Search results for "PROTEIN KINASE"

showing 10 items of 1188 documents

eIF2α confers cellular tolerance to S. aureus α-toxin

2015

We report on the role of conserved stress-response pathways for cellular tolerance to a pore forming toxin. First, we observed that small molecular weight inhibitors including of eIF2α-phosphatase, jun-N-terminal kinase (JNK), and PI3-kinase sensitized normal mouse embryonal fibroblasts (MEFs) to the small pore forming S. aureus α-toxin. Sensitization depended on expression of mADAM10, the murine ortholog of a proposed high-affinity receptor for α-toxin in human cells. Similarly, eIF2α (S51A/S51A) MEFs, which harbor an Ala knock-in mutation at the regulated Ser51 phosphorylation site of eukaryotic translation initiation factor 2α, were hyper-sensitive to α-toxin. Inhibition of translation w…

lcsh:Immunologic diseases. AllergyMAPK/ERK pathwayImmunologyeIF2αBiologyCycloheximide03 medical and health scienceschemistry.chemical_compoundCellular toleranceImmunology and AllergyInitiation factorpore forming toxinsReceptorOriginal Research030304 developmental biologyGenetics0303 health sciencesKinase030302 biochemistry & molecular biologyJNK Mitogen-Activated Protein KinasesADAM10Translation (biology)MAPKCell biologyEIF2AK4chemistryPhosphorylationCytolysinS. aureus α-toxinlcsh:RC581-607Frontiers in Immunology
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Increased autophagy and apoptosis contribute to muscle atrophy in a myotonic dystrophy type 1 Drosophila model

2015

ABSTRACT Muscle mass wasting is one of the most debilitating symptoms of myotonic dystrophy type 1 (DM1) disease, ultimately leading to immobility, respiratory defects, dysarthria, dysphagia and death in advanced stages of the disease. In order to study the molecular mechanisms leading to the degenerative loss of adult muscle tissue in DM1, we generated an inducible Drosophila model of expanded CTG trinucleotide repeat toxicity that resembles an adult-onset form of the disease. Heat-shock induced expression of 480 CUG repeats in adult flies resulted in a reduction in the area of the indirect flight muscles. In these model flies, reduction of muscle area was concomitant with increased apopto…

lcsh:MedicineMedicine (miscellaneous)Genes InsectApoptosisDystrophyInhibitor of Apoptosis ProteinsAnimals Genetically ModifiedCTG repeat expansion0302 clinical medicineImmunology and Microbiology (miscellaneous)Drosophila ProteinsMyotonic DystrophyMyocyte0303 health sciencesTOR Serine-Threonine KinasesMyotonin-protein kinaseNuclear ProteinsMuscle atrophyUp-RegulationCell biologyMuscular AtrophyDrosophila melanogastermedicine.anatomical_structureFemalemedicine.symptomSignal TransductionResearch Articlelcsh:RB1-214congenital hereditary and neonatal diseases and abnormalitiesProgrammed cell deathNeuroscience (miscellaneous)BiologyMyotonic dystrophyMyotonin-Protein KinaseMuscleblindGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesAutophagylcsh:PathologymedicineAnimalsHumans030304 developmental biologylcsh:RAutophagyDystrophySkeletal musclemedicine.diseaseMolecular biologyDisease Models AnimalMuscle atrophyTrinucleotide Repeat Expansion030217 neurology & neurosurgeryDisease Models & Mechanisms
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Artemisinin–Second Career as Anticancer Drug?

2015

Artemisinin represents a showcase example not only for the activity of medicinal herbs deriving from traditional chinese medicine, but for phytotherapy in general. Its isolation from Sweet Wormwood (qinhao, Artemisia annua L.) represents the starting point for an unprecedent success story in the treatment of malaria worldwide. Beyond the therapeutic value against Plasmodium parasites, it turned out in recent years that the bioactivity of artemisinin is not restricted to malaria. We and others found that this sesquiterpenoid also exerts profound anticancer activity in vitro and in vivo. Artemisinin-type drugs exert multi-factorial cellular and molecular actions in cancer cells. Ferrous iron …

lcsh:R5-920biologyChemistryKinaseKinase insert domain receptorPharmacologyArtemisia annuaMalariaQinhaosuComplementary and alternative medicineCyclin-dependent kinaseGSK-3parasitic diseasesbiology.proteinCancer researchE2F1ChemotherapyArtemisininProtein kinase Alcsh:Medicine (General)Protein kinase BTyrosine kinaseCancerPhytotherapyWorld Journal of Traditional Chinese Medicine
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A minireview on NHE1 inhibitors. A rediscovered hope in oncohematology.

2015

Background: Na+/H+ exchanger-1 (NHE-1) is involved in pH regulation and is up-regulated in different malignancies. Activation of NHE-1 is one way for allowing cells to avoid intracellular acidification and protect them against apoptosis. Inhibitors of NHE-1 are able to decrease intracellular pH and induce apoptosis. Some statins can also act by partial inhibition of NHE-1. This review presents progress in understanding the mechanisms of action of these inhibitors, connections with certain genetic mutations and acquired treatment resistance, as well as new patents on them. Methods: A MEDLINE search for original and review articles using key terms, Na+/H+ exchanger, leukemia, cariporide, and …

lovastatinlcsh:MedicineApoptosisPharmacologyGuanidinesAmiloridep-glycoproteinhemic and lymphatic diseasesDrug InteractionsSulfonesCation Transport ProteinsSodium-Hydrogen Exchanger 1leukemiaMyeloid leukemiaHydrogen-Ion ConcentrationSorafenibUp-RegulationLeukemiaLeukemia Myeloid AcuteImatinib MesylateSignal transductionTyrosine kinasemedicine.drugSignal TransductionSorafenibNiacinamideisoprenylationSodium-Hydrogen Exchangersbcr/ablAntineoplastic AgentsGenes ablGeneral Biochemistry Genetics and Molecular BiologystatinsPatents as TopicCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansProtein Kinase Inhibitorscariporidena+/h+ exchangerTumor hypoxiabusiness.industryPhenylurea Compoundslcsh:ROsmolar Concentrationintracellular phmedicine.diseaseImatinib mesylatefms-Like Tyrosine Kinase 3Fms-Like Tyrosine Kinase 3MutationCancer researchTumor Hypoxiaflt3/itdHydroxymethylglutaryl-CoA Reductase InhibitorsbusinessHeme Oxygenase-1DNA DamageBiomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia
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Mutant HRAS as novel target for MEK and mTOR inhibitors.

2015

HRAS is a frequently mutated oncogene in cancer. However, mutant HRAS as drug target has not been investigated so far. Here, we show that mutant HRAS hyperactivates the RAS and the mTOR pathway in various cancer cell lines including lung, bladder and esophageal cancer. HRAS mutation sensitized toward growth inhibition by the MEK inhibitors AZD6244, MEK162 and PD0325901. Further, we found that MEK inhibitors induce apoptosis in mutant HRAS cell lines but not in cell lines lacking RAS mutations. In addition, knockdown of HRAS by siRNA blocked cell growth in mutant HRAS cell lines. Inhibition of the PI3K pathway alone or in combination with MEK inhibitors did not alter signaling nor had an imp…

mTOR inhibitorMutantBlotting Western610 Medicine & healthApoptosisMice SCIDCell LineProto-Oncogene Proteins p21(ras)chemistry.chemical_compoundCell Line TumorNeoplasmsMedicineAnimalsHumansHRASHRAS mutationsProtein Kinase InhibitorsPI3K/AKT/mTOR pathwayCell ProliferationGeneticsMitogen-Activated Protein Kinase KinasesMEK inhibitorOncogeneCell growthbusiness.industryMEK inhibitorTOR Serine-Threonine KinasesDiphenylamineXenograft Model Antitumor AssaysTumor Burdenlung cancer10219 Clinic for Gastroenterology and HepatologyCell Transformation NeoplasticOncologychemistry10032 Clinic for Oncology and HematologyBenzamidesMutationCancer researchbladder cancer2730 OncologyBenzimidazolesRNA InterferenceSignal transductionGrowth inhibitionbusinessSignal TransductionResearch PaperOncotarget
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Mechanisms of arachidonic acid induced glial swelling

2000

Accumulation of arachidonic acid (AA) in the brain during ischaemia may contribute to development of brain oedema. In this study we investigated the effect of selected drugs on AA-induced cytotoxic brain oedema in C6 glioma cells. Suspended C6 glioma cells were preincubated with drugs and AA (0.1 mM) was added. When no drug was administered cell volume increased immediately after the addition of AA with a maximum cell swelling of 13.1+/-1.9% at 15 min (mean +/- S.E. M.). Preincubation of cells with BW 755C, a dual inhibitor of cyclo- and lipoxygenases, showed no reduction in cell swelling from AA, whereas superoxide dismutase, amiloride and the protein kinase inhibitor H-9370 led to a signi…

medicine.drug_classModels Neurological45-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyrazol-3-amineBrain EdemaPharmacologyAmilorideSuperoxide dismutaseCellular and Molecular Neurosciencechemistry.chemical_compoundTumor Cells CulturedmedicineAnimalsCytotoxic T cellEnzyme InhibitorsOuabainMolecular BiologyCell SizeArachidonic AcidbiologySuperoxide DismutaseGliomaProtein kinase inhibitorIn vitroAmiloridemedicine.anatomical_structurechemistryCell cultureImmunologybiology.proteinNeurogliaArachidonic acidNeurogliamedicine.drugMolecular Brain Research
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Development and biological investigations of hypoxia-sensitive prodrugs of the tyrosine kinase inhibitor crizotinib

2019

Despite the huge success of tyrosine kinase inhibitors as anticancer agents, severe side effects are a major problem. In order to overcome this drawback, the first hypoxia-activatable 2-nitroimidazole-based prodrugs of the clinically approved ALK and c-MET inhibitor crizotinib were developed. The 2-aminopyridine functionality of crizotinib (essential for target kinase binding) was considered as ideal position for prodrug derivatization. Consequently, two different prodrugs were synthesized with the nitroimidazole unit attached to crizotinib either via carbamoylation (A) or alkylation (B) of the 2-aminopyridine moiety. The successful prodrug design could be proven by docking studies and a dr…

medicine.drug_classTyrosine kinase inhibitorAntineoplastic Agents01 natural sciencesBiochemistryArticleTyrosine-kinase inhibitorStructure-Activity Relationshipchemistry.chemical_compoundDrug DevelopmentCrizotinibIn vivoDrug DiscoverymedicineHumansAnaplastic Lymphoma KinaseProdrugsHypoxiaProdrugProtein Kinase InhibitorsMolecular BiologyCells CulturedCell ProliferationNitroimidazoleDose-Response Relationship DrugMolecular StructureCrizotinib010405 organic chemistryChemistryNitroimidazoleOrganic ChemistryProto-Oncogene Proteins c-metProdrugCell Hypoxia0104 chemical sciences010404 medicinal & biomolecular chemistrySettore CHIM/03 - Chimica Generale E InorganicaDocking (molecular)Cancer researchDrug Screening Assays AntitumorKinase bindingTyrosine kinasemedicine.drugBioorganic Chemistry
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Adrenergic modulation of astroglial phospholipase D activity and cell proliferation.

1999

As phospholipase D (PLD) activation has been associated with mitogenic signalling in several cell types, we tested an association between adrenergic activation of PLD and cellular proliferation in primary cultures of rat cortical astrocytes. In 2-week old cultures, PLD activation by noradrenaline (EC50: 0.49 microM) was inhibited by prazosin, a specific antagonist at alpha1-adrenergic receptors (IC50: 0.23 microM). Adrenergic PLD activation was not affected by genistein, an inhibitor of tyrosine kinases, or by Ro 31-8220, an inhibitor of protein kinase C (PKC), but was dose-dependently depressed in the presence of brefeldin A (1-100 microg/ml), an inhibitor of ARF activation. In experiments…

medicine.medical_specialtyAdrenergic AntagonistsAdrenergicBiologyPharmacologychemistry.chemical_compoundNorepinephrineGTP-Binding ProteinsIsoprenalineInternal medicinemedicineAdrenergic antagonistPrazosinPhospholipase DPhospholipase D activityAnimalsMolecular BiologyProtein kinase CCells CulturedBrefeldin APhospholipase DGeneral NeurosciencePrazosinBrefeldin AAdrenergic AgonistsPropranololRatsReceptors AdrenergicEndocrinologychemistryAlcoholsAstrocyteslipids (amino acids peptides and proteins)Neurology (clinical)Cell DivisionDevelopmental Biologymedicine.drugSignal TransductionBrain research
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Age-dependent changes of nuclear envelope protein phosphokinase and protein phosphatase activities. Significance for altered nucleo-cytoplasmic mRNA …

1984

Nuclear envelopes are associated with a protein phosphokinase and a phosphoprotein phosphatase, whose activities are modulated by poly(A) in an opposite manner. The activities of these enzymes were determined in nuclear ghosts from liver and oviduct of quails of different age and of different hormone status. Under optimal conditions, kinase activity was found to increase in immature animals 8-fold in response to diethylstilbestrol; co-administration of progesterone had no marked effect on enzyme activity. After the initial burst, the activity of the enzyme increased only slightly during ageing. Two proteins present in nuclear ghosts of Mr 64 000 and of Mr 106 000 are phosphorylated during t…

medicine.medical_specialtyAgingNuclear Envelopemedicine.medical_treatmentPhosphataseOviductsQuailInternal medicinemedicinePhosphoprotein PhosphatasesAnimalsProtein phosphorylationRNA MessengerKinase activityPhosphorylationProtein kinase ADiethylstilbestrolProgesteronebiologyKinaseBiological TransportEnzyme assayMolecular WeightSteroid hormoneEndocrinologyLiverbiology.proteinPhosphorylationFemaleProtein KinasesDevelopmental BiologyMechanisms of ageing and development
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Estradiol or genistein prevent Alzheimer's disease-associated inflammation correlating with an increase PPAR gamma expression in cultured astrocytes.

2009

Inflammation has been implicated in neurodegenerative disorders such as Alzheimer's disease (AD). The main inflammatory players in AD are the glial cells which initiate the inflammatory response. One of the earliest neuropathological changes in AD is the accumulation of astrocytes at sites of A beta deposition. It is desirable to find methods of tipping the balance towards anti-inflammatory state. Estrogenic compounds have shown anti-inflammatory and also antioxidant activity. Astrocytes were pretreated with 17-beta estradiol or with genistein, and 48 h later treated with 5 microM amyloid beta (A beta) for 24 h. We found that A beta induces inflammatory mediators, such as cyclooxygenase 2 (…

medicine.medical_specialtyAmyloid betaInterleukin-1betaGenisteinPeroxisome proliferator-activated receptorNitric Oxide Synthase Type IIInflammationEnzyme-Linked Immunosorbent Assaychemistry.chemical_compoundInternal medicinemedicineAnimalsDrug InteractionsMolecular BiologyProtein Kinase InhibitorsCells Culturedchemistry.chemical_classificationCerebral CortexAmyloid beta-PeptidesbiologyDose-Response Relationship DrugEstradiolTumor Necrosis Factor-alphaGeneral NeuroscienceInterleukinEstrogensGenisteinPeptide FragmentsRatsPPAR gammaEndocrinologymedicine.anatomical_structurechemistryGene Expression RegulationCyclooxygenase 2Astrocytesbiology.proteinNeurogliaTumor necrosis factor alphaNeurology (clinical)medicine.symptomDevelopmental BiologyAstrocyteBrain research
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