria, tuberculosis, or AIDS, have driven the development of new alternative adjuvants such as QS-21, a triterpene saponin purified from Quillaja saponaria. Purpose The aim of this review is to attempt to clarify the mechanism of action of QS-21 through either receptors or signaling pathways in vitro and in vivo with special emphasis on the co-administration with other immunostimulants in new adjuvant formulations, called a…

InflammasomesT-Lymphocytesmedicine.medical_treatmentHerpes zosterPharmaceutical ScienceMonophosphoryl Lipid AAPCs antigen presenting cellsMiceCMI cell mediated immunity0302 clinical medicineDrug DiscoveryHerpes Zoster VaccineMedicineNSCLC non small cell lung carcinomaCancerImmunity CellularVaccines Synthetic0303 health sciencesImmunogenicityIl-2 interleukine 2HIV human immunodeficiency virusLipid A030220 oncology & carcinogenesisCytokinesMolecular MedicineDCs dendritic cellsNK natural killerAdjuvantTLR Toll-like receptorHerpes Zoster VaccineCD cluster of differentiationAntigen-Presenting CellsCTL cytotoxic T lymphocytesHZ herpes zosterMPL 3-deacylated monophosphoryl lipidVaccine adjuvantImmunoadjuvantArticleVZV varicella zoster virus03 medical and health sciencesImmune systemAdjuvants ImmunologicAntigenPAMPs pathogen-associated molecular patternsMalaria VaccinesPRRs pathogen recognition receptorsQS-21 Quillaja saponaria Molina-fraction 21AnimalsMHC major histocompatibility complexMtb Mycobacterium tuberculosis bacteriaSARS severe acute respiratory syndromeAntigen-presenting cellIFN-γ interferon-gamma030304 developmental biologyPharmacologybusiness.industryA-β amyloid-betaTNF-α tumor necrosis factor-alphaSaponinsQS-21MalariaQuillaja saponariaComplementary and alternative medicineTCR T-cell receptorLiposomesImmunologyKLH keyhole limpet hemocyaninbusinessdLN draining lymph nodesMAPK mitogen activated protein kinasePhytomedicine
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The collagen receptor integrins have distinct ligand recognition and signaling functions

2000

Distinct collagen subtypes are recognized by specific cell surface receptors. Two of the best known collagen receptors are members of the integrin family and are named alpha1beta1 and alpha2beta1. Integrin alpha1beta1 is abundant on smooth muscle cells, whereas the alpha2beta1 integrin is the major collagen receptor on epithelial cells and platelets. Many cell types, such as fibroblasts, osteoblasts, chondrocytes, endothelial cells, and lymphocytes may concomitantly express both of the receptors. We have studied the cell biology of these integrins at two levels. First, we have analyzed their ligand binding mechanism and specificity. Second, we have studied their signaling function inside th…

IntegrinsCell typeReceptors CollagenbiologyCell adhesion moleculeIntegrinLigandsLigand (biochemistry)p38 Mitogen-Activated Protein KinasesMolecular biologyIntegrin alpha1beta1Collagen receptorCell biologybiology.proteinAnimalsHumansPlateletMitogen-Activated Protein KinasesSignal transductionReceptorMolecular BiologySignal TransductionMatrix Biology
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Integrin alpha 2 beta 1 promotes activation of protein phosphatase 2A and dephosphorylation of Akt and glycogen synthase kinase 3 beta.

2002

The integrins are a large family of heterodimeric transmembrane receptors composed of α and β subunits (22). In addition to mediating cell-matrix interactions, integrins have been shown to activate intracellular signaling pathways which, in collaboration with growth factor-induced signals, regulate cellular functions (46). Some integrin signaling cascades are activated via the β subunit cytoplasmic domain, and they are therefore triggered by several integrin heterodimers. These signals include the activation of protein tyrosine kinases of the Src and focal adhesion kinase (FAK) families (9, 47). More-recent studies have revealed signaling events that are activated specifically by an α subun…

IntegrinsReceptors CollagenIntegrinProtein Serine-Threonine KinasesCD49cp38 Mitogen-Activated Protein KinasesCollagen receptorGlycogen Synthase Kinase 3Proto-Oncogene ProteinsCell AdhesionPhosphoprotein PhosphatasesHumansIntegrin-linked kinaseProtein Phosphatase 2cdc42 GTP-Binding ProteinMolecular BiologyCell Growth and DevelopmentCells CulturedbiologyAkt/PKB signaling pathwayCell adhesion moleculeGlycogen Synthase KinasesCell BiologyCell biologyEnzyme ActivationBiochemistryIntegrin alpha MCalcium-Calmodulin-Dependent Protein Kinasesbiology.proteinIntegrin beta 6CollagenMitogen-Activated Protein KinasesProto-Oncogene Proteins c-aktProtein BindingSignal TransductionMolecular and cellular biology
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Analysis of impaired in vitro immunoglobulin synthesis in rheumatoid arthritis.

1990

Decreased immunoglobulin production in pokeweed mitogen driven lymphocyte cultures has been reported in rheumatoid arthritis (RA). Here various activators and experimental designs have been used to determine the contribution of B cells, T cells, or monocytes to this low response. Sixty patients with RA and paired controls were studied at the onset of disease and again six months later. Concentrations of IgA, IgG, and IgM in cultures of RA peripheral blood mononuclear cells stimulated with thymus dependent activators were already decreased at the onset of the disease. Six months later RA mononuclear cells produced even lower concentrations of immunoglobulin. In contrast, stimulation with a T…

Interleukin 2AdultMalemedicine.medical_specialtyAdolescentLymphocyteT cellImmunologyImmunoglobulin ELymphocyte ActivationPeripheral blood mononuclear cellT-Lymphocytes RegulatoryGeneral Biochemistry Genetics and Molecular BiologyMonocytesArthritis RheumatoidRheumatologyInternal medicinemedicineImmunology and AllergyHumansCells CulturedAgedbiologybusiness.industryMonocytePokeweed mitogenT-Lymphocytes Helper-InducerMiddle AgedImmunoglobulin Isotypesmedicine.anatomical_structureEndocrinologyImmunologybiology.proteinInterleukin-2FemaleAntibodybusinessmedicine.drugResearch Article
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The Friedreich's Ataxia protein frataxin modulates DNA base excision repair in prokaryotes and mammals

2010

DNA-repair mechanisms enable cells to maintain their genetic information by protecting it from mutations that may cause malignant growth. Recent evidence suggests that specific DNA-repair enzymes contain ISCs (iron–sulfur clusters). The nuclearencoded protein frataxin is essential for the mitochondrial biosynthesis of ISCs. Frataxin deficiency causes a neurodegenerative disorder named Friedreich's ataxia in humans. Various types of cancer occurring at young age are associated with this disease, and hence with frataxin deficiency. Mice carrying a hepatocyte-specific disruption of the frataxin gene develop multiple liver tumours for unresolved reasons. In the present study, we show that frata…

Iron-Sulfur ProteinsDNA Repairmedicine.disease_causeBiochemistryDNA Glycosylases8-oxoG 78-dihydro-8-oxoguanineMice0302 clinical medicineIron-Binding Proteinsoxidative stressBER base excision repairCells CulturedMammalsMice Knockout0303 health sciencesfrataxinDMEM Dulbecco's modified Eagle's mediumbiologyLiver NeoplasmsSalmonella entericairon–sulfur clusterLife SciencesIron-binding proteinsTransfection3. Good healthLB Luria–BertaniOGG1 8-oxoguanine DNA glycosylase 1ISC iron–sulfur clusterFpg formamido-pyrimidine DNA glycosylaseHPRT hypoxanthine phosphoribosyltransferaseResearch ArticleDNA damageDNA repairSSB DNA single-strand breakTransfectionCell Line03 medical and health sciencesFRDA Friedreich's ataxiaROS reactive oxygen speciesmedicineAnimalsHumansMUTYH human mutY homologue (Escherichia coli)Molecular BiologyGene030304 developmental biologyFriedreich's ataxiaCell BiologyFibroblastsMolecular biologytumorigenesisProkaryotic CellsFriedreich AtaxiaDNA base excision repairDNA glycosylaseMutationHepatocytesFrataxinbiology.proteinInstitut für ErnährungswissenschaftCarcinogenesisMAPK mitogen-activated protein kinase030217 neurology & neurosurgeryDNA Damage
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Differential role of p38 mitogen activated protein kinase for cellular recovery from attack by pore-forming S. aureus alpha-toxin or streptolysin O.

2006

Following the observation that cells are able to recover from membrane lesions incurred by Staphylococcus aureus alpha-toxin and streptolysin O (SLO), we investigated the role of p38 in this process. p38 phosphorylation occurred in response to attack by both toxins, commencing within minutes after toxin treatment and waning after several hours. While SLO reportedly activates p38 via ASK1 and ROS, we show that this pathway does not play a major role for p38 induction in alpha-toxin-treated cells. Strikingly divergent effects of p38 blockade were noted depending on the toxin employed. In the case of alpha-toxin, inhibition of p38 within the time frame of its activation led to disruption of th…

KeratinocytesProgrammed cell deathStaphylococcus aureusCell Membrane Permeabilityp38 mitogen-activated protein kinasesBacterial ToxinsBiophysicsBiologymedicine.disease_causeMAP Kinase Kinase Kinase 5Biochemistryp38 Mitogen-Activated Protein KinasesMicrobiologyHemolysin ProteinsAdenosine TriphosphateBacterial ProteinsProto-Oncogene ProteinsmedicineHumansASK1PhosphorylationMolecular BiologyCells CulturedPore-forming toxinToxinCell MembraneCell BiologyProtein-Tyrosine KinasesBlockadeCell biologyEnzyme ActivationStreptolysinsPhosphorylationStreptolysinBiochemical and biophysical research communications
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Studies of Jak/STAT3 expression and signalling in psoriasis identifies STAT3-Ser727 phosphorylation as a modulator of transcriptional activity

2013

Jak/Tyk proteins have recently aroused as possible therapeutic targets for the treatment of psoriasis. In psoriasis, these proteins signal through STAT molecules including STAT3, and STAT3 expression and activation has been shown augmented in psoriatic lesions. Here, we characterized the expression of Jak/Tyk proteins in lesional compared with non-lesional psoriatic skin. Jak1, Jak2 mRNA and protein and Tyk2 mRNA appeared to be downregulated, whereas Jak3 mRNA expression was increased. Moreover, STAT3 expression and activation was examined in psoriasis. STAT3 is activated at two phosphorylation sites: Tyr705 and Ser727. Both phosphorylation sites were phosphorylated in lesional psoriatic sk…

KeratinocytesSTAT3 Transcription FactorTranscription GeneticMAP Kinase Signaling SystemBiopsyp38 mitogen-activated protein kinasesPrimary Cell CultureGene ExpressionDermatologyBiochemistrystatInterleukin 20PsoriasisSerinemedicineHumansPsoriasisRNA MessengerPhosphorylationSTAT3Molecular BiologySkinTYK2 KinasebiologyInterleukin-6InterleukinsJanus Kinase 3Janus Kinase 1Janus Kinase 2medicine.diseaseTyrosine kinase 2biology.proteinCancer researchPhosphorylationTumor necrosis factor alphaSignal Transduction
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STAT1 expression and activation is increased in lesional psoriatic skin

2013

Summary Background  The JAK (Janus kinase)/STAT (signal transducer and activator of transcription) signalling pathway is known to play an important role in many cellular processes including inflammation. The activation of STAT1 is dependent on tyrosine 701 and serine 727 phosphorylation, which leads to the formation of the STAT dimer and modulation of STAT1 activity, respectively. Objective  To determine STAT1 expression and activation in psoriatic skin. Methods  Biopsies were collected from patients with psoriasis. mRNA expression was evaluated by quantitative polymerase chain reaction, whereas the protein and phosphorylation level of STAT1 were evaluated by Western blotting. STAT1 localiz…

Kinasep38 mitogen-activated protein kinasesDermatologyBiologymedicine.diseaseMolecular biologyPsoriasismedicineSTAT proteinbiology.proteinPhosphorylationSTAT1Janus kinaseProtein kinase CBritish Journal of Dermatology
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Bisphenol-A impairs insulin action and up-regulates inflammatory pathways in human subcutaneous adipocytes and 3T3-L1 cells.

2013

Current evidence indicates that chemical pollutants may interfere with the homeostatic control of nutrient metabolism, thereby contributing to the increased prevalence of metabolic disorders. Bisphenol-A (BPA) is a lipophilic compound contained in plastic which is considered a candidate for impairing energy and glucose metabolism. We have investigated the impact of low doses of BPA on adipocyte metabolic functions. Human adipocytes derived from subcutaneous adipose tissue and differentiated 3T3-L1 cells were incubated with BPA, in order to evaluate the effect on glucose utilization, insulin sensitivity and cytokine secretion. Treatment with 1 nM BPA significantly inhibited insulin-stimulate…

Leptinmedicine.medical_treatmentAdipose tissuechemistry.chemical_compoundMice0302 clinical medicineAdipocyteAdipocytesInsulinPhosphorylation0303 health sciencesMultidisciplinaryPERSISTENT ORGANIC POLLUTANTS BODY-MASS INDEX METABOLIC SYNDROME ENVIRONMENTAL CONTAMINANTS CARDIOVASCULAR-DISEASE ENDOCRINE DISRUPTORS SERUM CONCENTRATIONS WIDESPREAD EXPOSURE PERINATAL EXPOSURE DIABETES-MELLITUSbiologyQRNF-kappa BCell Differentiation3. Good healthUp-RegulationAdipogenesisMedicinehormones hormone substitutes and hormone antagonistsResearch ArticleSignal TransductionSTAT3 Transcription Factormedicine.medical_specialtyendocrine systemScienceSubcutaneous FatDown-Regulation030209 endocrinology & metabolism03 medical and health sciencesDownregulation and upregulationPhenolsInternal medicine3T3-L1 CellsmedicineAnimalsHumansRNA MessengerBenzhydryl Compounds030304 developmental biologyInflammationurogenital systemInsulinJNK Mitogen-Activated Protein KinasesReceptor InsulinInsulin receptorEndocrinologyGlucosechemistry13. Climate actionbiology.proteinCytokine secretionGLUT4PloS one
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