Search results for "Proto-Oncogene Proteins c-akt"

showing 10 items of 129 documents

A Novel Loss-of-Function Mutation (N48K) in the PTEN Gene in a Spanish Patient with Cowden Disease

2003

Cowden disease, also known as multiple hamartoma syndrome, is a rare disease inherited in an autosomal dominant pattern, which confers a high risk of developing breast and thyroid carcinomas. Mutations in PTEN, a tumor suppressor gene located on chromosome 10q23, have been identified in patients with Cowden disease. In this work, the direct sequencing of all coding regions of the PTEN gene led us to the identification of N48K, a new germline PTEN missense mutation, in a patient suffering from Cowden disease. The genetic analysis of 200 chromosomes from healthy individuals revealed that the variant was not common in our population. Moreover, by functional analysis we found that the ability o…

AdultPTENcongenital hereditary and neonatal diseases and abnormalitiesTumor suppressor geneDNA Mutational AnalysisMolecular Sequence DataLoss of Heterozygositygenetic analysisDermatologyProtein Serine-Threonine Kinasesmedicine.disease_causeProto-Oncogene MasBiochemistryGenètica molecularfunctional analysisLoss of heterozygosityStructure-Activity RelationshipProto-Oncogene ProteinsmedicineLeukocytesMissense mutationPTENHumansPoint MutationCowden diseaseAmino Acid SequenceMolecular BiologyTumorsGeneticsMutationbiologySequence Homology Amino AcidPoint mutationTumor Suppressor ProteinsPTEN PhosphohydrolaseMultiple hamartoma syndromeCowden syndromeCell Biologymedicine.diseasePhosphoric Monoester HydrolasesN48KSpainbiology.proteinCancer researchFemaleHamartoma Syndrome MultipleProto-Oncogene Proteins c-akt
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Cellular stress induces cap-independent alpha-enolase/MBP-1 translation.

2015

AbstractMyc promoter-binding protein-1 (MBP-1) is a shorter protein variant of the glycolytic enzyme alpha-enolase. Although several lines of evidence indicate that MBP-1 acts as a tumor suppressor, the cellular mechanisms and signaling pathways underlying MBP-1 expression still remain largely elusive. To dissect these pathways, we used the SkBr3 breast cancer cell line and non-tumorigenic HEK293T cells ectopically overexpressing alpha-enolase/MBP-1. Here, we demonstrate that induced cell stresses promote MBP-1 expression through the AKT/PERK/eIF2α signaling axis. Our results contribute to shedding light on the molecular mechanisms underlying MBP-1 expression in non-tumorigenic and cancer c…

Alpha-enolaseCellEukaryotic Initiation Factor-2Alternative translationBiochemistryeIF-2 KinaseBreast cancerHEK293 CellStructural BiologyProtein IsoformsbiologyMedicine (all)Translation (biology)Recombinant ProteinEndoplasmic Reticulum StressRecombinant ProteinsNeoplasm ProteinsDNA-Binding ProteinsGene Expression Regulation Neoplasticmedicine.anatomical_structureFemaleSignal transductionMyc promoter-binding protein-1Breast NeoplasmHumanSignal TransductionCell SurvivalDNA-Binding ProteinRecombinant Fusion ProteinsBiophysicsBreast NeoplasmsNeoplasm ProteinGeneticCell Line TumorEndoplasmic reticulum streGeneticsmedicineBiomarkers TumorHumansGene SilencingMolecular BiologyProtein kinase BTumor Suppressor ProteinTumor Suppressor ProteinsHEK 293 cellsProtein IsoformCell BiologySettore BIO/18 - GeneticaHEK293 CellsBiophysicGene Expression RegulationPhosphopyruvate HydrataseCancer cellbiology.proteinUnfolded protein responseCancer researchProto-Oncogene Proteins c-aktRecombinant Fusion ProteinFEBS letters
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Endothelial Leptin Receptor Deletion Promotes Cardiac Autophagy and Angiogenesis Following Pressure Overload by Suppressing Akt/mTOR Signaling.

2019

Background: Cardiac remodeling is modulated by overnutrition or starvation. The adipokine leptin mediates energy balance between adipose tissue and brain. Leptin and its receptors are expressed in the heart. Methods and Results: To examine the importance of endothelial leptin signaling in cardiac hypertrophy, transverse aortic constriction was used in mice with inducible endothelium-specific deletion of leptin receptors (End.LepR-KO) or littermate controls (End.LepR-WT). End.LepR-KO was associated with improved left ventricular function (fractional shortening, 28.4% versus 18.8%; P =0.0114), reduced left ventricular dilation (end-systolic inner left ventricular diameter, 3.59 versus 4.08 m…

AngiogenesisAdipose tissueAdipokineCardiomegaly030204 cardiovascular system & hematologyVentricular Function Left03 medical and health sciences0302 clinical medicineAutophagyMedicineAnimalsHumansGenetic Predisposition to Disease030212 general & internal medicineProtein kinase BCells Cultured2. Zero hungerPressure overloadHeart FailureMice KnockoutLeptin receptorNeovascularization Pathologicbusiness.industryLeptinMyocardiumTOR Serine-Threonine KinasesAutophagyEndothelial CellsFibrosisCell biologyDisease Models AnimalPhenotypeReceptors LeptinFemaleCardiology and Cardiovascular MedicinebusinessProto-Oncogene Proteins c-aktGene DeletionSignal TransductionCirculation. Heart failure
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PTEN Mediates the Antioxidant Effect of Resveratrol at Nutritionally Relevant Concentrations

2014

Introduction.Antioxidant properties of resveratrol have been intensively studied for the last years, bothin vivoandin vitro. Its bioavailability after an oral dose is very low and therefore it is very important to make sure that plasma concentrations of free resveratrol are sufficient enough to be active as antioxidant.Aims.In the present study, using nutritionally relevant concentrations of resveratrol, we aim to confirm its antioxidant capacity on reducing peroxide levels and look for the molecular pathway involved in this antioxidant effect.Methods.We used mammary gland tumor cells (MCF-7), which were pretreated with different concentrations of resveratrol for 48 h, and/or a PTEN inhibit…

Antioxidantendocrine system diseasesArticle Subjectmedicine.medical_treatmentlcsh:MedicineResveratrolGeneral Biochemistry Genetics and Molecular BiologyAntioxidantschemistry.chemical_compoundDownregulation and upregulationStilbenesmedicinePTENHumansPhosphorylationskin and connective tissue diseasesHydrogen peroxidePI3K/AKT/mTOR pathwayGeneral Immunology and MicrobiologybiologyAkt/PKB signaling pathwaySuperoxide Dismutaseorganic chemicalslcsh:RPTEN Phosphohydrolasefood and beveragesGeneral MedicineHydrogen PeroxideCatalaseUp-RegulationEnzyme ActivationBiochemistrychemistryCatalaseResveratrolbiology.proteinMCF-7 CellsProto-Oncogene Proteins c-akthormones hormone substitutes and hormone antagonistsSignal TransductionResearch Article
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Different muscarinic receptor subtypes modulate proliferation of primary human detrusor smooth muscle cells via Akt/PI3K and map kinases.

2013

While acetylcholine (ACh) and muscarinic receptors in the bladder are mainly known for their role in the regulation of smooth muscle contractility, in other tissues they are involved in tissue remodelling and promote cell growth and proliferation. In the present study we have used primary cultures of human detrusor smooth muscle cells (HDSMCs), in order to investigate the role of muscarinic receptors in HDSMC proliferation. Samples were obtained as discarded tissue from men >65 years undergoing radical cystectomy for bladder cancer and cut in pieces that were either immediately frozen or placed in culture medium for the cell culture establishment. HDSMCs were isolated from samples, propagat…

AtropineMalePyrrolidinesMessenger030232 urology & nephrologyGene ExpressionPhosphatidylinositol 3-Kinases0302 clinical medicineAged Atropine; pharmacology Benzofurans; pharmacology Carbachol; pharmacology Cell Proliferation Cells; Cultured Cholinergic Agonists; pharmacology Gene Expression Humans Male Mitogen-Activated Protein Kinases; metabolism Muscarinic Antagonists; pharmacology Myocytes; Smooth Muscle; metabolism Phosphatidylinositol 3-Kinases; metabolism Piperidines; pharmacology Pirenzepine; analogs /&/ derivatives/pharmacology Proto-Oncogene Proteins c-akt; metabolism Pyrrolidines; pharmacology RNA; Messenger; metabolism Receptors; Muscarinic; physiology Urinary Bladder; cytologyPiperidinesSmooth MuscleReceptorsMuscarinic acetylcholine receptor M5Muscarinic acetylcholine receptorCells CulturedCulturedMuscarinic acetylcholine receptor M3Muscarinic acetylcholine receptor M2Smooth muscle contractionMuscarinic acetylcholine receptor M1Receptors Muscarinic030220 oncology & carcinogenesisMitogen-Activated Protein KinasesAcetylcholinemedicine.drugmedicine.medical_specialtyCarbacholCellsMyocytes Smooth MuscleUrinary BladderMuscarinic AntagonistsBiologyCholinergic Agonists03 medical and health sciencesInternal medicineMuscarinicmedicineHumansRNA MessengerAgedBenzofuransCell ProliferationPharmacologyMyocytesPirenzepineEndocrinologyphysiologycytologyRNACarbacholanalogs /&/ derivatives/pharmacologymetabolismProto-Oncogene Proteins c-aktPharmacological research
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Facilitation of Insulin Effects by Ranolazine in Astrocytes in Primary Culture

2022

Ranolazine (Rn) is a drug used to treat persistent chronic coronary ischemia. It has also been shown to have therapeutic benefits on the central nervous system and an anti-diabetic effect by lowering blood glucose levels and however, no effects of Rn on cellular sensitivity to insulin (Ins) have been demonstrated yet. The present study aimed to investigate the permissive effects of Rn on the actions of Ins in astrocytes in primary culture. Ins at 10-8 M, Rn (10-6 M) and Ins+Rn (10-8 M and 10−6 M respectively) were added to astrocytes during 24 h. In comparison to control cells, Rn and/or Ins caused modifications in cell viability and proliferation. p-AKT, p-ERK, p-eNOS, Mn-SOD, COX-2, and t…

Blood Glucoseranolazine; insulin; astrocytes; inflammation; antioxidantsSuperoxide DismutaseSistema nerviós central MalaltiesOrganic ChemistryAnti-Inflammatory AgentsNF-kappa Bendocrinology_metabolomicsGeneral MedicineCatalysisAntioxidantsComputer Science ApplicationsPPAR gammaInorganic ChemistryCyclooxygenase 2RanolazineAstrocytesInsulin Regular HumanInsulinPhysical and Theoretical ChemistryProto-Oncogene Proteins c-aktMolecular BiologySpectroscopy
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The histone deacetylase sirtuin 2 is a new player in the regulation of platelet function

2015

SummaryBackground Histone deacetylases (HDACs) play a key role in signaling in many cell types. However, little is known about the participation of HDACs, particularly sirtuins (SIRTs), in platelet reactivity. Objective To investigate the role of HDACs in platelets, we examined the effects of SIRT inhibition on platelet function and protein acetylation in human platelets. Methods We used washed platelets obtained from healthy subjects. Cambinol (SIRT1 and SIRT2 inhibitor), AGK2 (specific SIRT2 inhibitor) and EX527 (specific SIRT1 inhibitor) were used as SIRT inhibitors. Platelets were stimulated with collagen, thrombin, or U46619, and platelet responses were determined according to optical …

Blood PlateletsPlatelet AggregationCytoplasmic GranulesSIRT2Glycogen Synthase Kinase 3Akt3 protein kinaseSirtuin 2sirtuinsHumansPlateletRNA MessengerPhosphorylationProtein kinase Bacetylationblood plateletGlycogen Synthase Kinase 3 betabiologySecretory VesiclesAcetylationHematologyCell biologyHistone Deacetylase InhibitorsBiochemistryAcetylationSirtuinbiology.proteinPhosphorylationPlatelet aggregation inhibitorCalciumHistone deacetylaseProtein Processing Post-TranslationalProto-Oncogene Proteins c-aktPlatelet Aggregation Inhibitorssignal transductionSignal TransductionJournal of Thrombosis and Haemostasis
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A Neuroprotective Function for the Hematopoietic Protein Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF)

2007

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a hematopoietic cytokine responsible for the proliferation, differentiation, and maturation of cells of the myeloid lineage, which was cloned more than 20 years ago. Here we uncovered a novel function of GM-CSF in the central nervous system (CNS). We identified the GM-CSF α-receptor as an upregulated gene in a screen for ischemia-induced genes in the cortex. This receptor is broadly expressed on neurons throughout the brain together with its ligand and induced by ischemic insults. In primary cortical neurons and human neuroblastoma cells, GM-CSF counteracts programmed cell death and induces BCL-2 and BCL-Xl expression in a dose- a…

Brain InfarctionMaleProgrammed cell deathTime FactorsMyeloidmedicine.medical_treatmentDrug Evaluation Preclinicalbcl-X ProteinApoptosisBiologyNeuroprotectionBrain IschemiaPhosphatidylinositol 3-KinasesmedicineAnimalsHumansMyeloid CellsRats Long-EvansRats WistarProtein kinase BCell ProliferationCerebral CortexNeuronsDose-Response Relationship DrugGrowth factorGranulocyte-Macrophage Colony-Stimulating FactorCell DifferentiationNeurodegenerative DiseasesRatsUp-RegulationCell biologyDisease Models AnimalHaematopoiesisNeuroprotective Agentsmedicine.anatomical_structureGranulocyte macrophage colony-stimulating factorNeurologyBlood-Brain BarrierReceptors Granulocyte-Macrophage Colony-Stimulating FactorImmunologyNeurology (clinical)Signal transductionCardiology and Cardiovascular MedicineProto-Oncogene Proteins c-aktSignal Transductionmedicine.drugJournal of Cerebral Blood Flow & Metabolism
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Quercetin ameliorates dysregulation of lipid metabolism genes via the PI3K/AKT pathway in a diet-induced mouse model of nonalcoholic fatty liver dise…

2015

Scope Flavonoids and related compounds seem to have favorable effects on nonalcoholic fatty liver disease (NAFLD) progression, although the exact mechanisms implicated are poorly understood. In this study, we aimed to investigate the effect of the flanovol quercetin on gene expression deregulation involved in the development of NAFLD, as well as the possible implication of phosphatidylinositol 3-kinase (PI3K)/AKT pathway modulation. Methods and results We used an in vivo model based on methionine- and choline-deficient (MCD) diet-fed mice and an in vitro model consisting of Huh7 cells incubated with MCD medium. MCD-fed mice showed classical pathophysiological characteristics of nonalcoholic…

CD36 AntigensMalemedicine.medical_specialtyOxidative phosphorylationBiologyMicePhosphatidylinositol 3-Kinaseschemistry.chemical_compoundNon-alcoholic Fatty Liver DiseaseInternal medicineNonalcoholic fatty liver diseaseGene expressionmedicineTranscriptional regulationAnimalsLY294002PhosphatidylinositolCells CulturedPI3K/AKT/mTOR pathwayLipid metabolismLipid Metabolismmedicine.diseaseMice Inbred C57BLDisease Models AnimalOxidative StressEndocrinologyGene Expression RegulationchemistryCancer researchQuercetinLipid PeroxidationProto-Oncogene Proteins c-aktSignal TransductionFood ScienceBiotechnologyMolecular Nutrition & Food Research
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MHCII-independent CD4+ T cells protect injured CNS neurons via IL-4

2015

A body of experimental evidence suggests that T cells mediate neuroprotection following CNS injury; however, the antigen specificity of these T cells and how they mediate neuroprotection are unknown. Here, we have provided evidence that T cell-mediated neuroprotection after CNS injury can occur independently of major histocompatibility class II (MHCII) signaling to T cell receptors (TCRs). Using two murine models of CNS injury, we determined that damage-associated molecular mediators that originate from injured CNS tissue induce a population of neuroprotective, IL-4-producing T cells in an antigen-independent fashion. Compared with wild-type mice, IL-4-deficient animals had decreased functi…

CD4-Positive T-LymphocytesCancer ResearchMAP Kinase Signaling SystemPopulationReceptors Antigen T-CellInflammationBiologyNeuroprotectionMiceAntigenClinical investigationAnimalsMedicineExtracellular Signal-Regulated MAP KinaseseducationReceptorInterleukin 4Mice Knockouteducation.field_of_studybusiness.industryT-cell receptorHistocompatibility Antigens Class IINeurodegenerative DiseasesGeneral MedicineAxonsCell biologyBrain InjuriesMyeloid Differentiation Factor 88Immunologybiology.proteinInterleukin-4medicine.symptomFunction and Dysfunction of the Nervous SystemCorrigendumbusinessProto-Oncogene Proteins c-aktResearch ArticleNeurotrophinJournal of Clinical Investigation
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