Search results for "kinases"

showing 10 items of 929 documents

Protein kinase inhibitor β enhances the constitutive activity of G-protein-coupled zinc receptor GPR39.

2014

GPR39 is a G-protein-coupled zinc receptor that protects against diverse effectors of cell death. Its protective activity is mediated via constitutive activation of Gα13 and the RhoA pathway, leading to increased SRE (serum-response element)-dependent transcription; the zinc-dependent immediate activation of GPR39 involves Gq-mediated increases in cytosolic Ca2+ and Gs coupling leading to increased cAMP levels. We used the cytosolic and soluble C-terminus of GPR39 in a Y2H (yeast-2-hybrid) screen for interacting proteins, thus identifying PKIB (protein kinase A inhibitor β). Co-expression of GPR39 with PKIB increased the protective activity of GPR39 via the constitutive, but not the ligand-…

RHOAmedicine.drug_classG proteinCHO CellsBiochemistryCell LineReceptors G-Protein-CoupledMiceCricetulusTwo-Hybrid System TechniquesmedicineAnimalsHumansProtein kinase AReceptorMolecular BiologyProtein Kinase InhibitorsbiologyEffectorCell MembraneIntracellular Signaling Peptides and ProteinsCell BiologyProtein kinase inhibitorCyclic AMP-Dependent Protein KinasesProtein Kinase A InhibitorCytosolZincBiochemistrybiology.proteinHeLa CellsThe Biochemical journal
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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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Studying the phosphoryl transfer mechanism of the E. coli phosphofructokinase-2: from X-ray structure to quantum mechanics/molecular mechanics simula…

2019

Phosphofructokinases (Pfks) catalyze the ATP-dependent phosphorylation of fructose-6-phosphate (F6P) and they are regulated in a wide variety of organisms. Although numerous aspects of the kinetics and regulation have been characterized for Pfks, the knowledge about the mechanism of the phosphoryl transfer reaction and the transition state lags behind. In this work, we describe the X-ray crystal structure of the homodimeric Pfk-2 from E. coli, which contains products in one site and reactants in the other, as well as an additional ATP molecule in the inhibitory allosteric site adjacent to the reactants. This complex was previously predicted when studying the kinetic mechanism of ATP inhibit…

Reaction mechanism010405 organic chemistryChemistryMetaphosphateKineticsAllosteric regulationGeneral Chemistry010402 general chemistry01 natural sciencesMolecular mechanics0104 chemical sciencesMolecular dynamicschemistry.chemical_compoundBACTÉRIAS GRAM-NEGATIVASQuantum mechanicsMoleculePhosphofructokinasesChemical Science
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Entrectinib: a potent new TRK, ROS1, and ALK inhibitor

2015

Abstract: Introduction: Receptor tyrosine kinases (RTKs) and their signaling pathways, control normal cellular processes; however, their deregulation play important roles in malignant transformation. In advanced non-small cell lung cancer (NSCLC), the recognition of oncogenic activation of specific RTKs, has led to the development of molecularly targeted agents that only benefit roughly 20% of patients. Entrectinib is a pan-TRK, ROS1 and ALK inhibitor that has shown potent anti-neoplastic activity and tolerability in various neoplastic conditions, particularly NSCLC. Areas covered: This review outlines the pharmacokinetics, pharmacodynamics, mechanism of action, safety, tolerability, pre-cl…

Receptor Protein-Tyrosine KinasesEntrectinibNTRK1NTRK2NTRK3Receptor tyrosine kinaseEntrectinibMalignant transformationAntineoplastic AgentNeoplasmsProtein-Tyrosine KinaseALK; colorectal cancer; Entrectinib; non-small cell lung cancer; NTRK1; NTRK2; NTRK3; precision medicine; ROS1; salivary gland cancer; TrkA; TrkB; TrkC; Animals; Antineoplastic Agents; Benzamides; Humans; Indazoles; Neoplasms; Protein-Tyrosine Kinases; Proto-Oncogene Proteins; Receptor Protein-Tyrosine Kinases; Receptor; trkA; Receptor; trkB; Receptor; trkC; Pharmacology; Pharmacology (medical)Anaplastic Lymphoma KinasePharmacology (medical)salivary gland cancerProto-Oncogene ProteinbiologyTrkAPharmacology. TherapyTrkCTrkBGeneral MedicineProtein-Tyrosine KinasesReceptor Protein-Tyrosine KinaseBenzamidesmedicine.symptomROS1ReceptorHumanIndazolesmedicine.drug_classprecision medicineAntineoplastic Agentscolorectal cancerBenzamideProto-Oncogene ProteinsmedicineROS1AnimalsHumansReceptor trkBReceptor trkCReceptor trkAnon-small cell lung cancerPharmacologyAnimalReceptor Protein-Tyrosine KinasesALK inhibitorIndazoleMechanism of actionALKTrk receptorbiology.proteinCancer researchNeoplasmALK; colorectal cancer; Entrectinib; non-small cell lung cancer; NTRK1; NTRK2; NTRK3; precision medicine; ROS1; salivary gland cancer; TrkA; TrkB; TrkC; Animals; Antineoplastic Agents; Benzamides; Humans; Indazoles; Neoplasms; Protein-Tyrosine Kinases; Proto-Oncogene Proteins; Receptor Protein-Tyrosine Kinases; Receptor trkA; Receptor trkB; Receptor trkC; Pharmacology; Pharmacology (medical)Expert Opinion on Investigational Drugs
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Activation of mitogen-activated protein kinase by the bradykinin B2receptor is independent of receptor phosphorylation and phosphorylation-triggered …

1999

Recent evidence suggests that serine/threonine phosphorylation and internalization of beta2-adrenergic receptors play critical roles in signalling to the mitogen-activated protein kinase cascade. To investigate whether this represents a general mechanism employed by G protein-coupled receptors, we studied the requirement of these processes in the activation of mitogen-activated protein kinase by G alpha(q)-coupled bradykinin B2 receptors. Mutant B2 receptors impaired in receptor phosphorylation and internalization are fully capable to activate mitogen-activated protein kinase. Bradykinin-induced long-term effects on mitogenic signalling monitored by measuring the transcriptional activity of…

Receptor Bradykinin B2Bradykinin B2 receptorBiophysicsMitogen-activated protein kinase kinaseBradykininBiochemistryCell LineMAP2K7Structural BiologyMitogenic signallingGeneticsHumansPhosphorylationBradykinin receptorProtein kinase AMolecular BiologyProtein kinase CG protein-coupled receptorG protein-coupled receptor kinaseMAP kinase kinase kinaseChemistryReceptors BradykininCell BiologyMitogen-activated protein kinaseEnzyme ActivationBiochemistryCalcium-Calmodulin-Dependent Protein KinasesInternalizationSignal TransductionFEBS Letters
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Two distinct Ca2+ influx pathways activated by the bradykinin B2 receptor.

1996

The hormone-induced depletion of cellular Ca stores provides a signal for the Ca2+ influx into electrically non-excitable cells; however, the underlying molecular mechanisms remain elusive. Therefore, we analyzed bradykinin-activated Ca2+ influx into human foreskin fibroblast cells, HF-15, by fura-2 and 45Ca labeling to discriminate between Ca2+ influx into the fura-sensitive compartment and Ca uptake into fura-insensitive Ca stores. Bradykinin-activated CaZt influx into the fura-sensitive compartment was blocked by inhibitors of NO synthases. These inhibitors also suppressed bradykinin-activated increases in cGMP, indicating that the NO-dependent increase in cGMP is involved in the activat…

Receptor Bradykinin B2BradykininBradykininNitric OxideBiochemistryNitric oxideCell Linechemistry.chemical_compoundmedicineCyclic GMP-Dependent Protein KinasesHumansFibroblastCyclic GMPInterphaseFluorescent DyesIon TransportCell growthChemistryKinaseReceptors BradykininCa2 influxCompartment (chemistry)Calcium Channel BlockersCell biologymedicine.anatomical_structureBiochemistryCytoplasmCalciumFura-2Cell DivisionEuropean journal of biochemistry
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Novel therapeutic targets in esophageal cancer: impact of chemokine receptor CXCR4

2007

Ines Gockel†, Carl C Schimanski, Markus Moehler & Theodor Junginger †Author for correspondence Johannes GutenbergUniversity of Mainz, Department of General and Abdominal Surgery, Langenbeckstr. 1, 55131 Mainz, Germany Tel.: +49 6131 177 291; Fax: +49 6131 176 630; gockel@ach.klinik.unimainz.de ‘The interaction between esophageal cancer-expressed CXCR4 and SDF-1α may have a key role in directing malignant cells to ‘homing’ organs ... thus, this mechanism may account for metastasis.’

Receptors CXCR4Cancer ResearchEsophageal Neoplasmsbusiness.industryAntineoplastic AgentsGeneral MedicineEsophageal cancermedicine.diseaseCXCR4Chemokine CXCL12Cyclin-Dependent KinasesNeoadjuvant TherapyhumanitiesChemokine receptorDrug Delivery SystemsOncologyCancer researchmedicineHumansMalignant cellsbusinessChemokines CXCHoming (hematopoietic)Future Oncology
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Characterization of a Naturally Occurring Breast Cancer Subset Enriched in Epithelial-to-Mesenchymal Transition and Stem Cell Characteristics

2009

Abstract Metaplastic breast cancers (MBC) are aggressive, chemoresistant tumors characterized by lineage plasticity. To advance understanding of their pathogenesis and relatedness to other breast cancer subtypes, 28 MBCs were compared with common breast cancers using comparative genomic hybridization, transcriptional profiling, and reverse-phase protein arrays and by sequencing for common breast cancer mutations. MBCs showed unique DNA copy number aberrations compared with common breast cancers. PIK3CA mutations were detected in 9 of 19 MBCs (47.4%) versus 80 of 232 hormone receptor–positive cancers (34.5%; P = 0.32), 17 of 75 HER-2–positive samples (22.7%; P = 0.04), 20 of 240 basal-like c…

Receptors SteroidCancer ResearchPathologymedicine.medical_specialtyTranscription GeneticClass I Phosphatidylinositol 3-KinasesBreast NeoplasmsArticleCohort StudiesProto-Oncogene Proteins p21(ras)Phosphatidylinositol 3-KinasesBreast cancerProto-Oncogene ProteinsBiomarkers TumormedicineHumansRNA NeoplasmEpithelial–mesenchymal transitionskin and connective tissue diseasesComparative Genomic HybridizationMetaplasiabiologyGene Expression ProfilingCD44PTEN PhosphohydrolaseCancerEpithelial CellsMesenchymal Stem CellsSarcomaDNA NeoplasmMetaplastic Breast Carcinomamedicine.diseaseClaudin-LowOncologyMutationCarcinoma Squamous Cellras Proteinsbiology.proteinCancer researchFemaleBreast diseaseStem cellProto-Oncogene Proteins c-aktCancer Research
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Antagonistic feedback loops involving Rau and Sprouty in the Drosophila eye control neuronal and glial differentiation.

2013

During development, differentiation is often initiated by the activation of different receptor tyrosine kinases (RTKs), which results in the tightly regulated activation of cytoplasmic signaling cascades. In the differentiation of neurons and glia in the developing Drosophila eye, we found that the proper intensity of RTK signaling downstream of fibroblast growth factor receptor (FGFR) or epidermal growth factor receptor required two mutually antagonistic feedback loops. We identified a positive feedback loop mediated by the Ras association (RA) domain-containing protein Rau that sustained Ras activity and counteracted the negative feedback loop mediated by Sprouty. Rau has two RA domains t…

Receptors SteroidGTP'Blotting WesternIn situ hybridizationEyeBiochemistryReceptor tyrosine kinaseMicroscopy Electron TransmissionAnimalsDrosophila ProteinsEpidermal growth factor receptorReceptorMolecular BiologyTranscription factorIn Situ HybridizationFeedback PhysiologicalbiologyIntracellular Signaling Peptides and ProteinsMembrane ProteinsReceptor Protein-Tyrosine KinasesCell DifferentiationCell BiologyAnatomyPhenotypeImmunohistochemistryCell biologyProtein Structure TertiaryDNA-Binding ProteinsEnzyme ActivationCOUP Transcription FactorsGene Expression RegulationFibroblast growth factor receptorbiology.proteinDrosophilaNeurogliaProtein BindingSignal TransductionScience signaling
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Suppressor of fused links Fused and Cubitus interruptus on the Hedgehog signalling pathway

1998

0960-9822 doi: DOI: 10.1016/S0960-9822(98)70227-1; The Hedgehog (Hh) family of signalling proteins [1] mediate inductive interactions either directly or by controlling the transcription of other secreted proteins through the action of Gli transcription factors, such as Cubitus interruptus (Ci) [2]. In Drosophila, the transcription of Hh targets requires the activation of the protein kinase Fused (Fu) and the inactivation of both Suppressor of fused (Su(fu)) and Costal-2 (Cos-2) [3]. Fu is required for Hh signalling in the embryo and in the wing imaginal disc and acts also as an antitumorigen in ovaries [4]. All fu– phenotypes are suppressed by the loss of function of Su(fu) [5]. Fu, Cos-2 a…

Recombinant Fusion ProteinsBiologyProtein Serine-Threonine KinasesGeneral Biochemistry Genetics and Molecular Biologylaw.invention03 medical and health sciences0302 clinical medicinelawTranscription (biology)AnimalsDrosophila ProteinsHedgehog ProteinsProtein kinase AIntracellular partTranscription factorHedgehog030304 developmental biology0303 health sciencesAgricultural and Biological Sciences(all)Biochemistry Genetics and Molecular Biology(all)AnatomyCi proteinCell biologyDNA-Binding ProteinsRepressor ProteinsImaginal discSuppressorInsect ProteinsRabbitsGeneral Agricultural and Biological Sciences030217 neurology & neurosurgerySignal TransductionTranscription Factors
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