Search results for "Activating Transcription Factor 2"

showing 5 items of 5 documents

Structure-Activity Relationships and X-ray Structures Describing the Selectivity of Aminopyrazole Inhibitors for c-Jun N-terminal Kinase 3 (JNK3) ove…

2009

c-Jun N-terminal kinase 3alpha1 (JNK3alpha1) is a mitogen-activated protein kinase family member expressed primarily in the brain that phosphorylates protein transcription factors, including c-Jun and activating transcription factor-2 (ATF-2) upon activation by a variety of stress-based stimuli. In this study, we set out to design JNK3-selective inhibitors that had >1000-fold selectivity over p38, another closely related mitogen-activated protein kinase family member. To do this we employed traditional medicinal chemistry principles coupled with structure-based drug design. Inhibitors from the aminopyrazole class, such as SR-3576, were found to be very potent JNK3 inhibitors (IC(50) = 7 nm)…

Models MolecularStereochemistryProtein ConformationPyrazoleCrystallography X-RayBiochemistryp38 Mitogen-Activated Protein Kinaseschemistry.chemical_compoundStructure-Activity RelationshipProtein structureMitogen-Activated Protein Kinase 10Insulin-Secreting CellsStructure–activity relationshipAnimalsHumansEnzyme InhibitorsPhosphorylationProtein kinase AMolecular BiologyCells CulturedIndazolebiologyActivating Transcription Factor 2Active siteCell BiologyActivating transcription factor 2RatschemistryProtein Structure and Foldingbiology.proteinPyrazolesSelectivityJournal of Biological Chemistry
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Transcriptional activation of apurinic/apyrimidinic endonuclease (Ape, Ref-1) by oxidative stress requires CREB.

1999

Abstract Apurinic/apyrimidinic endonuclease (APE alias Ref-1) is a multifunctional enzyme involved in DNA repair and redox regulation of transcription factors (e.g., AP-1). It also acts as a repressor of its own and other genes. Recently, it was shown that the level of APE mRNA and protein is enhanced upon treatment of cells with oxidative agents, such as hydrogen peroxide (H 2 O 2 ), which gives rise to an adaptive response of cells to oxidative stress. Induction of APE is due to APE promoter activation. To elucidate the mechanism of transcriptional activation of APE by oxidative agents, we introduced mutations into the cloned human APE promoter and checked its activity in transient transf…

Transcription GeneticDNA repairProto-Oncogene Proteins c-junvirusesCarbon-Oxygen LyasesBiophysicsRepressorContext (language use)CHO CellsCREBTransfectionBiochemistryPolymerase Chain ReactionEndonucleasestomatognathic systemCricetinaeDNA-(Apurinic or Apyrimidinic Site) LyaseAnimalsHumansAP siteBinding siteCyclic AMP Response Element-Binding ProteinPromoter Regions GeneticMolecular BiologyTranscription factorBinding SitesbiologyActivating Transcription Factor 2social sciencesCell BiologyHydrogen PeroxideOxidantsMolecular biologybody regionsOxidative Stressbiology.proteinMutagenesis Site-DirectedTranscription FactorsBiochemical and biophysical research communications
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Activation of Cardiac c-Jun NH 2 -Terminal Kinases and p38-Mitogen–Activated Protein Kinases With Abrupt Changes in Hemodynamic Load

2001

Abstract —The role of mitogen-activated protein kinase (MAPK) pathways as signal transduction intermediates of hemodynamic stress leading to cardiac hypertrophy in the adult heart is not fully established. In a rat model of pressure-overload hypertrophy, we examined whether activation of MAPK pathways, namely, the extracellular signal–regulated protein kinase (ERK), c-Jun NH 2 -terminal kinase (JNK), and the p38-MAPK pathways, occurs during rapid changes in hemodynamic load in vivo. A slight activation of ERK2 and marked increases in JNK1 and p38-MAPK activities were observed 30 minutes after aortic banding. The increase in p38-MAPK activity was accompanied by an increase in the phosphoryl…

MAPK/ERK pathwaymedicine.medical_specialtyProto-Oncogene Proteins c-junp38 mitogen-activated protein kinasesp38 Mitogen-Activated Protein KinasesVentricular Function LeftStress PhysiologicalInternal medicineInternal MedicinemedicineAnimalsASK1PhosphorylationRats WistarCyclic AMP Response Element-Binding ProteinProtein kinase AProtein kinase CMAPK14Activating Transcription Factor 2biologyKinaseMyocardiumJNK Mitogen-Activated Protein KinasesRatsCell biologyEnzyme ActivationTranscription Factor AP-1Disease Models AnimalEndocrinologyMitogen-activated protein kinasebiology.proteinFemaleMitogen-Activated Protein KinasesTranscription FactorsHypertension
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Age-dependent regulation of antioxidant genes by p38α MAPK in the liver

2018

p38α is a redox sensitive MAPK activated by pro-inflammatory cytokines and environmental, genotoxic and endoplasmic reticulum stresses. The aim of this work was to assess whether p38α controls the antioxidant defense in the liver, and if so, to elucidate the mechanism(s) involved and the age-related changes. For this purpose, we used liver-specific p38α-deficient mice at two different ages: young-mice (4 months-old) and old-mice (24 months-old). The liver of young p38α knock-out mice exhibited a decrease in GSH levels and an increase in GSSG/GSH ratio and malondialdehyde levels. However, old mice deficient in p38α had higher hepatic GSH levels and lower GSSG/GSH ratio than young p38α knock-…

ROS Reactive oxygen species;RSK1 Ribosomal S6 kinase10301 basic medicineMAPK/ERK pathwayAgingHPLC High-performance liquid chromatographyAntioxidantmedicine.medical_treatmentTBP TATA-binding proteinClinical BiochemistryDEN Diethyl nitrosamine;MKP-1 MAPK phosphatase-1IκB kinaseGCLc Glutamate cysteine ligase catalytic subunitp38 Mitogen-Activated Protein KinasesG6PDH Glucose-6-phosphate dehydrogenaseBiochemistryAntioxidantsMicechemistry.chemical_compoundSuperoxide Dismutase-1Akt Protein kinase B0302 clinical medicineNrf2 Nuclear factor erythroid 2-related factor-2IL InterleukinSOD1 Cu/Zn-superoxide dismutaselcsh:QH301-705.5Mice KnockoutMK2 MAP-activated protein kinase 2;PGC-1α Peroxisome proliferator-activated receptor gamma coactivator 1-alphachemistry.chemical_classificationlcsh:R5-920Trx ThioredoxinGlutathione DisulfideTNF-α Tumor necrosis factor-alphabiologyLPS Lipopolysaccharide;GSSG Oxidized glutathione;MEF Mouse embryonic fibroblastsNF-kappa BGstm1 Glutathione S-transferase mu 1CatalaseEndoplasmic Reticulum StressGlutathioneLiverGSH Reduced glutathione;Catalase030220 oncology & carcinogenesisJNK c-Jun N-terminal kinaselcsh:Medicine (General)Research Papermedicine.medical_specialtyNF-E2-Related Factor 2Glutamate-Cysteine LigaseMKK MAPK kinaseAP-1 Activator protein-1IKK IƙB KinaseGene Expression Regulation EnzymologicSuperoxide dismutase03 medical and health sciencesInternal medicineGlutamate cysteine ligaseEGFR Epidermal growth factor receptormedicineAnimalsNuclear factor ƙBAnd catalaseChIP Chromatin immunoprecipitation;Protein kinase BNF-ƙB Nuclear factor kappa BSuperoxide DismutaseSuperoxide dismutase 1Superoxide dismutase 2Organic ChemistryGlutathioneASK1 Apoptosis signal-regulating kinase 1ATF2 activating transcription factor 2;030104 developmental biologyEndocrinologyEnzymeHsp Heat shock proteinlcsh:Biology (General)chemistrybiology.proteinSOD2 Mn-superoxide dismutaseMAPK mitogen activated protein kinaseNEM N-ethyl maleimide;Redox Biology
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A53T-Alpha-Synuclein Overexpression Impairs Dopamine Signaling and Striatal Synaptic Plasticity in Old Mice

2010

BACKGROUND: Parkinson's disease (PD), the second most frequent neurodegenerative disorder at old age, can be caused by elevated expression or the A53T missense mutation of the presynaptic protein alpha-synuclein (SNCA). PD is characterized pathologically by the preferential vulnerability of the dopaminergic nigrostriatal projection neurons. METHODOLOGY/PRINCIPAL FINDINGS: Here, we used two mouse lines overexpressing human A53T-SNCA and studied striatal dysfunction in the absence of neurodegeneration to understand early disease mechanisms. To characterize the progression, we employed young adult as well as old mice. Analysis of striatal neurotransmitter content demonstrated that dopamine (DA…

AgingDopaminelcsh:MedicineMicechemistry.chemical_compoundHomer Scaffolding ProteinsReceptor Cannabinoid CB1lcsh:ScienceLong-term depressionNeurotransmitterChromatography High Pressure LiquidIn Situ Hybridization FluorescenceOligonucleotide Array Sequence AnalysisMice KnockoutNeuronal PlasticityMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionDopaminergicNeurodegenerationGenetics and Genomics/Gene ExpressionElectrophysiologyalpha-SynucleinResearch ArticleRadioimmunoprecipitation Assaymedicine.medical_specialtyNeuronal Calcium-Sensor ProteinsHOMER1Substantia nigraNeurotransmissionBiologyNeurological DisordersInternal medicinemedicineAnimalsHumansddc:610Cyclic Nucleotide Phosphodiesterases Type 7Activating Transcription Factor 2lcsh:RNeuropeptidesmedicine.diseaseMolecular biologyCorpus StriatumMice Mutant StrainsEndocrinologyGenetics and Genomics/Disease ModelschemistrySynaptic plasticitylcsh:QCarrier ProteinsPLoS ONE
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