Search results for "MAPK"

showing 10 items of 238 documents

Exercise and hormesis: activation of cellular antioxidant signaling pathway.

2006

Contraction-induced production of reactive oxygen species (ROS) has been shown to cause oxidative stress to skeletal muscle. As an adaptive response, muscle antioxidant defense systems are upregulated after heavy exercise. Nuclear factor (NF) kappaB and mitogen-activated protein kinases (MAPKs) are the major oxidative stress-sensitive signal transduction pathways in mammalian tissues. Activation of NF-kappaB signaling cascade has been shown to enhance the gene expression of important enzymes, such as mitochondrial superoxide dismutase (MnSOD) and inducible nitric oxide synthase (iNOS). MAPK activations are involved in a variety of cellular functions including growth, proliferation, and adap…

MAPK/ERK pathwayNitric Oxide Synthase Type IIBiologymedicine.disease_causeModels BiologicalGeneral Biochemistry Genetics and Molecular BiologyAntioxidantsGene Expression Regulation EnzymologicHistory and Philosophy of ScienceDownregulation and upregulationPhysical Conditioning AnimalmedicineAnimalsMuscle Skeletalchemistry.chemical_classificationReactive oxygen speciesKinaseSuperoxide DismutaseGeneral NeuroscienceNF-kappa BSkeletal muscleCell biologyMitochondriaNitric oxide synthaseEnzyme ActivationKineticsmedicine.anatomical_structurechemistrybiology.proteinSignal transductionMitogen-Activated Protein KinasesReactive Oxygen SpeciesOxidative stressSignal TransductionAnnals of the New York Academy of Sciences
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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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Mutations and Deregulation of Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Cascades Which Alter Therapy Response.

2012

The Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascades are often activated by genetic alterations in upstream signaling molecules such as receptor tyrosine kinases (RTK). Certain components of these pathways, RAS, NF1, BRAF, MEK1, DUSP5, PP2A, PIK3CA, PIK3R1, PIK3R4, PIK3R5, IRS4, AKT, NFKB1, MTOR, PTEN, TSC1, and TSC2 may also be activated/inactivated by mutations or epigenetic silencing. Upstream mutations in one signaling pathway or even in downstream components of the same pathway can alter the sensitivity of the cells to certain small molecule inhibitors. These pathways have profound effects on proliferative, apoptotic and differentiation pathways. Dysregulation of components of these cas…

MAPK/ERK pathwayPremature agingMAP Kinase Signaling SystemTargeted Therapy Therapy Resistance Mutations Raf Akt PI3K mTORMtorReviewsPi3kPI3KReceptor tyrosine kinaseAkt; Mtor; Mutations; Pi3k; Raf; Targeted therapy; Therapy resistance;Targeted therapyPhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineAnimalsHumansPTENExtracellular Signal-Regulated MAP KinasesProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biology0303 health sciencesbiologyChemistryTOR Serine-Threonine KinasesAktTherapy resistancePTEN PhosphohydrolaseTargeted TherapyTherapy ResistanceRafProtein phosphatase 2MAP Kinase Kinase Kinases3. Good healthCell biologyOncology030220 oncology & carcinogenesisMutationras ProteinsmTORCancer researchbiology.proteinraf KinasesMitogen-Activated Protein KinasesSignal transductionProto-Oncogene Proteins c-aktMutationsSignal TransductionOncotarget
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Characteristic ERK Signaling Dynamics Distinguishes Necroptosis from Apoptosis

2021

ERK involvement in cell death remains unclear, although many studies have demonstrated the importance of ERK dynamics in determining cellular responses. To untangle ERK’s contribution in two cell death programs, we investigated ERK signaling dynamics during hFasL-induced apoptosis and TNF-induced necroptosis in L929sAhFas cells. We observed that ERK inhibition sensitizes cells to apoptosis while delaying necroptosis. By monitoring ERK activity by live-cell imaging using an improved ERK biosensor (EKAR4.0), we reported differential ERK signaling dynamics between cell survival, apoptosis, and necroptosis. We also decrypted a temporally shifted amplitude- and frequency-modulated (AM/FM) ERK ac…

MAPK/ERK pathwayProgrammed cell deathActivity profileChemistryApoptosisNecroptosisErk signalingTumor necrosis factor alphaCell survivalCell biologySSRN Electronic Journal
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The role of death effector domain (DED)-containing proteins in acute oxidative cell injury in hepatocytes

2012

Abstract Apoptosis is a mechanism that regulates hepatic tissue homeostasis and contributes to both acute and chronic injury in liver disease. The apoptotic signaling cascade involves activation of the death-inducing signaling complex (DISC) and subsequent recruitment of proteins containing death effector domains (DED), which regulate downstream effector molecules. Prominent among these are the Fas-associated death domain (FADD) and the cellular caspase 8-like inhibitory protein (cFLIP), and alterations in these proteins can lead to severe disruption of physiological processes, including acute liver failure or hepatocellular carcinoma. Their role in cell signaling events independent of the …

MAPK/ERK pathwayProgrammed cell deathDeath Domain Receptor Signaling Adaptor ProteinsbiologyBlotting WesternBiochemistryArticleCell biologyMiceMicroscopy FluorescencePhysiology (medical)Cell Line TumorDeath-inducing signaling complexModels Animalbiology.proteinHepatocytesAnimalsHumansDeath effector domainFADDSignal transductionCaspaseDeath domainSignal Transduction
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Emerging Raf inhibitors

2009

The Raf/MAPK kinase/extracellular-signal-regulated kinase pathway is often activated by genetic alterations in upstream signaling molecules. An integral component of this pathway, BRAF, is also activated by mutation, especially in melanoma and thyroid cancers. The Raf/MAPK kinase/extracellular-signal-regulated kinase pathway has profound effects on proliferative, apoptotic and differentiation pathways as well as the sensitivity and resistance to chemotherapeutic drugs.This review discusses targeting of Raf which could control abnormal proliferation in cancer and other proliferative diseases. The important roles that genetics plays in the response of patients to Raf inhibitors is also evalua…

MAPK/ERK pathwayProto-Oncogene Proteins B-rafCell signalingMAP Kinase Signaling SystemSignal transductionrafmedicine.disease_causemekerkmedicineHumanscancerPharmacology (medical)raf inhibitorsExtracellular Signal-Regulated MAP KinasesMelanomaProtein Kinase InhibitorsPharmacologyapoptosis cancer ERK proliferative disorderssignal transductionMitogen-Activated Protein Kinase KinasesApoptosis; Cancer; ERK; Kinases; MEK; Proliferative disorders; Protein phosphorylation; Raf; Raf inhibitors; Signal transductionMutationproliferative disordersapoptosis; cancer; erk; kinases; mek; proliferative disorders; protein phosphorylation; raf; raf inhibitors; signal transduction read more: http://informahealthcare.com/doi/abs/10.1517/14728210903232633business.industryKinaseMelanomaapoptosisCancermedicine.diseaseXenograft Model Antitumor Assaysprotein phosphorylationCell Transformation Neoplastickinasessignal transduction read more: http://informahealthcare.com/doi/abs/10.1517/14728210903232633ApoptosisDrug Resistance NeoplasmCancer researchSignal transductionMitogen-Activated Protein Kinasesbusiness
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B-Raf-mediated signaling pathway regulates T cell development

2008

The activities of the Raf kinase family proteins control extracellular signal-regulated kinase (ERK) activation in many aspects of cellular responses. However, the relative contributions of individual isozymes to cellular functions including T cell responses are still unclear. In addition to Raf-1, another Raf family kinase, B-Raf, is expressed in murine thymocytes and peripheral T cells, and its activation was induced by TCR stimulation. Here, we investigated the function of B-Raf in development of T cells by generating chimeric mice in which a T cell-compromised host was reconstituted with fetal liver-derived cells from embryonic lethal B-Raf-deficient mice. Although B-Raf was dispensable…

MAPK/ERK pathwayProto-Oncogene Proteins B-rafT cellCellular differentiationT-LymphocytesImmunologyThymus GlandBiologyLymphocyte ActivationJurkat cellsArticleJurkat CellsMicemedicineImmunology and AllergyCytotoxic T cellAnimalsHumansExtracellular Signal-Regulated MAP KinasesCells CulturedRetrospective StudiesMice KnockoutZAP70T-cell receptorCell DifferentiationMolecular biologyCoculture TechniquesCell biologyMice Inbred C57BLmedicine.anatomical_structureEnzyme InductionCD8Signal Transduction
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BRAF mutations in non-small cell lung cancer : has finally Janus opened the door?

2016

Abstract: B-Raf mutations occur in about 1-2% of non-small cell lung cancers (NSCLC). These mutations generate a permanent activation of the mitogen activated protein kinase (MAPK) pathway, which promotes tumor growth and proliferation. In the present review, we discuss B-Raf mutation epidemiology, diagnostic methods to detect B-Raf mutations, the role of B-Raf as a driver mutation and a potential therapeutic target in NSCLC. The results of clinical trials involving B-Raf or MAPK pathway inhibitors for the treatment of NSCLC are also discussed. Clinical trials evaluating B-Raf inhibitors in BRAF mutated NSCLC patients have shown promising results, and larger prospective studies are warrante…

MAPK/ERK pathwayProto-Oncogene Proteins B-rafmedicine.medical_specialtyLung Neoplasmsmedicine.medical_treatmentCellProtein Kinase Inhibitormedicine.disease_causeBioinformaticsNSCLCTargeted therapy03 medical and health sciences0302 clinical medicineInternal medicineCarcinoma Non-Small-Cell LungmedicineHumans030212 general & internal medicineB-Raf inhibitorLung cancerProtein Kinase InhibitorsB-Raf inhibitorsMutationHematologybiologybusiness.industryB-RafB-Raf; B-Raf inhibitors; Drug; Mutation; NSCLC; Oncology; Hematology; Geriatrics and GerontologyHematologymedicine.diseaseLung NeoplasmClinical trialmedicine.anatomical_structureOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisMitogen-activated protein kinaseMutationbiology.proteinCancer researchHuman medicineDrugGeriatrics and GerontologybusinessHumanCritical reviews in oncology, hematology
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