Search results for "MAPK signaling cascades"

showing 6 items of 6 documents

Direct estrogen receptor (ER) / HER family crosstalk mediating sensitivity to lumretuzumab and pertuzumab in ER+ breast cancer.

2017

Bidirectional cross talk between members of the human epidermal growth factor family of receptors (HER) and the estrogen receptor (ER) is believed to underlie resistance mechanisms that develop in response to treatment with anti-HER agents and endocrine therapy. We investigated the interaction between HER2, HER3 and the ER in vitro using human embryonic kidney cells transfected with human HER2, HER3, and ERα. We also investigated the additive efficacy of combination regimens consisting of anti-HER3 (lumretuzumab), anti-HER2 (pertuzumab), and endocrine (fulvestrant) therapy in vivo. Our data show that both HER2 and HER3 can directly complex with the ER and can mediate phosphorylation of the …

0301 basic medicineCell signalingReceptor ErbB-3Receptor ErbB-2Cancer TreatmentEstrogen receptorlcsh:MedicineSignal transductionBiochemistryMice0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsBreast TumorsMedicine and Health SciencesReceptorlcsh:Scienceskin and connective tissue diseasesMultidisciplinaryRemission InductionEndocrine TherapySignaling cascadesPrecipitation TechniquesTreatment OutcomeReceptors EstrogenOncology030220 oncology & carcinogenesisMonoclonalCell linesFemalePertuzumabBiological culturesmedicine.drugResearch ArticleAdultCell biologyMAPK signaling cascadesPaclitaxelBreast NeoplasmsAntibodies Monoclonal Humanized03 medical and health sciencesBreast cancerCell Line TumorBreast CancermedicineEndocrine systemAnimalsHumansImmunoprecipitationFulvestrantbusiness.industrylcsh:RHEK 293 cellsCancers and NeoplasmsBiology and Life SciencesEstrogensReceptor Cross-TalkLumretuzumabmedicine.diseaseXenograft Model Antitumor AssaysHormonesResearch and analysis methods030104 developmental biologyCancer researchlcsh:QbusinessPloS one
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Impact of Glutathione Peroxidase-1 Deficiency on Macrophage Foam Cell Formation and Proliferation: Implications for Atherogenesis

2013

Clinical and experimental evidence suggests a protective role for the antioxidant enzyme glutathione peroxidase-1 (GPx-1) in the atherogenic process. GPx-1 deficiency accelerates atherosclerosis and increases lesion cellularity in ApoE(-/-) mice. However, the distribution of GPx-1 within the atherosclerotic lesion as well as the mechanisms leading to increased macrophage numbers in lesions is still unknown. Accordingly, the aims of the present study were (1) to analyze which cells express GPx-1 within atherosclerotic lesions and (2) to determine whether a lack of GPx-1 affects macrophage foam cell formation and cellular proliferation. Both in situ-hybridization and immunohistochemistry of l…

CD36 AntigensMAPK/ERK pathwayMouseMitogen-Activated Protein Kinase 3lcsh:MedicineGene ExpressionSignal transductionCardiovascularMiceMolecular cell biologyGlutathione Peroxidase GPX1lcsh:ScienceIn Situ HybridizationFoam cellMice KnockoutMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MultidisciplinaryReverse Transcriptase Polymerase Chain ReactionKinaseSignaling cascadesScavenger Receptors Class AAnimal ModelsImmunohistochemistryLipoproteins LDLMedicineFemaleSignal transductionResearch ArticleMacrophage colony-stimulating factorMAPK signaling cascadesBlotting WesternBiologyCell GrowthModel OrganismsApolipoproteins EVascular BiologyAnimalsHumansProtein kinase ABiologyCell ProliferationGlutathione PeroxidaseMacrophage Colony-Stimulating Factorlcsh:RAtherosclerosisMolecular biologyMacrophages Peritoneallcsh:QMacrophage proliferationFoam CellsPLoS ONE
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Differences in the signaling pathways of α(1A)- and α(1B)-adrenoceptors are related to different endosomal targeting.

2013

AIMS: To compare the constitutive and agonist-dependent endosomal trafficking of α(1A)- and α(1B)-adrenoceptors (ARs) and to establish if the internalization pattern determines the signaling pathways of each subtype. METHODS: Using CypHer5 technology and VSV-G epitope tagged α(1A)- and α(1B)-ARs stably and transiently expressed in HEK 293 cells, we analyzed by confocal microscopy the constitutive and agonist-induced internalization of each subtype, and the temporal relationship between agonist induced internalization and the increase in intracellular calcium (determined by FLUO-3 flouorescence), or the phosphorylation of ERK1/2 and p38 MAP kinases (determined by Western blot). RESULTS AND C…

MAPK signaling cascadesEndosomemedia_common.quotation_subjecteducationIntracellular Spacelcsh:MedicineEndosomesSignal transductionERK signaling cascadeBiologyEndocytosisp38 Mitogen-Activated Protein KinasesSignaling PathwaysCell LineMolecular cell biologyReceptors Adrenergic alpha-1Calcium-Mediated Signal TransductionHumansMembrane Receptor SignalingCalcium SignalingInternalizationlcsh:ScienceBiologyCalcium signalingmedia_commonMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MultidisciplinaryHEK 293 cellslcsh:RNeurotransmitter Receptor SignalingSignaling cascadesNeurotransmittersLipid signalingEndocytosisCell biologyTransport proteinProtein TransportHEK293 CellsCalcium signaling cascadeMembranes and Sortinglcsh:QAdrenergic alpha-1 Receptor AgonistsMolecular NeuroscienceSignal transductionResearch ArticleAdrenergic Signal TransductionNeurosciencePLoS ONE
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Candida albicans Yeast and Hyphae are Discriminated by MAPK Signaling in Vaginal Epithelial Cells

2011

We previously reported that a bi-phasic innate immune MAPK response, constituting activation of the mitogen-activated protein kinase (MAPK) phosphatase MKP1 and c-Fos transcription factor, discriminates between the yeast and hyphal forms of Candida albicans in oral epithelial cells (ECs). Since the vast majority of mucosal Candida infections are vaginal, we sought to determine whether a similar bi-phasic MAPK-based immune response was activated by C. albicans in vaginal ECs. Here, we demonstrate that vaginal ECs orchestrate an innate response to C. albicans via NF-κB and MAPK signaling pathways. However, unlike in oral ECs, the first MAPK response, defined by c-Jun transcription factor acti…

MAPK/ERK pathwaylcsh:MedicineYeast and Fungal ModelsPathogenesisSignal transductionMolecular cell biologyCandida albicansGranulocyte Colony-Stimulating FactorCandida albicanslcsh:ScienceImmune Response0303 health sciencesMultidisciplinarybiologyCandidiasisNF-kappa BSignaling cascadesObstetrics and GynecologyCorpus albicansInnate ImmunityHost-Pathogen InteractionInfectious DiseasesVaginaCytokinesMedicineFemaleSignal transductionCandidalysinResearch ArticleMAPK signaling cascadesMAP Kinase Signaling SystemUrologyImmunologySexually Transmitted DiseasesHyphaeMycologyMicrobiologyMicrobiologyImmune Activation03 medical and health sciencesModel OrganismsHumansTranscription factorBiology030304 developmental biologyInnate immune systemChemokine CCL20030306 microbiologyGenitourinary InfectionsInterleukin-6lcsh:RImmunityFungiMouth MucosaImmune DefenseEpithelial Cellsbiology.organism_classificationImmunity InnateCCL20Immune Systemlcsh:QClinical ImmunologyPLoS ONE
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Additive effects of cherlerythrine chloride combination with erlotinib in human non-small cell lung cancer cells

2017

Several studies implicate that lung cancer progression is governed by the interaction between epidermal growth factor receptor (EGFR) signaling and protein kinase C (PKC) pathways. Combined the targeting of EGFR and PKC may have an additive or synergistic effects in lung cancer treatment. The aim of this study is to explore the potential utility by inhibiting these two pathways with the combination of erlotinib and chelerythrine chloride in non-small cell lung cancer (NSCLC) cell lines. The erlotinib-less sensitive cell lines SK-MES-1 and A549 were treated with erlotinib or chelerythrine by themselves or in combination with each other. The cell viability, clonogenic survival, cell migration…

Male0301 basic medicineOncologyCell signalingLung NeoplasmsCancer Treatmentlcsh:MedicineApoptosisMice SCIDSignal transductionLung and Intrathoracic TumorsMicechemistry.chemical_compoundMice Inbred NODCarcinoma Non-Small-Cell LungMedicine and Health SciencesEpidermal growth factor receptorPhosphorylationlcsh:ScienceErlotinib HydrochlorideMultidisciplinaryCell DeathbiologyPharmaceuticsChemistrySignaling cascadesFlow CytometryErbB ReceptorsCell MotilityOncologyCell ProcessesDrug Therapy CombinationErlotinibSignal transductionEGFR signalingResearch Articlemedicine.drugmedicine.medical_specialtyMAPK signaling cascadesCell MigrationErlotinib Hydrochloride03 medical and health sciencesDrug TherapyCell Line TumorInternal medicinemedicineAnimalsHumansViability assayLung cancerBenzophenanthridineslcsh:RCancers and NeoplasmsBiology and Life SciencesCell Biologymedicine.diseaseXenograft Model Antitumor AssaysNon-Small Cell Lung Cancerrespiratory tract diseases030104 developmental biologyChelerythrineApoptosisCancer researchbiology.proteinlcsh:QDevelopmental BiologyPLOS ONE
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Inhibition of Xanthine Oxidase by Allopurinol Prevents Skeletal Muscle Atrophy: Role of p38 MAPKinase and E3 Ubiquitin Ligases

2012

International audience; Abstract Top Alterations in muscle play an important role in common diseases and conditions. Reactive oxygen species (ROS) are generated during hindlimb unloading due, at least in part, to the activation of xanthine oxidase (XO). The major aim of this study was to determine the mechanism by which XO activation causes unloading-induced muscle atrophy in ratsand its possible prevention by allopurinol, a well-known inhibitor of this enzyme. For this purpose we studied one of the main redox sensitive signalling cascades involved in skeletal muscle atrophy i.e. p38 MAPKinaseand the expression of two well known muscle specific E3 ubiquitin ligases involved in proteolysis, …

MaleAgingAnatomy and Physiology[SDV]Life Sciences [q-bio]lcsh:MedicineMuscle ProteinsGene ExpressionHindlimbSignal transductionmedicine.disease_causep38 Mitogen-Activated Protein KinasesTripartite Motif Proteinschemistry.chemical_compound0302 clinical medicineMolecular cell biologySignaling in Cellular Processeslcsh:ScienceMusculoskeletal System0303 health sciencesMultidisciplinarySignaling cascadesMuscle BiochemistryAnimal ModelsMuscle atrophy3. Good healthMuscular Atrophymedicine.anatomical_structureBiochemistryHindlimb SuspensionMuscleMedicinemedicine.symptomCellular Typesmedicine.drugResearch Articlemedicine.medical_specialtyXanthine OxidaseMAPK signaling cascadesAllopurinolUbiquitin-Protein LigasesAllopurinolBiology03 medical and health sciencesAtrophyModel OrganismsInternal medicinemedicineAnimalsRats WistarXanthine oxidaseMuscle SkeletalBiology030304 developmental biologySoleus muscleMuscle CellsSKP Cullin F-Box Protein LigasesSuperoxide Dismutaselcsh:RSkeletal musclemedicine.diseaseRatsEnzyme ActivationOxidative StressEndocrinologychemistryRatlcsh:QPhysiological Processes030217 neurology & neurosurgeryOxidative stress
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