Search results for "pi3k"

showing 10 items of 240 documents

A Regulatory Mechanism Involving TBP-1/Tat-Binding Protein 1 and Akt/PKB in the Control of Cell Proliferation

2011

Abstract TBP-1 /Tat-Binding Protein 1 (also named Rpt-5, S6a or PSMC3) is a multifunctional protein, originally identified as a regulator of HIV-1-Tat mediated transcription. It is an AAA-ATPase component of the 19S regulative subunit of the proteasome and, as other members of this protein family, fulfils different cellular functions including proteolysis and transcriptional regulation. We and others reported that over expression of TBP-1 diminishes cell proliferation in different cellular contexts with mechanisms yet to be defined. Accordingly, we demonstrated that TBP-1 binds to and stabilizes the p14ARF oncosuppressor increasing its anti-oncogenic functions. However, TBP-1 restrains cell…

TBP-1/Tat-Binding Protein 1lcsh:Medicinemacromolecular substancesBiologymTORC2Cell GrowthTBP-1/Tat-Binding Protein 1; cell proliferationp14arfMolecular Cell BiologyGeneticsCancer GeneticsTranscriptional regulationGene Networkslcsh:ScienceBiologyProtein kinase BPI3K/AKT/mTOR pathwayMultidisciplinaryCell growthAKTBinding proteinlcsh:RMolecular biologySignaling CascadesCell biologyTBP-1enzymes and coenzymes (carbohydrates)cell proliferationbiology.proteinMdm2lcsh:QCell DivisionResearch ArticleSignal TransductionPLoS ONE
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Sustained activation of mTOR pathway in embryonic neural stem cells leads to development of tuberous sclerosis complex-associated lesions

2011

SummaryTuberous Sclerosis Complex (TSC) is a multisystem genetic disorder characterized by hamartomatous neurological lesions that exhibit abnormal cell proliferation and differentiation. Hyperactivation of mTOR pathway by mutations in either the Tsc1 or Tsc2 gene underlies TSC pathogenesis, but involvement of specific neural cell populations in the formation of TSC-associated neurological lesions remains unclear. We deleted Tsc1 in Emx1-expressing embryonic telencephalic neural stem cells (NSCs) and found that mutant mice faithfully recapitulated TSC neuropathological lesions, such as cortical lamination defects and subependymal nodules (SENs). These alterations were caused by enhanced gen…

Telencephaloncongenital hereditary and neonatal diseases and abnormalitiesCellular differentiationNeuroepithelial CellsEmbryonic DevelopmentBiologyTuberous Sclerosis Complex 1 Proteinmurine modelCerebral VentriclesMiceNeural Stem CellsCell MovementTuberous SclerosismedicineGeneticsAnimalsAnimals; Animals Newborn; Cell Differentiation; Cell Movement; Cell Proliferation; Cerebral Ventricles; Embryonic Development; Embryonic Stem Cells; Epilepsy; Gene Silencing; Gene Targeting; Megalencephaly; Mice; Mutation; Neural Stem Cells; Neuroepithelial Cells; Neurons; TOR Serine-Threonine Kinases; Telencephalon; Tuberous Sclerosis; Tuberous Sclerosis Complex 1 Protein; Tumor Suppressor Proteins; Signal TransductionGene SilencingNeural cellPI3K/AKT/mTOR pathwayEmbryonic Stem CellsCell ProliferationNeuronsEpilepsymTOR; Neural Stem Cells; Tuberous Sclerosis; murine modelTOR Serine-Threonine KinasesTumor Suppressor ProteinsCell DifferentiationCell BiologyNewbornEmbryonic stem cellNeural stem cellMegalencephalyCell biologynervous system diseasesNeuroepithelial cellmedicine.anatomical_structureAnimals NewbornImmunologyGene TargetingMutationmTORMolecular MedicineTSC1TSC2Signal Transduction
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Coordinated Sumoylation and Ubiquitination Modulate EGF Induced EGR1 Expression and Stability

2011

Background Human early growth response-1 (EGR1) is a member of the zing-finger family of transcription factors induced by a range of molecular and environmental stimuli including epidermal growth factor (EGF). In a recently published paper we demonstrated that integrin/EGFR cross-talk was required for Egr1 expression through activation of the Erk1/2 and PI3K/Akt/Forkhead pathways. EGR1 activity and stability can be influenced by many different post-translational modifications such as acetylation, phosphorylation, ubiquitination and the recently discovered sumoylation. The aim of this work was to assess the influence of sumoylation on EGF induced Egr1 expression and/or stability. Methods We …

Time FactorsTranscription GeneticSUMO proteinlcsh:MedicineUbiquitin-conjugating enzymeBiochemistrychemistry.chemical_compoundEpidermal growth factorMG132protein 1lcsh:ScienceMitogen-Activated Protein Kinase 1Regulation of gene expressionMitogen-Activated Protein Kinase 3MultidisciplinaryProtein translationProtein Stabilitygene expression regulationCell biologyepidermal growth factorResearch Articlemedicine.drugProteasome Endopeptidase Complexendocrine systemkinase 1SUMO-1 ProteinBiologyDNA-binding proteinsGeneticsmedicineHumansBiologySettore BIO/10 - BIOCHIMICAProtein kinase BPI3K/AKT/mTOR pathwayEarly Growth Response Protein 1lcsh:RMitogen-activated proteinProteinsSumoylationRegulatory proteinsenzyme activationRNA stabilityMolecular biologychemistryProteolysisUbiquitin-Conjugating EnzymesProteasome inhibitorlcsh:QEarly growth responseGene expressionCell linePLoS ONE
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mTOR Driven Gene Transcription Is Required for Cholesterol Production in Neurons of the Developing Cerebral Cortex

2021

AbstractDysregulated mammalian target of rapamycin (mTOR) activity is associated with various neurodevelopmental disorders ranging from idiopathic autism spectrum disorders to syndromes caused by single gene defects. This suggests that maintaining mTOR activity levels in a physiological range is essential for brain development and functioning. Upon activation, mTOR regulates a variety of cellular processes such as cell growth, autophagy and metabolism. On a molecular level, however, the consequences of mTOR activation in the brain are not well understood.Low levels of cholesterol are associated with a wide variety of neurodevelopmental disorders. We here describe numerous genes of the stero…

Transcription GeneticQH301-705.5Primary Cell CulturemTORC1Mechanistic Target of Rapamycin Complex 1BiologySREBPCatalysisArticleInorganic ChemistryMiceAutophagyTranscriptional regulationmedicineAnimalsPhysical and Theoretical ChemistryBiology (General)Molecular BiologyTranscription factorQD1-999mTORC1SpectroscopyPI3K/AKT/mTOR pathwayCerebral CortexNeuronsSterol Regulatory Element Binding ProteinsCell growthTOR Serine-Threonine KinasesOrganic Chemistrycholesterol ; NF-Y ; neurogenesis ; mTOR ; mTORC1 ; SP1 ; SREBPAutophagyGene Expression Regulation DevelopmentalcholesterolGeneral MedicineComputer Science ApplicationsSterol regulatory element-binding proteinCell biologySP1Chemistryneurogenesismedicine.anatomical_structureCCAAT-Binding FactorCerebral cortexmTORNF-YProtein KinasesSignal TransductionInternational Journal of Molecular Sciences
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A compound-based proteomic approach discloses 15-ketoatractyligenin methyl ester as a new PPARγ partial agonist with anti-proliferative ability

2017

AbstractProteomics based approaches are emerging as useful tools to identify the targets of bioactive compounds and elucidate their molecular mechanisms of action. Here, we applied a chemical proteomic strategy to identify the peroxisome proliferator-activated receptor γ (PPARγ) as a molecular target of the pro-apoptotic agent 15-ketoatractyligenin methyl ester (compound 1). We demonstrated that compound 1 interacts with PPARγ, forms a covalent bond with the thiol group of C285 and occupies the sub-pocket between helix H3 and the β-sheet of the ligand-binding domain (LBD) of the receptor by Surface Plasmon Resonance (SPR), mass spectrometry-based studies and docking experiments. 1 displayed…

Transcriptional Activation0301 basic medicinenatural productTime FactorsPeroxisome proliferator-activated receptorApoptosisLigandsPartial agonistArticleRosiglitazonePPAR_gammaJurkat Cells03 medical and health sciencesTransactivation0302 clinical medicineproteomicsHumansBinding siteReceptorMode of actionPI3K/AKT/mTOR pathwayCell Proliferationchemistry.chemical_classificationBinding SitesMultidisciplinaryProtein StabilityProtein Proliferator-Activated-Receptor PPARs Ligand-Binding Domain Chemical Proteomics Accurate Docking Pi3k/Akt Pathway Drug Discovery Anticancer compoundsReproducibility of ResultsEstersSurface Plasmon ResonanceMolecular Docking SimulationPPAR gammaKineticsHEK293 Cells030104 developmental biologychemistryBiochemistryDocking (molecular)030220 oncology & carcinogenesisThermodynamicsThiazolidinedionesproteomics PPAR_gamma natural productDiterpenes KauraneHT29 CellsScientific Reports
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Acidic Environment Leads to ROS-Induced MAPK Signaling in Cancer Cells

2011

Tumor micromilieu often shows pronounced acidosis forcing cells to adapt their phenotype towards enhanced tumorigenesis induced by altered cellular signalling and transcriptional regulation. In the presents study mechanisms and potential consequences of the crosstalk between extra- and intracellular pH (pH(e), pH(i)) and mitogen-activated-protein-kinases (ERK1/2, p38) was analyzed. Data were obtained mainly in AT1 R-3327 prostate carcinoma cells, but the principle importance was confirmed in 5 other cell types. Extracellular acidosis leads to a rapid and sustained decrease of pH(i) in parallel to p38 phosphorylation in all cell types and to ERK1/2 phosphorylation in 3 of 6 cell types. Furth…

Tumor PhysiologyIntracellular Spacelcsh:MedicineSignal transductionERK signaling cascadeMolecular cell biologyNeoplasmsBasic Cancer ResearchTumor MicroenvironmentSignaling in Cellular ProcessesPhosphorylationCyclic AMP Response Element-Binding ProteinCreb Signalinglcsh:ScienceCellular Stress ResponsesMultidisciplinaryKinaseMechanisms of Signal TransductionSignaling cascadesHydrogen-Ion ConcentrationProtein-Tyrosine KinasesCell biologyOncologyMedicinePhosphorylationMitogen-Activated Protein KinasesSodium-Potassium-Exchanging ATPaseIntracellularResearch ArticleCell SurvivalMAP Kinase Signaling Systemp38 mitogen-activated protein kinasesIntracellular pHBiologyCREBModels BiologicalCell GrowthDogsCell Line TumorAnimalsHumansProtein Kinase InhibitorsBiologyPI3K/AKT/mTOR pathwaylcsh:RRatsEnzyme ActivationCancer cellbiology.proteinlcsh:QExtracellular SpaceReactive Oxygen SpeciesAcidsPLoS ONE
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The deubiquitinase USP11 is a versatile and conserved regulator of autophagy

2021

Autophagy is a major cellular quality control system responsible for the degradation of proteins and organelles in response to stress and damage to maintain homeostasis. Ubiquitination of autophagy-related proteins or regulatory components is important for the precise control of autophagy pathways. Here, we show that the deubiquitinase ubiquitin-specific protease 11 (USP11) restricts autophagy and that KO of USP11 in mammalian cells results in elevated autophagic flux. We also demonstrate that depletion of the USP11 homolog H34C03.2 in Caenorhabditis elegans triggers hyperactivation of autophagy and protects the animals against human amyloid-β peptide 42 aggregation-induced paralysis. USP11…

autophagyhAβ42 human amyloid-β protein 1 to 42Lipid kinase activityPI(3)P phosphatidylinositol-3-phosphatemTORC1BiochemistryCell LineGene Knockout Techniqueschemistry.chemical_compoundubiquitinAnimalsHumansULK1 unc-51-like autophagy activating kinase 1WIPI WD-repeat domain phosphoinositide-interacting proteinPI3KC3-C1Caenorhabditis elegansCaenorhabditis elegans ProteinsmTORC1Molecular BiologyMechanistic target of rapamycinUSP11 ubiquitin-specific protease 11proteostasisAmyloid beta-PeptidesS6K S6 kinasebiologyPhosphatidylinositol 3-phosphateAutophagyDUB deubiquitinaseLFQ label-free quantificationIP immunoprecipitationNHT nonhuman targetingPI3KC3-C1 class III phosphatidylinositol 3-kinase complex ICell BiologyACN acetonitrile amyloid-βNRBF2 nuclear receptor-binding factor 2Peptide FragmentsCell biologydeubiquitinase (DUB)ProteostasischemistryProteotoxicitymTORC1 mechanistic target of rapamycin complex 1biology.proteinAutophagy-Related Protein-1 HomologBSA bovine serum albuminThiolester HydrolasesResearch ArticleJournal of Biological Chemistry
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Drivers of topoisomerase II poisoning mimic and complement cytotoxicity in AML cells

2019

Recently approved cancer drugs remain out-of-reach to most patients due to prohibitive costs and only few produce clinically meaningful benefits. An untapped alternative is to enhance the efficacy and safety of existing cancer drugs. We hypothesized that the response to topoisomerase II poisons, a very successful group of cancer drugs, can be improved by considering treatment-associated transcript levels. To this end, we analyzed transcriptomes from Acute Myeloid Leukemia (AML) cell lines treated with the topoisomerase II poison etoposide. Using complementary criteria of co-regulation within networks and of essentiality for cell survival, we identified and functionally confirmed 11 druggabl…

biologyCombination therapybusiness.industryTopoisomeraseMyeloid leukemiatopoisomerase II poisonscombination therapyCell killingOncologygene expressioncancer essentialitybiology.proteinmedicineCancer researchDNA damageCytotoxic T cellCytotoxicitybusinessEtoposidePI3K/AKT/mTOR pathwayResearch Papermedicine.drugOncotarget
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Overcoming of P-glycoprotein-mediated multidrug resistance of tumors in vivo by drug combinations

2014

Summary Inhibition of P-glycoprotein represents an attractive possibility to modulate resistance of cancer cells to anticancer drugs. One major strategy to overcome P-glycoprotein-mediated multidrug resistance (MDR) of tumors is to increase intracellular concentrations of anticancer drugs. This can be achieved by blocking of P-glycoprotein-mediated drug efflux using synthetic or natural small molecules or monoclonal antibodies, which bind to various parts of the efflux channel. Another possibility to increase intracellular drug concentrations can be reached by nanoparticles. A further major strategy to overcome MDR involves the downregulation of P-glycoprotein expression either by therapeut…

biologyMedicine (miscellaneous)Cell BiologyPharmacologySmall moleculeMultiple drug resistanceRNA interferenceIn vivoCancer cellbiology.proteinPharmacology (medical)EffluxMolecular BiologyPI3K/AKT/mTOR pathwayP-glycoproteinSynergy
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Advances in Targeting Signal Transduction Pathways

2012

// James A. McCubrey 1 , Linda S. Steelman 1 , William H. Chappell 1 , Lin Sun 1,2 , Nicole M. Davis 1 , Stephen L. Abrams 1 , Richard A. Franklin 1 , Lucio Cocco 3 , Camilla Evangelisti 4 , Francesca Chiarini 4 , Alberto M. Martelli 3,4 , Massimo Libra 5 , Saverio Candido 5 , Giovanni Ligresti 5 , Grazia Malaponte 5 , Maria C. Mazzarino 5 , Paolo Fagone 5 , Marco Donia 5 , Ferdinando Nicoletti 5 , Jerry Polesel 6 , Renato Talamini 6 , Jorg Basecke 7 , Sanja Mijatovic 8 , Danijela Maksimovic-Ivanic 8 , Michele Milella 9 , Agostino Tafuri 10 , Joanna Dulinska-Litewka 11 , Piotr Laidler 11 , Antonio B. D’Assoro 12 , Lyudmyla Drobot 13 , Kazuo Umezawa 14 , Giuseppe Montalto 15 , Melchiorre Cer…

cancer stem cellsAMPKtherapy resistanceReviewsLibrary scienceAntineoplastic AgentsrafBiologyPI3Kampk03 medical and health sciences0302 clinical medicineCANCER STEM CELLSNeoplasmsAnimalsHumansUniversity medicalMolecular Targeted TherapyAkt; AMPK; Cancer stem cells; Metformin; MTOR; PI3K; Raf; Targeted therapy; Therapy resistanceTreatment resistanceProtein Kinase Inhibitors030304 developmental biology0303 health sciencesRoswell Park Cancer InstituteAktCancer stem cellAKTMTORAMP-ACTIVATED PROTEIN KINASE (AMPK)Raftargeted therapyMetformin3. Good healthGene Expression Regulation NeoplasticCell stressOncologyDrug Resistance NeoplasmDrug Designtargeted therapy; metformin; therapy resistance; pi3k; akt; ampk; cancer stem cells; raf; mtor030220 oncology & carcinogenesisMutationmTORMolecular targetsCancer researchmetforminSignal Transduction
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