Search results for "Protein Serine-Threonine Kinases"

showing 10 items of 152 documents

Dietary protein restriction reduces circulating VLDL triglyceride levels via CREBH-APOA5-dependent and -independent mechanisms

2018

Hypertriglyceridemia is an independent risk factor for cardiovascular disease. Dietary interventions based on protein restriction (PR) reduce circulating triglycerides (TGs), but underlying mechanisms and clinical relevance remain unclear. Here, we show that 1 week of a protein-free diet without enforced calorie restriction significantly lowered circulating TGs in both lean and diet-induced obese mice. Mechanistically, the TG-lowering effect of PR was due, in part, to changes in very low-density lipoprotein (VLDL) metabolism both in liver and peripheral tissues. In the periphery, PR stimulated VLDL-TG consumption by increasing VLDL-bound APOA5 expression and promoting VLDL-TG hydrolysis and…

0301 basic medicineMalemedicine.medical_specialtyVery low-density lipoproteinDietary proteinFGF21Calorie restrictionmTORC1Lipoproteins VLDLMechanistic Target of Rapamycin Complex 1Protein Serine-Threonine Kinases03 medical and health sciencesMice0302 clinical medicineRisk FactorsInternal medicinemedicineDiet Protein-RestrictedIntegrated stress responseAnimalsHumansCyclic AMP Response Element-Binding ProteinTriglyceridesRandomized Controlled Trials as TopicHypertriglyceridemiaChemistryHydrolysisHypertriglyceridemianutritional and metabolic diseasesGeneral Medicinemedicine.diseaseLipid Metabolism030104 developmental biologyEndocrinologyApolipoproteinsHypotriglyceridemiaLiverApolipoprotein A-Vlipids (amino acids peptides and proteins)Female030217 neurology & neurosurgeryLipoproteinResearch Article
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Role of the HIPPO pathway as potential key player in the cross talk between oncology and cardiology.

2021

The HIPPO pathway (HP) is a highly conserved kinase cascade that affects organ size by regulating proliferation, cell survival and differentiation. Discovered in Drosophila melanogaster to early 2000, it immediately opened wide frontiers in the field of research. Over the last years the field of knowledge on HP is quickly expanding and it is thought will offer many answers on complex pathologies. Here, we summarized the results of several studies that have investigated HP signaling both in oncology than in cardiology field, with an overview on future perspectives in cardiology research.

0301 basic medicineOncologymedicine.medical_specialtyCardiologyProtein Serine-Threonine KinasesCardiac regeneration03 medical and health sciences0302 clinical medicineInternal medicinemedicineAnimalsHumansHippo Signaling PathwayCardio oncologyCell survivalCell ProliferationHippo signaling pathwaybiologybusiness.industryHematologybiology.organism_classificationKinase cascade030104 developmental biologyDrosophila melanogasterOncologyCardiology fieldAnimals Cardiac development Cardiac regeneration Cardio-oncology Cardiology Cell Proliferation Drosophila melanogaster HIPPO signaling pathway Humans Protein Serine-Threonine Kinases030220 oncology & carcinogenesisCardiologyDrosophila melanogasterbusinessSignal TransductionCritical reviews in oncology/hematology
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Kinase-independent functions of RIPK1 regulate hepatocyte survival and liver carcinogenesis.

2017

The mechanisms that regulate cell death and inflammation play an important role in liver disease and cancer. Receptor-interacting protein kinase 1 (RIPK1) induces apoptosis and necroptosis via kinase-dependent mechanisms and exhibits kinase-independent prosurvival and proinflammatory functions. Here, we have used genetic mouse models to study the role of RIPK1 in liver homeostasis, injury, and cancer. While ablating either RIPK1 or RelA in liver parenchymal cells (LPCs) did not cause spontaneous liver pathology, mice with combined deficiency of RIPK1 and RelA in LPCs showed increased hepatocyte apoptosis and developed spontaneous chronic liver disease and cancer that were independent of TNF…

0301 basic medicineProgrammed cell deathLiver tumorCell SurvivalNecroptosisMice TransgenicBiologyChronic liver diseaseProinflammatory cytokine03 medical and health sciencesLiver diseaseMiceLiver Neoplasms ExperimentalmedicineAnimalsDiethylnitrosamineKinase activityTranscription Factor RelAGeneral Medicinemedicine.disease3. Good healthNeoplasm Proteins030104 developmental biologymedicine.anatomical_structureCell Transformation NeoplasticReceptors Tumor Necrosis Factor Type IHepatocyteReceptor-Interacting Protein Serine-Threonine KinasesCancer researchHepatocytesSignal TransductionResearch ArticleThe Journal of clinical investigation
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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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Herbicide glufosinate inhibits yeast growth and extends longevity during wine fermentation.

2017

Glufosinate ammonium (GA) is a widely used herbicide that inhibits glutamine synthetase. This inhibition leads to internal amino acid starvation which, in turn, causes the activation of different nutrient sensing pathways. GA also inhibits the enzyme of the yeast Saccharomyces cerevisiae in such a way that, although it is not used as a fungicide, it may alter yeast performance in industrial processes like winemaking. We describe herein how GA indeed inhibits the yeast growth of a wine strain during the fermentation of grape juice. In turn, GA extends longevity in a variety of growth media. The biochemical analysis indicates that GA partially inhibits the nutrient sensing TORC1 pathway, whic…

0301 basic medicineSaccharomyces cerevisiae ProteinsSaccharomyces cerevisiaelcsh:MedicineWineSaccharomyces cerevisiaeProtein Serine-Threonine KinasesArticle03 medical and health scienceschemistry.chemical_compoundGlutamine synthetaselcsh:ScienceAmino acid synthesisWinemakingchemistry.chemical_classificationFermentation in winemakingMultidisciplinarybiologyHerbicidesAminobutyrateslcsh:Rbiology.organism_classificationYeast030104 developmental biologychemistryBiochemistryGlufosinateFermentationlcsh:QFermentationTranscription FactorsScientific reports
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Characterisation of CDKL5 Transcript Isoforms in Human and Mouse.

2016

Mutations in the X-linked Cyclin-Dependent Kinase-Like 5 gene (CDKL5) cause early onset infantile spasms and subsequent severe developmental delay in affected children. Deleterious mutations have been reported to occur throughout the CDKL5 coding region. Several studies point to a complex CDKL5 gene structure in terms of exon usage and transcript expression. Improvements in molecular diagnosis and more extensive research into the neurobiology of CDKL5 and pathophysiology of CDKL5 disorders necessitate an updated analysis of the gene. In this study, we have analysed human and mouse CDKL5 transcript patterns both bioinformatically and experimentally. We have characterised the predominant brai…

0301 basic medicineUntranslated regionTranscription GeneticCDKL5lcsh:MedicineGene ExpressionArtificial Gene Amplification and ExtensionPolymerase Chain ReactionBiochemistryExonMice0302 clinical medicineCoding regionProtein Isoformslcsh:ScienceGeneticsRegulation of gene expressionMultidisciplinaryMammalian GenomicsHigh-Throughput Nucleotide SequencingExonsGenomicsNucleic acidsRNA isolationPhenotypeSpasms InfantileResearch ArticleGene isoformBiologyProtein Serine-Threonine KinasesPolyadenylationResearch and Analysis MethodsBiomolecular isolation03 medical and health sciencesGeneticsAnimalsHumansAdultsAmino Acid SequenceMolecular Biology TechniquesGeneMolecular BiologyAlternative splicinglcsh:RGene MappingInfant NewbornBiology and Life SciencesReverse Transcriptase-Polymerase Chain ReactionAlternative Splicing030104 developmental biologyGene Expression RegulationRNA processingAge GroupsAnimal GenomicsMutationPeople and PlacesExon MappingRNAlcsh:QPopulation Groupings030217 neurology & neurosurgeryPloS one
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Effects of muscular dystrophy, exercise and blocking activin receptor IIB ligands on the unfolded protein response and oxidative stress

2016

Protein homeostasis in cells, proteostasis, is maintained through several integrated processes and pathways and its dysregulation may mediate pathology in many diseases including Duchenne muscular dystrophy (DMD). Oxidative stress, heat shock proteins, endoplasmic reticulum (ER) stress and its response, i.e. unfolded protein response (UPR), play key roles in proteostasis but their involvement in the pathology of DMD are largely unknown. Moreover, exercise and activin receptor IIB blocking are two strategies that may be beneficial to DMD muscle, but studies to examine their effects on these proteostasis pathways are lacking. Therefore, these pathways were examined in the muscle of mdx mice, …

0301 basic medicineX-Box Binding Protein 1Activin Receptors Type IIEukaryotic Initiation Factor-2MyostatinUPRBiochemistryMiceeIF-2 KinaseThioredoxinsSirtuin 1ENDOPLASMIC-RETICULUM STRESSDISULFIDE-ISOMERASEPhosphorylationta315Endoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsIN-VIVOta3141Activin receptorMOUSE MODELER STRESSEndoplasmic Reticulum Stress3. Good healthmedicine.anatomical_structuremyostatinPRESERVES MUSCLE FUNCTIONER-stressSKELETAL-MUSCLEmdxSignal TransductionEXPRESSIONmedicine.medical_specialtyXBP1MDX MICEBiologyProtein Serine-Threonine Kinases03 medical and health sciencesPhysiology (medical)Internal medicineHeat shock proteinPhysical Conditioning AnimalEndoribonucleasesmedicineAnimalsHumansRNA MessengerMuscle SkeletalSkeletal muscleMyostatinGENEActivating Transcription Factor 6Immunoglobulin Fc FragmentsMuscular Dystrophy DuchenneDisease Models Animal030104 developmental biologyProteostasisEndocrinologyGene Expression RegulationUnfolded protein responsebiology.proteinMice Inbred mdxProteostasisUnfolded Protein Response3111 BiomedicineCarrier ProteinsACVR2B
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STRIPAK Members Orchestrate Hippo and Insulin Receptor Signaling to Promote Neural Stem Cell Reactivation

2019

Summary Adult stem cells reactivate from quiescence to maintain tissue homeostasis and in response to injury. How the underlying regulatory signals are integrated is largely unknown. Drosophila neural stem cells (NSCs) also leave quiescence to generate adult neurons and glia, a process that is dependent on Hippo signaling inhibition and activation of the insulin-like receptor (InR)/PI3K/Akt cascade. We performed a transcriptome analysis of individual quiescent and reactivating NSCs harvested directly from Drosophila brains and identified the conserved STRIPAK complex members mob4, cka, and PP2A (microtubule star, mts). We show that PP2A/Mts phosphatase, with its regulatory subunit Widerbors…

0301 basic medicinereactivationendocrine systemMitosisNerve Tissue ProteinsProtein Serine-Threonine KinasesBiologyArticleGeneral Biochemistry Genetics and Molecular BiologyAnimals Genetically ModifiedPhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineNeural Stem CellsAnimalsDrosophila ProteinsquiescenceProtein Phosphatase 2lcsh:QH301-705.5Protein kinase BCells CulturedPI3K/AKT/mTOR pathwayTissue homeostasisAdaptor Proteins Signal TransducingCell ProliferationHippo signaling pathwayGene Expression ProfilingHippo signalingInR/PI3K/Akt signalingfungiIntracellular Signaling Peptides and ProteinsBrainSTRIPAK membersProtein phosphatase 2Receptor InsulinNeural stem cellCell biologyDrosophila melanogaster030104 developmental biologylcsh:Biology (General)nervous systemHippo signalingSingle-Cell AnalysisTranscriptomeProto-Oncogene Proteins c-akt030217 neurology & neurosurgeryAdult stem cellCell Reports
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Epigenetic dysregulation in the developing Down syndrome cortex

2016

Using Illumina 450K arrays, 1.85% of all analyzed CpG sites were significantly hypermethylated and 0.31% hypomethylated in fetal Down syndrome (DS) cortex throughout the genome. The methylation changes on chromosome 21 appeared to be balanced between hypo- and hyper-methylation, whereas, consistent with prior reports, all other chromosomes showed 3–11 times more hyper- than hypo-methylated sites. Reduced NRSF/REST expression due to upregulation of DYRK1A (on chromosome 21q22.13) and methylation of REST binding sites during early developmental stages may contribute to this genome-wide excess of hypermethylated sites. Upregulation of DNMT3L (on chromosome 21q22.4) could lead to de novo methyl…

Adult0301 basic medicineCancer ResearchDown syndromeDown syndromeNeuronal OutgrowthDNMT3BProtein Serine-Threonine KinasesBiologyDNA Methyltransferase 3AEpigenesis Genetic03 medical and health sciencesfetal brain developmentddc:570medicineHumansDNA (Cytosine-5-)-MethyltransferasesEpigeneticsddc:610Molecular BiologyCerebral CortexGeneticsDNA methylationfrontal cortexGene Expression Regulation DevelopmentalChromosomeMethylationProtein-Tyrosine KinasesCadherinsmedicine.diseaseMolecular biologyprotocadherin gamma cluster030104 developmental biologyCpG siteDNA methylationChromosome 21Research Paper
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Erratum: By promoting cell differentiation, miR-100 sensitizes basal-like breast cancer stem cells to hormonal therapy

2019

Basal-like breast cancer is an aggressive tumor subtype with a poor response to conventional therapies. Tumor formation and relapse are sustained by a cell subset of Breast Cancer Stem Cells (BrCSCs). Here we show that miR-100 inhibits maintenance and expansion of BrCSCs in basal-like cancer through Polo-like kinase1 (Plk1) down-regulation. Moreover, miR-100 favors BrCSC differentiation, converting a basal like phenotype into luminal. It induces the expression of a functional estrogen receptor (ER) and renders basal-like BrCSCs responsive to hormonal therapy. The key role played by miR-100 in breast cancer free-survival is confirmed by the analysis of a cohort of patients' tumors, which sho…

AdultAntineoplastic Agents HormonalTransplantation HeterologousBreast cancer basal-like differentiation miR-100Breast NeoplasmsCell Cycle ProteinsKaplan-Meier EstimateMice SCIDProtein Serine-Threonine KinasesMice Inbred NODCell Line TumorProto-Oncogene ProteinsAnimalsHumansAgedAged 80 and overReverse Transcriptase Polymerase Chain ReactionCorrectionCell DifferentiationMiddle AgedPrognosisImmunohistochemistryGene Expression Regulation NeoplasticMicroRNAsTamoxifenOncologyReceptors EstrogenMCF-7 CellsNeoplastic Stem CellsFemale
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