Search results for "Protein kinase b"

showing 10 items of 191 documents

Roles of signaling pathways in drug resistance, cancer initiating cells and cancer progression and metastasis

2014

The EGFR/PI3K/PTEN/Akt/mTORC pathway plays prominent roles in malignant transformation, prevention of apoptosis, drug resistance, cancer initiating cells (CICs) and metastasis. The expression of this pathway is frequently altered in breast and other cancers due to mutations at or aberrant expression of: HER2, EGFR1, PIK3CA, and PTEN as well as other oncogenes and tumor suppressor genes. miRs and epigenetic mechanisms of gene regulation are also important events which regulate this pathway. In some breast cancer cases, mutations at certain components of this pathway (e.g., PIK3CA) are associated with a better prognosis than breast cancers lacking these mutations. The expression of this pathw…

MaleOncologyCancer Researchmedicine.medical_treatmentTargeted therapyMetastasisTargeted therapyBreast cancerNeoplasmsNeoplasm MetastasisCancer stem cellsMedicine (all)Neoplasm ProteinsNeoplasm MetastasiGene Expression Regulation NeoplasticCell Transformation NeoplasticMolecular MedicineFemaleHormonal therapyHumanSignal Transductionmedicine.medical_specialtyEGFRBiologyNeoplasm ProteinBreast cancerGeneticCancer stem cellInternal medicineHER2GeneticsmedicineAnimalsHumansPTENMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayCell ProliferationAnimalCancer stem cellTherapy resistanceCancermedicine.diseaseERDrug Resistance NeoplasmBreast cancer; Cancer stem cells; EGFR; ER; HER2; Hormonal therapy; Targeted therapy; Therapy resistancebiology.proteinCancer researchNeoplasm
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Human periodontal fibroblast response to a nanostructured hydroxyapatite bone replacement graft in vitro

2007

Abstract Objective The efficacy of nanostructured hydroxyapatite (NHA) for the treatment of osseous defects has been demonstrated in recent studies, even though the underlining biological mechanism is still poorly known. This study examined the alterations in cellular adhesion and mitogenic responses in human periodontal ligament (PDL) cells treated with a novel nanostructured hydroxyapatite bone graft substitute and characterized associated changes in cellular signalling pathways. Methods Cultured PDL cells were stimulated with NHA in a surface coated form. Proliferation was determined by bromodeoxyuridine (BrdU) incorporation and cell adhesion was analysed by a colorimetric assay. In orde…

MalePeriodontal LigamentIntegrinBiocompatible MaterialsFocal adhesionstomatognathic systemCell AdhesionHumansEpidermal growth factor receptorCell adhesionProtein kinase AGeneral DentistryProtein kinase BCells CulturedCell ProliferationbiologyChemistryCell BiologyGeneral MedicineAnatomyFibroblastsNanostructuresCell biologyErbB ReceptorsDurapatiteOtorhinolaryngologyFocal Adhesion Kinase 1Mitogen-activated protein kinasebiology.proteinPhosphorylationFemaleMitogen-Activated Protein KinasesSignal TransductionArchives of Oral Biology
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Cytotoxic activity of the novel small molecule AKT inhibitor SC66 in hepatocellular carcinoma cells

2014

Hepatocellular carcinoma (HCC) is characterized by limited response to current drug therapies. Here, we report that SC66, a novel AKT inhibitor, reduced cell viability in a dose- and time-dependent manner, inhibited colony formation and induced apoptosis in HCC cells. SC66 treatment led to a reduction in total and phospho-AKT levels. This was associated with alterations in cytoskeleton organization, a reduction in expression levels of E-cadherin, β-catenin and phospho-FAK, together with up-regulation of Snail protein levels. All these alterations were coupled with anoikis cell death induction. In addition, SC66 induced the production of reactive oxygen species (ROS) and DNA damage. Pre-trea…

MaleProgrammed cell deathCarcinoma HepatocellularCytoskeleton organizationPyridinesMice NudeApoptosisBiologyMice03 medical and health sciences0302 clinical medicineanoikisCell Line TumorAnimalsHumansAnoikisViability assayHCCProtein Kinase InhibitorsProtein kinase BPI3K/AKT/mTOR pathwayCell Proliferation030304 developmental biologySC660303 health sciencesCyclohexanonesCell growthAKTLiver NeoplasmsXenograft Model Antitumor AssaysMolecular biology3. Good healthOncologyApoptosis030220 oncology & carcinogenesismTORCancer researchHCC AKT mTOR SC66 anoikisProto-Oncogene Proteins c-aktResearch Paper
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Inducible NO synthase confers chemoresistance in head and neck cancer by modulating survivin

2009

The dual role of the inducible NO synthase (iNOS) and NO signaling in head and neck squamous cell carcinoma (HNSCC) is a complex and can both promote or inhibit tumor progression. However, the underlying molecular mechanisms are not yet resolved in detail. We show for the first time that conditions, favoring low NO levels conferred resistance against cisplatin/taxol-induced apoptosis in HNSCC cell lines. Cytoprotection was mediated by survivin, because we observed its upregulation subsequent to low doses of the NO donors S-nitroso-N-acetyl-penicillamine (SNAP) and sodium nitroprusside (SNP) or ectopic expression of physiologic amounts of iNOS. Also, RNAi-mediated depletion of survivin block…

MaleUmbilical VeinsCancer ResearchSurvivinFluorescent Antibody TechniqueNitric Oxide Synthase Type IIApoptosisp38 Mitogen-Activated Protein KinasesInhibitor of Apoptosis ProteinsImmunoenzyme TechniquesPhosphatidylinositol 3-Kinaseschemistry.chemical_compoundLY294002Enzyme InhibitorsRNA Small InterferingAged 80 and overReverse Transcriptase Polymerase Chain ReactionCell CycleMiddle AgedCell cycleOncologyHead and Neck NeoplasmsCarcinoma Squamous CellFemaleMicrotubule-Associated ProteinsNitroprussidePaclitaxelImmunoblottingAntineoplastic AgentsS-Nitroso-N-AcetylpenicillamineBiologyCell LineDownregulation and upregulationSurvivinmedicineHumansNitric Oxide DonorsRNA MessengerneoplasmsProtein kinase BNitritesPI3K/AKT/mTOR pathwayAgedmedicine.diseaseAntineoplastic Agents PhytogenicHead and neck squamous-cell carcinomachemistryDrug Resistance NeoplasmTumor progressionImmunologyCancer researchEndothelium VascularCisplatinProto-Oncogene Proteins c-aktInternational Journal of Cancer
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Perlecan-Induced Suppression of Smooth Muscle Cell Proliferation Is Mediated Through Increased Activity of the Tumor Suppressor PTEN

2004

We were interested in the elucidation of the interaction between the heparan sulfate proteoglycan, perlecan, and PTEN in the regulation of vascular smooth muscle cell (SMC) growth. We verified serum-stimulated DNA synthesis, and Akt and FAK phosphorylation were significantly reduced in SMCs overexpressing wild-type PTEN. Our previous studies showed perlecan is a potent inhibitor of serum-stimulated SMC growth. We report in the present study, compared with SMCs plated on fibronectin, serum-stimulated SMCs plated on perlecan exhibited increased PTEN activity, decreased FAK and Akt activities, and high levels of p27, consistent with SMC growth arrest. Adenoviral-mediated overexpression of cons…

MaleVascular smooth musclePhysiology:CIENCIAS MÉDICAS ::Farmacodinámica [UNESCO]Aorta ThoracicBasement MembraneCulture Media Serum-FreeMuscle Smooth VascularRats Sprague-DawleyMicePhosphorylationCells CulturedGlycosaminoglycansbiologyProtein-Tyrosine KinasesCell cycle:CIENCIAS MÉDICAS [UNESCO]musculoskeletal systemUNESCO::CIENCIAS MÉDICAS ::FarmacodinámicaUNESCO::CIENCIAS MÉDICAScardiovascular systemPhosphorylationSmooth muscle cell proliferationCardiology and Cardiovascular MedicineCell DivisionDNA ReplicationBasement membraneRecombinant Fusion ProteinsPerlecanProtein Serine-Threonine KinasesVascular injurySmooth muscle cell proliferation ; Restenosis ; Vascular injury ; Vascular development ; Basement membraneCatheterizationProto-Oncogene ProteinsAnimalsPTENProtein kinase BRestenosisCell growthVascular developmentOligonucleotides AntisenseFibronectinsRatsFibronectinFocal Adhesion Kinase 1Focal Adhesion Protein-Tyrosine Kinasesbiology.proteinCancer researchHeparitin SulfateCarotid Artery InjuriesProtein Processing Post-TranslationalProto-Oncogene Proteins c-aktHeparan Sulfate ProteoglycansCirculation Research
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Altered REDD1, myostatin, and Akt/mTOR/FoxO/MAPK signaling in streptozotocin-induced diabetic muscle atrophy

2011

Type 1 diabetes, if poorly controlled, leads to skeletal muscle atrophy, decreasing the quality of life. We aimed to search highly responsive genes in diabetic muscle atrophy in a common diabetes model and to further characterize associated signaling pathways. Mice were killed 1, 3, or 5 wk after streptozotocin or control. Gene expression of calf muscles was analyzed using microarray and protein signaling with Western blotting. We identified translational repressor protein REDD1 (regulated in development and DNA damage responses) that increased seven- to eightfold and was associated with muscle atrophy in diabetes. The diabetes-induced increase in REDD1 was confirmed at the protein level. …

Malemedicine.medical_specialtyMAP Kinase Signaling SystemPhysiologyEndocrinology Diabetes and MetabolismFOXO1P70-S6 Kinase 1MyostatinBiologyMiceRandom Allocation03 medical and health sciences0302 clinical medicinePhysiology (medical)Internal medicinemedicineAnimalsRNA MessengerPhosphorylationMuscle SkeletalProtein kinase BPI3K/AKT/mTOR pathwayOligonucleotide Array Sequence Analysis030304 developmental biology0303 health sciencesForkhead Box Protein O1Gene Expression ProfilingTOR Serine-Threonine KinasesUbiquitinationForkhead Transcription FactorsOrgan SizeMyostatinProtein ubiquitinationMuscle atrophyMuscular AtrophyDNA Repair EnzymesDiabetes Mellitus Type 1EndocrinologyGene Expression Regulationbiology.proteinPhosphorylationmedicine.symptomProto-Oncogene Proteins c-akt030217 neurology & neurosurgeryTranscription FactorsAmerican Journal of Physiology-Endocrinology and Metabolism
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Imeglimin Normalizes Glucose Tolerance and Insulin Sensitivity and Improves Mitochondrial Function in Liver of a High-Fat, High-Sucrose Diet Mice Mod…

2015

International audience; Imeglimin is the first in a new class of oral glucose-lowering agents currently in phase 2b development. Although imeglimin improves insulin sensitivity in humans, the molecular mechanisms are unknown. This study used a model of 16-week high-fat, high-sucrose diet (HFHSD) mice to characterize its antidiabetic effects. Six-week imeglimin treatment significantly decreased glycemia, restored normal glucose tolerance, and improved insulin sensitivity without modifying organs, body weights, and food intake. This was associated with an increase in insulin-stimulated protein kinase B phosphorylation in the liver and muscle. In liver mitochondria, imeglimin redirects substra…

Malemedicine.medical_specialtyMale Animals Mice Inbred C57BL Insulin Resistance/*physiology Diet High-Fat/adverse effects Hypoglycemic Agents/*therapeutic use Liver/*drug effects/*metabolism Mitochondria/*drug effects/*metabolism Triazines/*therapeutic useImegliminMitochondria/*drug effects/*metabolismEndocrinology Diabetes and Metabolism[SDV]Life Sciences [q-bio]High-Fat/adverse effectsBiologyMitochondrionDiet High-Fatmedicine.disease_causeInbred C57BLchemistry.chemical_compoundMiceLipid oxidationInternal medicineInternal MedicinemedicineHypoglycemic Agents/*therapeutic useHypoglycemic AgentsAnimalsProtein kinase BBeta oxidationComputingMilieux_MISCELLANEOUS2. Zero hungerchemistry.chemical_classificationReactive oxygen speciesTriazines/*therapeutic useTriazinesMitochondria3. Good healthDietMice Inbred C57BL[SDV] Life Sciences [q-bio]EndocrinologyLiver/*drug effects/*metabolismLiverchemistryInsulin Resistance/*physiologyCoenzyme Q – cytochrome c reductaseInsulin ResistanceOxidative stress
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Benfotiamine accelerates the healing of ischaemic diabetic limbs in mice through protein kinase B/Akt-mediated potentiation of angiogenesis and inhib…

2006

Benfotiamine, a vitamin B1 analogue, reportedly prevents diabetic microangiopathy. The aim of this study was to evaluate whether benfotiamine is of benefit in reparative neovascularisation using a type I diabetes model of hindlimb ischaemia. We also investigated the involvement of protein kinase B (PKB)/Akt in the therapeutic effects of benfotiamine. Streptozotocin-induced diabetic mice, given oral benfotiamine or vehicle, were subjected to unilateral limb ischaemia. Reparative neovascularisation was analysed by histology. The expression of Nos3 and Casp3 was evaluated by real-time PCR, and the activation state of PKB/Akt was assessed by western blot analysis and immunohistochemistry. The f…

Malemedicine.medical_specialtyProgrammed cell deathAngiogenesisEndocrinology Diabetes and MetabolismBlotting WesternNeovascularization PhysiologicApoptosisMice Inbred StrainsBiologyDiabetes Mellitus ExperimentalNeovascularizationMiceRandom AllocationIschemiaInternal medicineInternal MedicinemedicineAnimalsThiamineMuscle SkeletalProtein kinase BCell ProliferationCaspase 3Stem Cellsprotein kinase PKB/AktBody WeightHemodynamicsEndothelial CellsCaspase InhibitorsImmunohistochemistryEndothelial stem cellEnzyme ActivationOxidative StressEndocrinologyBenfotiamineApoptosisCaspasesDietary SupplementsTransketolase activitymedicine.symptomProto-Oncogene Proteins c-aktDiabetic Angiopathiesmedicine.drugDiabetologia
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Overlapping phenotypes between SHORT and Noonan syndromes in patients with PTPN11 pathogenic variants

2020

Overlapping syndromes such as Noonan, Cardio-Facio-Cutaneous, Noonan syndrome (NS) with multiple lentigines and Costello syndromes are genetically heterogeneous conditions sharing a dysregulation of the RAS/mitogen-activated protein kinase (MAPK) pathway and are known collectively as the RASopathies. PTPN11 was the first disease-causing gene identified in NS and remains the more prevalent. We report seven patients from three families presenting heterozygous missense variants in PTPN11 probably responsible for a disease phenotype distinct from the classical Noonan syndrome. The clinical presentation and common features of these seven cases overlap with the SHORT syndrome. The latter is the c…

Malemusculoskeletal diseases0301 basic medicineMAPK/ERK pathwaycongenital hereditary and neonatal diseases and abnormalitiesMAP Kinase Signaling SystemProtein Tyrosine Phosphatase Non-Receptor Type 11030105 genetics & heredityBiologyGene productPhosphatidylinositol 3-Kinases03 medical and health sciencesMetabolic DiseasesGeneticsmedicineHumansMissense mutationskin and connective tissue diseasesProtein kinase BGrowth DisordersGenetics (clinical)GeneticsGenetic heterogeneityNoonan SyndromeGenetic Variationmedicine.diseasePTPN11NephrocalcinosisPhenotype030104 developmental biologySHORT syndromeHypercalcemiaNoonan syndromeFemaleMitogen-Activated Protein KinasesSignal TransductionClinical Genetics
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Ionizing radiation-engineered nanogels as insulin nanocarriers for the development of a new strategy for the treatment of Alzheimer's disease

2016

A growing body of evidence shows the protective role of insulin in Alzheimer's disease (AD). A nanogel system (NG) to deliver insulin to the brain, as a tool for the development of a new therapy for Alzheimer's Disease (AD), is designed and synthetized. A carboxyl-functionalized poly(N-vinyl pyrrolidone) nanogel system produced by ionizing radiation is chosen as substrate for the covalent attachment of insulin or fluorescent molecules relevant for its characterization. Biocompatibility and hemocompatibility of the naked carrier is demonstrated. The insulin conjugated to the NG (NG-In) is protected by protease degradation and able to bind to insulin receptor (IR), as demonstrated by immunofl…

Materials scienceIonizing radiation processingmedicine.medical_treatmentBiophysicsBioengineering02 engineering and technologyBlood–brain barrierNeuroprotectionBiomaterialsInsulin nanocarrier03 medical and health sciencesNanogel0302 clinical medicineDrug Delivery SystemsAlzheimer DiseaseCell Line TumorRadiation Ionizingmedicinenanogels; ionizing radiation processing; insulin nanocarriers; Alzheimer's Disease; targeted drug deliveryAnimalsHumansInsulinNanotechnologyProtein kinase BDrug CarriersTargeted drug deliverybiologyInsulinBrainPovidoneAlzheimer's disease021001 nanoscience & nanotechnologyReceptor InsulinCell biologyNanostructuresMice Inbred C57BLInsulin receptormedicine.anatomical_structureTargeted drug deliveryBiochemistryMechanics of MaterialsCeramics and Compositesbiology.proteinSettore CHIM/07 - Fondamenti Chimici Delle TecnologieNanocarriers0210 nano-technology030217 neurology & neurosurgeryNanogel
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