Search results for "protein kinase A"

showing 10 items of 231 documents

Arrestin-β-1 Physically Scaffolds TSH and IGF1 Receptors to Enable Crosstalk

2019

Endogenously expressed TSH receptors (TSHRs) on orbital fibroblasts of patients with Graves ophthalmopathy (GO) use crosstalk with IGF1 receptors (IGF1R) to synergistically stimulate secretion of hyaluronan (HA), a major component of GO pathology. We previously showed crosstalk occurred upstream of mitogen-activated protein kinase (ERK) phosphorylation. Because other G protein-coupled receptors engage arrestin-β-1 (ARRB1) and ERK, we tested whether ARRB1 was a necessary component of TSHR/IGF1R crosstalk. HA secretion was stimulated by the TSHR-stimulating monoclonal antibodies M22 and KSAb1, or immunoglobulins from patients with GO (GO-Igs). Treatment with M22, as previously shown, resulted…

0301 basic medicineMAPK/ERK pathwaymedicine.medical_specialty030209 endocrinology & metabolismStimulationReceptor tyrosine kinaseCell LineReceptor IGF Type 103 medical and health sciencesMice0302 clinical medicineEndocrinologyInternal medicinemedicineArrestinAnimalsHumansPhosphorylationProtein kinase AReceptorResearch ArticlesbiologyChemistryReceptors Thyrotropinbody regionsGraves OphthalmopathyCrosstalk (biology)030104 developmental biologyEndocrinologybeta-Arrestin 1Thyroid Epithelial CellsGene Knockdown Techniquesbiology.proteinPhosphorylationSignal Transduction
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AMPK phosphorylation modulates pain by activation of NLRP3 inflammasome

2016

et al.

0301 basic medicineMESH : Carrier Proteins/geneticsMaleMESH: Fibromyalgia/geneticsFibromyalgiaIndolesPhysiologyInflammasomesClinical BiochemistryInterleukin-1betaInjuryAMP-Activated Protein KinasesNeuropathic painBiochemistryPyrin domainMice0302 clinical medicineAMP-activated protein kinaseRestrictionSunitinibDiseasePhosphorylationGeneral Environmental Sciencebiologyintegumentary systemChemistryInterleukin-18InflammasomePain Perception[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism[ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismMiddle AgedMetforminCell biologyOriginal Research CommunicationsMESH : Fibromyalgia/geneticsHyperalgesiaPhosphorylationFemalemedicine.symptommedicine.drugMESH : Inflammasomes/metabolismAdultmedicine.medical_specialtyPain03 medical and health sciencesMESH: Carrier Proteins/geneticsInternal medicineNLR Family Pyrin Domain-Containing 3 ProteinmedicineAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyPyrrolesProtein kinase AMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Inflammasomes/metabolismFibromialgia patientsAMPK ; fibromyalgia ; NLRP3 InflammasomeDangerAMPKCell BiologyAdenosineMESH: AMP-Activated Protein Kinases/genetics030104 developmental biologyEndocrinologyMetabolismProtein-Kinase AMPKbiology.proteinGeneral Earth and Planetary SciencesMESH : AMP-Activated Protein Kinases/geneticsAnalgesiaCarrier Proteins030217 neurology & neurosurgery
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Mitochondrial Fatty Acid β-Oxidation Inhibition Promotes Glucose Utilization and Protein Deposition through Energy Homeostasis Remodeling in Fish.

2020

BACKGROUND: Fish cannot use carbohydrate efficiently and instead utilize protein for energy supply, thus limiting dietary protein storage. Protein deposition is dependent on protein turnover balance, which correlates tightly with cellular energy homeostasis. Mitochondrial fatty acid β-oxidation (FAO) plays a crucial role in energy metabolism. However, the effect of remodeled energy homeostasis caused by inhibited mitochondrial FAO on protein deposition in fish has not been intensively studied. OBJECTIVES: This study aimed to identify the regulatory role of mitochondrial FAO in energy homeostasis maintenance and protein deposition by studying lipid, glucose, and protein metabolism in fish. M…

0301 basic medicineMaleProtein metabolismMedicine (miscellaneous)MitochondrionEnergy homeostasis03 medical and health scienceschemistry.chemical_compoundNile tilapia0302 clinical medicineAdjuvants ImmunologicmedicineAnimalsHomeostasisInsulinCarnitineProtein kinase ACells CulturedZebrafishNutrition and DieteticsbiologyCarnitine O-PalmitoyltransferaseChemistryFatty AcidsProtein turnoverProteinsMetabolismCichlidsDNACytochromes bbiology.organism_classificationMitochondria030104 developmental biologyGlucoseBiochemistryMutationHepatocytesNutrient Physiology Metabolism and Nutrient-Nutrient InteractionsEnergy MetabolismOxidation-Reduction030217 neurology & neurosurgerymedicine.drugMethylhydrazinesThe Journal of nutrition
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H89 Treatment Reduces Intestinal Inflammation and Candida albicans Overgrowth in Mice

2020

Deregulation of the dynamic crosstalk between the gut microbiota, intestinal epithelial cells, and immune cells is critically involved in the development of inflammatory bowel disease and the overgrowth of opportunistic pathogens, including the human opportunistic fungus Candida albicans. In the present study, we assessed the effect of N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H89), a protein kinase A inhibitor, on the migration of macrophages to C. albicans through dextran sulphate sodium (DSS)-challenged Caco-2 cells. We also investigated the impact of H89 on intestinal inflammation and C. albicans clearance from the gut, and determined the diversity of the gut microbio…

0301 basic medicineMicrobiology (medical)<i>Lactobacillus johnsonii</i>colitisH89030106 microbiologyInflammationGut floraMicrobiologydigestive systemArticleMicrobiology03 medical and health sciences<i>Enterococcus faecalis</i>Immune system[SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseasesVirologyCandida albicansmedicineEscherichia coliEnterococcus faecalismicrobiotaColitisCandida albicanslcsh:QH301-705.5Lactobacillus johnsoniiLactobacillus johnsoniiDSSH89;Candida albicans;Escherichia coli;Enterococcus faecalis;Lactobacillus johnsonii;microbiota;DSS;colitis;protein kinase AInnate immune systembiology<i>Escherichia coli</i>[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterologymedicine.diseasebiology.organism_classificationCorpus albicans3. Good health<i>Candida albicans</i>030104 developmental biologylcsh:Biology (General)[SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacologyprotein kinase Amedicine.symptomMicroorganisms
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Regulatory T Cells Prevent Neutrophilic Infiltration of Skin during Contact Hypersensitivity Reactions by Strengthening the Endothelial Barrier

2020

The healing phase of contact hypersensitivity reactions is critically dependent on regulatory T cells (Tregs), but even the early inflammatory phase, that is, 6-24 hours after induction of a contact hypersensitivity reaction, is susceptible to Treg-mediated suppression. To investigate the underlying mechanisms, we injected Tregs before the challenge and analyzed the skin-infiltrating cells as early as 6 hours later. Early on, we found mainly neutrophils in the challenged skin, but only a few T cells. This influx of neutrophils was blocked by the injection of Tregs, indicating that they were able to prevent the first wave of leukocytes, which are responsible for starting an immune reaction. …

0301 basic medicineNeutrophilsRegulatory T cellchemical and pharmacologic phenomenaCell CommunicationPicryl ChlorideDermatologyFilaminT-Lymphocytes RegulatoryBiochemistryProinflammatory cytokineMice03 medical and health sciences0302 clinical medicineDownregulation and upregulationNectinmedicineAnimalsHumansProtein kinase AMolecular BiologySkinChemistryChemotaxisCell BiologyCell biologyEndothelial stem cellDisease Models Animal030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisDermatitis Allergic ContactEndothelium VascularIntracellularJournal of Investigative Dermatology
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N-Desmethyldauricine Induces Autophagic Cell Death in Apoptosis-Defective Cells via Ca2+ Mobilization

2017

Resistance of cancer cells to chemotherapy remains a significant problem in oncology. Mechanisms regulating programmed cell death, including apoptosis, autophagy or necrosis, in the treatment of cancers have been extensively investigated over the last few decades. Autophagy is now emerging as an important pathway in regulating cell death or survival in cancer therapy. Recent studies demonstrated variety of natural small-molecules could induce autophagic cell death in apoptosis-resistant cancer cells, therefore, discovery of novel autophagic enhancers from natural products could be a promising strategy for treatment of chemotherapy-resistant cancer. By computational virtual docking analysis,…

0301 basic medicinePharmacologyProgrammed cell deathautophagyKinaseDrug discoveryAutophagylcsh:RM1-950BiologyCell biology03 medical and health sciences030104 developmental biologylcsh:Therapeutics. PharmacologyApoptosisautophagic cell deathN-desmethyldauricineSERCACancer cellCytotoxic T cellPharmacology (medical)apoptosis-resistantProtein kinase AOriginal ResearchFrontiers in Pharmacology
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Tetrandrine, an Activator of Autophagy, Induces Autophagic Cell Death via PKC-α Inhibition and mTOR-Dependent Mechanisms

2017

Emerging evidence suggests the therapeutic role of autophagic modulators in cancer therapy. This study aims to identify novel traditional Chinese medicinal herbs as potential anti-tumor agents through autophagic induction, which finally lead to autophagy mediated-cell death in apoptosis-resistant cancer cells. Using bioactivity-guided purification, we identified tetrandrine (Tet) from herbal plant, Radix stephaniae tetrandrae, as an inducer of autophagy. Across a number of cancer cell lines, we found that breast cancer cells treated with tetrandrine show an increase autophagic flux and formation of autophagosomes. In addition, tetrandrine induces cell death in a panel of apoptosis-resistant…

0301 basic medicinePharmacologyProgrammed cell deathautophagylcsh:RM1-950AutophagyCaspase 3BiologytetrandrineCaspase 7Cell biologyTetrandrine03 medical and health scienceschemistry.chemical_compoundlcsh:Therapeutics. Pharmacology030104 developmental biologychemistryCancer cellmTORPharmacology (medical)apoptosis-resistantPKC-αProtein kinase API3K/AKT/mTOR pathwayOriginal ResearchFrontiers in Pharmacology
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Comparative Proteomics Unveils LRRFIP1 as a New Player in the DAPK1 Interactome of Neurons Exposed to Oxygen and Glucose Deprivation

2020

Altres ajuts: The group has received funding from 'la Caixa Foundation' CI15-00009, from the European Institute of Innovation and Technology (EIT) PoC-2016-SPAIN-04, which receives support from the European Union's Horizon 2020 research and innovation program, and from the 'Fundación para la Innovación y la Prospectiva en Salud en España (FIPSE)' program 3594-18. Death-associated protein kinase 1 (DAPK1) is a pleiotropic hub of a number of networked distributed intracellular processes. Among them, DAPK1 is known to interact with the excitotoxicity driver NMDA receptor (NMDAR), and in sudden pathophysiological conditions of the brain, e.g., stroke, several lines of evidence link DAPK1 with t…

0301 basic medicinePhysiologyClinical BiochemistryExcitotoxicitymedicine.disease_causeProteomicsBiochemistryInteractomeNeuroprotectionArticle03 medical and health sciences0302 clinical medicinemedicineDAPK1Protein kinase AMolecular Biologychemistry.chemical_classificationReactive oxygen specieslcsh:RM1-950OGDROSCell BiologyneuronferroptosisCell biology030104 developmental biologymedicine.anatomical_structurelcsh:Therapeutics. Pharmacologychemistrynervous systemNMDANeuronLRRFIP1MCAO030217 neurology & neurosurgeryIntracellularAntioxidants
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Inappropriate translation inhibition and P-body formation cause cold-sensitivity in tryptophan-auxotroph yeast mutants

2017

In response to different adverse conditions, most eukaryotic organisms, including Saccharomyces cerevisiae, downregulate protein synthesis through the phosphorylation of eIF2α (eukaryotic initiation factor 2α) by Gcn2, a highly conserved protein kinase. Gcn2 also controls the translation of Gcn4, a transcription factor involved in the induction of amino acid biosynthesis enzymes. Here, we have studied the functional role of Gcn2 and Gcn2-regulating proteins, in controlling translation during temperature downshifts of TRP1 and trp1 yeast cells. Our results suggest that neither cold-instigated amino acid limitation nor Gcn2 are involved in the translation suppression at low temperature. Howev…

0301 basic medicineSaccharomyces cerevisiae ProteinsSaccharomyces cerevisiaeeIF2αSaccharomyces cerevisiaeProtein Serine-Threonine KinasesBiology03 medical and health sciencesPolysomeEukaryotic initiation factormedicineProtein biosynthesisLow temperatureEukaryotic Initiation FactorsPhosphorylationProtein kinase AMolecular BiologyTryptophanTranslation (biology)Cell Biologybiology.organism_classificationAdaptation PhysiologicalYeastHog1Cold TemperatureBasic-Leucine Zipper Transcription Factors030104 developmental biologyBiochemistryProtein BiosynthesisPolysomesSnf1Cold sensitivityPhosphorylationMitogen-Activated Protein Kinasesmedicine.symptomEnergy MetabolismGcn2 pathwayTranscription FactorsBiochimica et Biophysica Acta (BBA) - Molecular Cell Research
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Therapeutic potential of polyphenols in cardiovascular diseases: Regulation of mTOR signaling pathway

2020

Cardiovascular diseases comprise of non-communicable disorders that involve the heart and/or blood vessels and have become the leading cause of death worldwide with increased prevalence by age. mTOR is a serine/threonine-specific protein kinase which plays a central role in many physiological processes including cardiovascular diseases, and also integrates various proliferative signals, nutrient and energy abundance and stressful situations. mTOR also acts as central regulator during chronic stress, mitochondrial dysfunction and deregulated autophagy which are associated with senescence. Under oxidative stress, mTOR has been reported to exert protective effects regulating apoptosis and auto…

0301 basic medicineSenescenceRegulatorDiseasemedicine.disease_causeNatural product03 medical and health sciences0302 clinical medicineAnimalsHumansMedicineChronic stressProtein kinase API3K/AKT/mTOR pathwayPharmacologybusiness.industryTOR Serine-Threonine KinasesAutophagyPolyphenols030104 developmental biologyCardiovascular Diseases030220 oncology & carcinogenesismTORCancer researchTranscription factorbusinessOxidative stressSignal TransductionPharmacological Research
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