Search results for "Phosphorylation"

showing 10 items of 975 documents

Regulation of the proapoptotic functions of prostate apoptosis response-4 (Par-4) by casein kinase 2 in prostate cancer cells

2013

International audience; The proapoptotic protein, prostate apoptosis response-4 (Par-4), acts as a tumor suppressor in prostate cancer cells. The serine/threonine kinase casein kinase 2 (CK2) has a well-reported role in prostate cancer resistance to apoptotic agents or anticancer drugs. However, the mechanistic understanding on how CK2 supports survival is far from complete. In this work, we demonstrate both in rat and humans that (i) Par-4 is a new substrate of the survival kinase CK2 and (ii) phosphorylation by CK2 impairs Par-4 proapoptotic functions. We also unravel different levels of CK2-dependent regulation of Par-4 between species. In rats, the phosphorylation by CK2 at the major si…

MaleCancer Researchanimal structuresCK2[SDV]Life Sciences [q-bio]ImmunologyAmino Acid MotifsPAWR[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]Biology[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biology[SDV.MHEP.UN]Life Sciences [q-bio]/Human health and pathology/Urology and NephrologyCellular and Molecular NeuroscienceProstate cancer[SDV.CAN] Life Sciences [q-bio]/CancerProstateCell Line Tumor[SDV.BC.BC] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]medicineAnimalsHumansCasein Kinase IIComputingMilieux_MISCELLANEOUSGene knockdownKinasephosphorylationfungita1182apoptosisProstatic Neoplasms[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyCell Biologymedicine.diseaseprostate cancer[SDV.MHEP.UN] Life Sciences [q-bio]/Human health and pathology/Urology and NephrologyRatsmedicine.anatomical_structureApoptosisembryonic structuresCancer researchPhosphorylationOriginal ArticleCasein kinase 2Apoptosis Regulatory ProteinsPar-4
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Cannabinoid modulation of hippocampal long-term memory is mediated by mTOR signaling.

2009

Cognitive impairment is one of the most important negative consequences associated with cannabis consumption. We found that CB1 cannabinoid receptor (CB1R) activation transiently modulated the mammalian target of rapamycin (mTOR)/p70S6K pathway and the protein synthesis machinery in the mouse hippocampus, which correlated with the amnesic properties of delta9-tetrahydrocannabinol (THC). In addition, non-amnesic doses of either the mTOR blocker rapamycin or the protein synthesis inhibitor anisomycin abrogated the amnesic-like effects of THC, pointing to a mechanism involving new protein synthesis. Moreover, using pharmacological and genetic tools, we found that THC long-term memory deficits …

MaleCannabinoid receptormedicine.medical_treatmentGlutamic AcidHippocampusReceptors N-Methyl-D-AspartateGlutamatergicchemistry.chemical_compoundMiceCognitionReceptor Cannabinoid CB1Memorymental disordersmedicineAnimalsDronabinolPI3K/AKT/mTOR pathwayAnisomycingamma-Aminobutyric AcidMice KnockoutNeuronsProtein Synthesis InhibitorsSirolimusMemory DisordersChemistryGeneral NeuroscienceTOR Serine-Threonine KinasesRibosomal Protein S6 Kinases 70-kDanervous systemKnockout mouseNMDA receptorPhosphorylationCannabinoidNeuroscienceProtein KinasesAnisomycinCentral Nervous System AgentsSignal TransductionNature neuroscience
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Induction of hepatic heme oxygenase-1 by diclofenac in rodents: role of oxidative stress and cytochrome P-450 activity

2003

Abstract Background/Aims : The role of oxidative stress in diclofenac hepatotoxicity is still not clear. This study examined whether the drug induced heme oxygenase-1 (HO-1), a stress protein. Methods : HO-1 mRNA and HO activity were measured in mouse liver and in rat hepatocytes after treatment with diclofenac parallel to release of serum alanine aminotransferase (ALT) and sorbitol dehydrogenase (SDH) as a marker of hepatic damage. Results : HO-1 was transcriptionally and dose-dependently induced by diclofenac in mouse liver and rat hepatocytes. HO-1 mRNA, ALT and SDH peaked at the same time. Mechanistic studies revealed that the drug synergized with buthionine sulfoximine (BSO) in lowerin…

MaleCarcinoma HepatocellularDiclofenacCytochromeMice Inbred StrainsOxidative phosphorylationPharmacologymedicine.disease_causeMicechemistry.chemical_compoundCytochrome P-450 Enzyme SystemCell Line TumormedicineAnimalsCytochrome P-450 Enzyme InhibitorsHumansButhionine sulfoximineEnzyme InhibitorsButhionine SulfoximineDose-Response Relationship DrugHepatologybiologyLiver NeoplasmsMembrane ProteinsCytochrome P450GlutathioneAcetylcysteineRatsHeme oxygenaseOxidative Stressstomatognathic diseasesmedicine.anatomical_structureLiverchemistryBiochemistryEnzyme InductionHepatocyteHeme Oxygenase (Decyclizing)Hepatocytesbiology.proteinFemaleHeme Oxygenase-1Oxidative stressJournal of Hepatology
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Redox state alteration modulates astrocyte glucuronidation.

2004

We have investigated the effects of mild oxidative conditions on drug-metabolizing enzyme activity in rat cultured astrocytes. These experimental conditions promoting an oxidative environment were obtained by short exposure to a low concentration of menadione (5 microM) for a short duration (15 min). This resulted in the rapid and transient production of reactive oxygen species (+130%), associated with a decrease in GSH cellular content (-24%), and an increase in total protein oxidation (+26%), but promoted neither PGE(2) nor NO production. This treatment induced a rapid and persistent decrease in astrocyte glucuronidation activities, which was totally prevented by N-acetyl-l-cysteine. Thes…

MaleCell SurvivalGlucuronidationApoptosisGlucuronatesOxidative phosphorylationmedicine.disease_causeProtein oxidationBiochemistryRedoxchemistry.chemical_compoundMenadionePhysiology (medical)CricetinaemedicineAnimalsProtein IsoformsRNA MessengerGlucuronosyltransferaseRats WistarPromoter Regions GeneticCells Culturedchemistry.chemical_classificationInflammationReactive oxygen speciesBase SequenceVitamin K 3GlutathioneHydrogen PeroxideMolecular biologyGlutathioneCell biologyRatschemistryAstrocytesFemaleReactive Oxygen SpeciesOxidation-ReductionOxidative stressFree radical biologymedicine
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p38 MAP kinase drives the expression of mast cell-derived IL-9 via activation of the transcription factor GATA-1.

2007

Mast cells are able to produce a huge panel of mediators including the Th2-type cytokine IL-9, which is considered to be a key mediator for the pathogenesis of allergic asthma, but detailed information on the regulation of IL-9 transcription in mast cells has been scarce. Herein we provide evidence that the erythroid/myeloid transcription factor GATA-1, which is not expressed in Th2 cells, is a potent activator of IL-9 expression in murine bone marrow-derived mast cells (BMMC). Furthermore, in mast cells, but not in Th2 cells, production of IL-9 is sensitive to inhibition of p38 MAP kinase. As transactivation mediated by GATA-1 is also sensitive to inhibition of p38 MAP kinase, and GATA-1 i…

MaleCell signalingmedicine.medical_treatmentImmunologyBone Marrow CellsGATA3 Transcription FactorBiologyp38 Mitogen-Activated Protein KinasesTransactivationMiceTh2 CellsmedicineAnimalsGATA1 Transcription FactorMast CellsRNA MessengerPhosphorylationPromoter Regions GeneticMolecular BiologyInterleukin 5Mice Inbred BALB CGATA2Interleukin-9Mast cellCell biologyInterleukin 33GATA2 Transcription FactorCytokinemedicine.anatomical_structureGene Expression RegulationInterleukin 15MutationFemaleMolecular immunology
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Toll-like receptor 5 deficiency exacerbates cardiac injury and inflammation induced by myocardial ischaemia-reperfusion in the mouse

2015

Myocardial ischaemia-reperfusion (MIR) triggers a sterile inflammatory response important for myocardial healing, but which may also contribute to adverse ventricular remodelling. Such inflammation is initiated by molecular danger signals released by damaged myocardium, which induce innate immune responses by activating toll-like receptors (TLRs). Detrimental roles have been recently reported for TLR2, TLR3 and TLR4. The role of other TLRs is unknown. We therefore evaluated the role of TLR5, expressed at high level in the heart, in the development of myocardial damage and inflammation acutely triggered by MIR. TLR5−/− and wild-type (WT) mice were exposed to MIR (30 min ischaemia, 2 h reperf…

MaleChemokinemedicine.medical_specialtyGenotypep38 mitogen-activated protein kinasesMyocardial InfarctionMyocardial Reperfusion InjuryInflammation030204 cardiovascular system & hematologyBiologyp38 Mitogen-Activated Protein KinasesVentricular Function LeftProinflammatory cytokineVentricular Dysfunction Left03 medical and health sciences0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemInternal medicinemedicineAnimalsPhosphorylationProtein kinase B030304 developmental biologyInflammationMice Knockout0303 health sciencesToll-like receptorMyocardiumGeneral MedicineImmunity Innate3. Good healthMice Inbred C57BLDisease Models AnimalOxidative StressToll-Like Receptor 5CXCL2PhenotypeEndocrinologybiology.proteinTLR4Inflammation Mediatorsmedicine.symptomProto-Oncogene Proteins c-aktClinical Science
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Hepatoprotective and anti-inflammatory effects of total flavonoids of Qu Zhi Ke (peel of Citrus changshan-huyou) on non-alcoholic fatty liver disease…

2019

Abstract Background Citrus flavonoids, consisting of naringin, narirutin, neohesperidine, etc., have therapeutic activities for the treatment of lipometabolic disorders. The peel of Citrus changshan-huyou (Qu Zhi Ke, QZK) is a new source of flavonoids, but attracted little attention so far. Hypothesis QZK should possess therapeutic effects against lipometabolic disorders due to the flavonoids it contains. Study design In this study, we extracted and purified the flavonoids of QZK (TFCH) and established an obesity-induced non-alcoholic fatty liver disease (NAFLD) model of rats. TFCH was given orally for 8 weeks, and its anti-NAFLD effects and potential mechanism were evaluated. Methods The f…

MaleCitrusmedicine.drug_classFlavonoidPharmaceutical SciencePharmacologyDiet High-FatProtective AgentsAnti-inflammatoryProinflammatory cytokineRats Sprague-Dawley03 medical and health scienceschemistry.chemical_compound0302 clinical medicineWestern blotNon-alcoholic Fatty Liver DiseaseDrug DiscoveryNonalcoholic fatty liver diseasemedicineAnimalsPhosphorylationNaringin030304 developmental biologyFlavonoidsPharmacologychemistry.chemical_classification0303 health sciencesNarirutinmedicine.diagnostic_testPlant ExtractsAnti-Inflammatory Agents Non-SteroidalFatty liverNF-kappa Bfood and beveragesmedicine.diseaseGene Expression RegulationLiverComplementary and alternative medicinechemistry030220 oncology & carcinogenesisMolecular MedicineMitogen-Activated Protein KinasesPhytomedicine
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Effect of nitrite on microsomal cytochrome P-450.

1978

1. Addition of nitrite to anaerobic rat liver microsomes leads to the appearance of a difference spectrum similar to the spectrum of the ferrous cytochrome P-450-NO complex. A Soret band is found at 444 nm in phenobarbital-stimulated microsomes but at 442 nm in 3-methylcholanthrene-stimulated microsomes. An alpha-band is located at 583 nm in both types of microsome. 2. The initial nitrite-induced difference spectrum is converted into a spectrum lacking a Soret band but with a prominent absorbance minimum at 417 nm. This is more rapid in microsomes from phenobarbital-treated animals where it is completed in 8 min than in microsomes from 3-methylcholanthrene-treated animals. A similar spectru…

MaleCytochromeLightHealth Toxicology and MutagenesisOxidative phosphorylationIn Vitro TechniquesToxicologyNitric OxideBiochemistryFerrousAbsorbancechemistry.chemical_compoundCytochrome P-450 Enzyme SystemAnimalsNitriteNitritesPharmacologybiologyGeneral MedicineRatsBiochemistrychemistrySpectrophotometrybiology.proteinMicrosomeMicrosomes LiverAnaerobic exerciseDrug metabolismXenobiotica; the fate of foreign compounds in biological systems
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Regio- and stereoselective regulation of monooxygenase activities by isoenzyme-selective phosphorylation of cytochrome P450.

1989

The phosphorylation of the two major phenobarbital-inducible cytochrome P450 isoenzymes IIB1 and IIB2 was increased in hepatocytes by the action of the membrane permeating cAMP derivatives N6-dibutyryl-cAMP and 8-thiomethyl-cAMP. Under these conditions the dealkylation of 7-pentoxyresorufin, a selective substrate of cytochrome P450IIB1 and P450IIB2 was markedly reduced. 16 beta-Hydroxylation of testosterone which is catalyzed specifically only by cytochrome P450IIB1 and IIB2 was strongly reduced; for 16 alpha-hydroxylation which is also catalyzed by cytochrome P450IIB1 and IIB2 but additionally by 3 further cytochrome P450 isoenzymes, this reduction was less pronounced; for the oxidation of…

MaleCytochromeStereochemistry25-Hydroxyvitamin D3 1-alpha-hydroxylaseBiophysicsHydroxylationBiochemistryMixed Function OxygenasesCytochrome P-450 Enzyme SystemCyclic AMPCytochrome c oxidaseAnimalsTestosteronePhosphorylationMolecular BiologybiologyChemistryCytochrome c peroxidaseCytochrome cCYP1A2Cytochrome P450 reductaseRats Inbred StrainsCell BiologyRatsIsoenzymesBiochemistryLiverSteroid 16-alpha-HydroxylaseCoenzyme Q – cytochrome c reductasePhenobarbitalbiology.proteinProtein Processing Post-TranslationalBiochemical and biophysical research communications
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Muscle NAD+ depletion and Serpina3n as molecular determinants of murine cancer cachexia—the effects of blocking myostatin and activins

2020

Objective Cancer cachexia and muscle loss are associated with increased morbidity and mortality. In preclinical animal models, blocking activin receptor (ACVR) ligands has improved survival and prevented muscle wasting in cancer cachexia without an effect on tumour growth. However, the underlying mechanisms are poorly understood. This study aimed to identify cancer cachexia and soluble ACVR (sACVR) administration-evoked changes in muscle proteome. Methods Healthy and C26 tumour-bearing (TB) mice were treated with recombinant sACVR. The sACVR or PBS control were administered either prior to the tumour formation or by continued administration before and after tumour formation. Muscles were an…

MaleEXPRESSIONActivin receptor; APR; C26; Cancer cachexia; Nrk2; OXPHOSlcsh:Internal medicineCachexiaREVERSALActivin ReceptorsMETABOLISMactivin receptorOxidative PhosphorylationCell Line TumorAnimalsMuscle Skeletallcsh:RC31-1245aineenvaihduntaSerpinslihassolut318 Medical biotechnologyNrk2Cancer cachexiaMyostatinNADOXPHOSMUSCULAR-DYSTROPHYActivinsMitochondriaActivin receptorDisease Models AnimalMuscular AtrophyMICESIRTUINSOriginal ArticlesyöpätauditproteiinitC26lihassurkastumasairaudetAPRAcute-Phase Proteinscancer cachexia
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