Search results for "Protein kinase b"

showing 10 items of 191 documents

Activity-dependent survival of developing neocortical neurons depends on PI3K signalling

2011

J. Neurochem. (2012) 120, 495–501. Abstract Spontaneous electrical network activity plays a major role in the control of cell survival in the developing brain. Several intracellular pathways are implicated in transducing electrical activity into gene expression dependent and independent survival signals. These include activation of phosphatidylinositol 3-kinase (PI3K) and its downstream effector Akt, activation of Ras and subsequently MAPK/extracellular signal-regulated kinase (MEK) and extracellular signal-regulated kinase and signalling via calcium/calmodulin-dependent protein kinase (CaMK). In the present study, we analyzed the role of these pathways for the control of neuronal survival …

MAPK/ERK pathwayCellular and Molecular NeuroscienceKinaseExtracellularBiologyProtein kinase ABiochemistryProtein kinase BCAMKPI3K/AKT/mTOR pathwayIntracellularCell biologyJournal of Neurochemistry
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Bis(1H-indol-2-yl)methanones are effective inhibitors of FLT3-ITD tyrosine kinase and partially overcome resistance to PKC412A in vitro.

2009

Inhibition of the mutated fms-like tyrosine kinase 3 (FLT3) receptor tyrosine kinase is a promising therapeutic strategy in acute myeloid leukaemia (AML). However, development of resistance to FLT3 tyrosine kinase inhibitors (TKI), such as PKC412A, has been described recently. This observation may have an increasing impact on the duration of response and relapse rates in upcoming clinical trials employing FLT3-TKI. Herein we investigated two representatives of a novel class of FLT3-TKI: Bis(1H-indol-2-yl)methanones. Both compounds effectively induced apoptosis in FLT3-internal tandem duplicate (ITD)-transfected murine myeloid cells and in primary FLT3-ITD positive blasts. Combination of bot…

MAPK/ERK pathwayIndolesmedicine.drug_classAntineoplastic AgentsApoptosisTransfectionTyrosine-kinase inhibitorReceptor tyrosine kinaseCell Linefluids and secretionshemic and lymphatic diseasesmedicineTumor Cells CulturedHumansProtein kinase Bbiologyhemic and immune systemsHematologyStaurosporineIn vitroLeukemia Myeloid Acutefms-Like Tyrosine Kinase 3Drug Resistance NeoplasmTandem Repeat SequencesTrk receptorembryonic structuresFms-Like Tyrosine Kinase 3Cancer researchbiology.proteinTyrosine kinasepsychological phenomena and processesBritish journal of haematology
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Divide and rule: The role of ubiquitination in inactivation of the ERK5-MAPK cascade

2014

Recently, we revealed that ubiquitination of MEKK2 and MEKK3 by inhibitor of apoptosis proteins (IAPs) directly disrupts MEK5/ERK5 interaction and subsequently attenuates ERK5 activation. In addition, loss of XIAP promotes human myogenic differentiation in an ERK5-dependent manner. These results reveal another layer of MAPK regulation and a novel role for XIAP in controlling myogenic differentiation.

MAPK/ERK pathwayInhibitor of apoptosis domainCancer ResearchAkt/PKB signaling pathwayChemistryMAPK cascadeInhibitor of apoptosisMAP2K7XIAPCell biologyCancer researchMolecular MedicineAuthor's ViewProtein kinase BMolecular & Cellular Oncology
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The JAK2 Kinase Inhibitor LS104 Induces Growth-Arrest and Apoptosis in JAK2V617F Positive Cells.

2007

Abstract The JAK2V617F-mutation (V617F) is a novel, highly prevalent molecular marker in Ph-negative myeloproliferative disease (MPD). In vitro, the V617F mutation confers cytokine independent growth of Ba/F3 cells expressing erythropoietin receptor (EpoR) and constitutive activation of the JAK2 kinase and of the JAK-STAT pathway. In a murine bone-marrow transplant model the V617F-mutation alone is sufficient to induce a polycythemia vera-like phenotype. Therefore, mutant JAK2 kinase is a promising target for kinase inhibitor development. In this report, we characterize the small molecule LS104 (previously CR4; Grunberger et al., Blood 2003) as a novel non-ATP-competitive JAK2V617F kinase i…

MAPK/ERK pathwayKinasemedicine.medical_treatmentImmunologyAutophosphorylationfood and beveragesCell BiologyHematologyTransfectionBiologyBiochemistryMolecular biologyErythropoietin receptorCytokinehemic and lymphatic diseasesmedicineCancer researchKinase activityProtein kinase BBlood
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Increased radioresistance via G12S K-Ras by compensatory upregulation of MAPK and PI3K pathways in epithelial cancer

2011

Background Irradiation-induced signaling via the 2 pathways, Raf-MEK-ERK and PI3K-Akt, is known to be closely associated with a limited response to radiotherapy. In the present study we analyzed the relevance of constitutively active K-Ras for postradiogenic pathway stimulation and the option of coordinated inhibition to overcome these rescue mechanisms. Methods We used 2 epithelial tumor cell lines as a model system, one of them harboring a G12S K-Ras mutation. Cells were irradiated and the effect of combined treatment with ionizing radiation and inhibitors on the expression of pERK and pAkt was determined by Western blotting. Additionally, clonogenic assays were performed to functionally …

MAPK/ERK pathwayMAP Kinase Signaling SystemBlotting WesternPolymerase Chain ReactionRadiation ToleranceSensitivity and SpecificityPhosphatidylinositol 3-KinasesDownregulation and upregulationCell Line TumorRadioresistanceHumansMedicineRadiosensitivityClonogenic assayProtein kinase BPI3K/AKT/mTOR pathwayMitogen-Activated Protein Kinase Kinasesbusiness.industryEpithelial CellsUp-RegulationGenes rasOtorhinolaryngologyHead and Neck NeoplasmsCell cultureImmunologyCarcinoma Squamous CellCancer researchElectrophoresis Polyacrylamide GelbusinessSignal TransductionHead & Neck
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Inhibition of c-MYC with involvement of ERK/JNK/MAPK and AKT pathways as a novel mechanism for shikonin and its derivatives in killing leukemia cells

2015

Leukemia remains life-threatening despite remarkable advances in chemotherapy. The poor prognosis and drug resistance are challenging treatment. Novel drugs are urgently needed. Shikonin, a natural naphthoquinone, has been previously shown by us to be particularly effective towards various leukemia cell lines compared to solid tumors. However, the underlying mechanisms are still poorly understood. Here, we investigated shikonin and 14 derivatives on U937 leukemia cells. Four derivatives (isobutyrylshikonin, 2-methylbutyrylshikonin, isovalerylshikonin and β,β-dimethylacrylshikonin) were more active than shikonin. AnnexinV-PI analysis revealed that shikonins induced apoptosis. Cell cycle G1/S…

MAPK/ERK pathwayMAP Kinase Signaling Systemshikonin and its derivativesJurkat cellsProto-Oncogene Proteins c-mycCell Line TumormedicineHumansacute leukemiaExtracellular Signal-Regulated MAP KinasesProtein kinase BPI3K/AKT/mTOR pathwayMitogen-Activated Protein Kinase KinasesLeukemiaU937 cellERK/JNK/MAP kinasesbusiness.industryAnti-Inflammatory Agents Non-SteroidalJNK Mitogen-Activated Protein KinasesU937 CellsCell cyclemedicine.diseaseLeukemiac-MYCAKT pathwayOncologyCancer researchSignal transductionbusinessProto-Oncogene Proteins c-aktResearch PaperNaphthoquinonesSignal TransductionOncotarget
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Influences of TP53 and the anti-aging DDR1 receptor in controlling Raf/MEK/ERK and PI3K/Akt expression and chemotherapeutic drug sensitivity in prost…

2020

Background TP53 plays critical roles in sensitivity to chemotherapy, and aging. Collagen is very important in aging. The molecular structure and biochemical properties of collagen changes during aging. The discoidin domain receptor (DDR1) is regulated in part by collagen. Elucidating the links between TP53 and DDR1 in chemosensitivity and aging could improve therapies against cancer and aging. Results Restoration of WT-TP53 activity resulted in increased sensitivity to chemotherapeutic drugs and elevated expression of key components of the Raf/MEK/ERK, PI3K/Akt and DDR1 pathways. DDR1 could modulate the levels of Raf/MEK/ERK and PI3K/Akt pathways as well as sensitize the cells to chemothera…

MAPK/ERK pathwayMalecollagenAgingRAF/MEK/ERKMAP Kinase Signaling SystemAntineoplastic Agentsdiscoidin domain receptor (DDR1)DDRCollagen receptorPhosphatidylinositol 3-KinasesDiscoidin Domain Receptor 1Cell Line TumorHumansRapamycinTP53ReceptorProtein kinase BPI3K/AKT/mTOR pathwayDDR1ChemistryWild typeProstateProstatic NeoplasmschemoresistanceCell Biologyprostate cancerDrug Resistance NeoplasmMutationCancer researchraf KinasesTumor Suppressor Protein p53Discoidin domainResearch Paper
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Erythropoietin activates cell survival pathways in breast cancer stem-like cells to protect them from chemotherapy

2013

Abstract Recombinant erythropoietin (EPO) analogs [erythropoiesis-stimulating agents (ESA)] are clinically used to treat anemia in patients with cancer receiving chemotherapy. After clinical trials reporting increased adverse events and/or reduced survival in ESA-treated patients, concerns have been raised about the potential role of ESAs in promoting tumor progression, possibly through tumor cell stimulation. However, evidence is lacking on the ability of EPO to directly affect cancer stem–like cells, which are thought to be responsible for tumor progression and relapse. We found that breast cancer stem–like cells (BCSC) isolated from patient tumors express the EPO receptor and respond to …

MAPK/ERK pathwayOncologyCancer Researchmedicine.medical_treatmentFluorescent Antibody TechniqueApoptosisMice SCIDImmunoenzyme TechniquesMiceCell MovementMice Inbred NODhemic and lymphatic diseasesTumor Cells CulturedCulturedBlottingAnemiaFlow CytometryTumor CellsTRIALSOncologyDisease ProgressionNeoplastic Stem CellsFemaleWesternSignal Transductionmedicine.drugSTIMULATING AGENTSEXPRESSIONmedicine.medical_specialtyBlotting WesternAntineoplastic AgentsBreast NeoplasmsSCIDRECOMBINANT-HUMAN-ERYTHROPOIETIN STIMULATING AGENTS EXPRESSION MORTALITY TRIALS ANEMIA ALPHA ALDH1Breast cancerIn vivoInternal medicinemedicineAnimalsHumansBreast cancer Cancer stem cellsALDH1ErythropoietinProtein kinase BCell ProliferationSettore MED/04 - Patologia GeneraleChemotherapybusiness.industryMORTALITYCancerRECOMBINANT-HUMAN-ERYTHROPOIETINmedicine.diseaseALPHAErythropoietinTumor progressionInbred NODAnemia; Animals; Antineoplastic Agents; Apoptosis; Blotting Western; Breast Neoplasms; Cell Movement; Cell Proliferation; Disease Progression; Erythropoietin; Female; Flow Cytometry; Fluorescent Antibody Technique; Humans; Immunoenzyme Techniques; Mice; Mice Inbred NOD; Mice SCID; Neoplastic Stem Cells; Signal Transduction; Tumor Cells Cultured; Cancer Research; Oncologybusiness
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Therapeutic resistance resulting from mutations in Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR signaling pathways.

2011

Chemotherapy remains a commonly used therapeutic approach for many cancers. Indeed chemotherapy is relatively effective for treatment of certain cancers and it may be the only therapy (besides radiotherapy) that is appropriate for certain cancers. However, a common problem with chemotherapy is the development of drug resistance. Many studies on the mechanisms of drug resistance concentrated on the expression of membrane transporters and how they could be aberrantly regulated in drug resistant cells. Attempts were made to isolate specific inhibitors which could be used to treat drug resistant patients. Unfortunately most of these drug transporter inhibitors have not proven effective for ther…

MAPK/ERK pathwayPTENTumor suppressor genekinase inhibitorPhysiologymedicine.medical_treatmentClinical Biochemistrygrowth factor receptorAntineoplastic AgentsDrug resistancePharmacologyBiologyTargeted therapy03 medical and health sciencesMicePhosphatidylinositol 3-Kinases0302 clinical medicineGrowth factor receptormedicinePTENAnimalsHumansExtracellular Signal-Regulated MAP KinasesProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biology0303 health sciencesTOR Serine-Threonine KinasesPTEN PhosphohydrolaseCell BiologyMAP Kinase Kinase Kinases3. Good healthErbB ReceptorsDrug Resistance Neoplasm030220 oncology & carcinogenesisMutationCancer researchbiology.proteinraf KinasesProto-Oncogene Proteins c-aktDrug resistance therapeutic sensitivity targeted therapy RAF ERKACUTE MYELOID LEUKAEMIASignal TransductionJournal of cellular physiology
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Ability of nanocrystalline hydroxyapatite paste to promote human periodontal ligament cell proliferation.

2008

Recent studies indicate that nanocrystalline hydroxyapatite (nano-HA) paste represents a promising class of bone graft substitute. However, the underlying molecular mechanisms of nano-HA function have not yet been determined. This study was conducted to investigate the proliferation of human periodontal ligament (PDL) cells cultured in the presence of nano-HA paste and to characterize associated changes in intracellular signaling pathways. Cultured PDL cells were stimulated with nano-HA paste and enamel matrix derivative (EMD) in a soluble form. Proliferation of PDL cells was determined by incorporation of bromodeoxyuridine (BrdU) in the DNA of proliferating cells. In order to understand th…

MAPK/ERK pathwayPeriodontal LigamentBlotting Westernchemistry.chemical_compoundDental Enamel ProteinsPeriodontal fiberHumansRegenerationEpidermal growth factor receptorPhosphorylationGeneral DentistryProtein kinase BCells CulturedCell ProliferationMitogen-Activated Protein Kinase 1biologyChemistryCell growthKinaseAnatomyFibroblastsCell biologyErbB ReceptorsDurapatiteBone Substitutesbiology.proteinPhosphorylationNanoparticlesProto-Oncogene Proteins c-aktBromodeoxyuridineJournal of oral science
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