Search results for "ERK1"

showing 7 items of 17 documents

mGluR2/3 agonist LY379268, by enhancing the production of GDNF, induces a time-related phosphorylation of RET receptor and intracellular signaling Er…

2011

In the present study we aimed to verify if the enhancement of glial cell line-derived neurotrophic factor (GDNF) production in mouse striatum following treatment with LY379268 may also induce in the nigrostriatal system a time-related activation of RET receptor and its specific intracellular signaling. For this purpose, we have investigated the effects of LY379268 treatment on RET phosphorylation at the Tyr1062 and on downstream signaling Erk1/2, Akt and PLCγ1 pathway activation. The results showed that treatment with LY379268 (3 mg/kg) induces a significant increase of GDNF levels and time-related RET and Erk1/2 phosphorylation in the striatum. These increases were detected at 24 h and 48 …

Intracellular FluidMalemedicine.medical_specialtyTime FactorsMAP Kinase Signaling SystemSubstantia nigraStriatumReceptors Metabotropic GlutamateSettore BIO/09 - FisiologiaCellular and Molecular NeuroscienceMiceErk1/2Neurotrophic factorsInternal medicinemedicineGlial cell line-derived neurotrophic factorAnimalsGlial Cell Line-Derived Neurotrophic FactorAmino AcidsPhosphorylationReceptormGluR2/3Protein kinase BPharmacologyMitogen-Activated Protein Kinase 3biologyChemistryProto-Oncogene Proteins c-retLY379268Bridged Bicyclo Compounds HeterocyclicGDNFCorpus StriatumUp-RegulationMice Inbred C57BLEndocrinologynervous systembiology.proteinPhosphorylationTrK phosphorylationRETGDNF family of ligandsNeuropharmacology
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The three α1-adrenoceptor subtypes show different spatio-temporal mechanisms of internalization and ERK1/2 phosphorylation

2013

AbstractWe analyzed the kinetic and spatial patterns characterizing activation of the MAP kinases ERK 1 and 2 (ERK1/2) by the three α1-adrenoceptor (α1-AR) subtypes in HEK293 cells and the contribution of two different pathways to ERK1/2 phosphorylation: protein kinase C (PKC)-dependent ERK1/2 activation and internalization-dependent ERK1/2 activation. The different pathways of phenylephrine induced ERK phosphorylation were determined by western blot, using the PKC inhibitor Ro 31-8425, the receptor internalization inhibitor concanavalin A and the siRNA targeting β-arrestin 2. Receptor internalization properties were studied using CypHer5 technology and VSV-G epitope-tagged receptors. Activ…

MAPK/ERK pathwayArrestinsmedia_common.quotation_subjectBlotting WesternKidneyReal-Time Polymerase Chain ReactionImmunoenzyme TechniquesConstitutive activityReceptors Adrenergic alpha-1Concanavalin AHumansRNA MessengerPKCEnzyme InhibitorsPhosphorylationRNA Small InterferingInternalizationProtein kinase AMolecular BiologyCells CulturedProtein Kinase Cbeta-ArrestinsProtein kinase Cmedia_commonMitogen-Activated Protein Kinase 1G protein-coupled receptor kinaseMitogen-Activated Protein Kinase 3ERK1/2biologyReverse Transcriptase Polymerase Chain ReactionKinaseChemistryCell Biologybeta-Arrestin 2Molecular biologyAdrenaline α1 receptorsEndocytosisMitogen-activated protein kinasebiology.proteinPhosphorylationInternalizationSignal TransductionBiochimica et Biophysica Acta (BBA) - Molecular Cell Research
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Potentiation of the antitumor effects of both selective cyclooxygenase-1 and cyclooxygenase-2 inhibitors in human hepatic cancer cells by inhibition …

2007

The molecular mechanisms behind the anti-neoplastic effects of non-steroidal anti-inflammatory drugs (NSAIDs) are not completely understood and cannot be explained by the inhibition of the cyclooxygenase (COX) enzymes COX-1 and COX-2 alone. We previously reported that both the selective COX-1 inhibitor SC-560 and the selective COX-2 inhibitor CAY10404 exhibit anti-tumor effects in human hepatoma cells. NSAID inhibitors have many COX-independent actions and, among others, the mitogen-activated protein kinase (MAPK) pathways are targets for NSAIDs. Here, we examined the role of MEK/ERK1/2 signaling in the anti-neoplastic effects of both selective COX-1 and COX-2 inhibitors in two human hepato…

MAPK/ERK pathwayCancer ResearchCarcinoma HepatocellularTime FactorsBlotting WesternApoptosisPharmacologyCOX-1 COX-2 NSAIDs MEK1/2 ERK1/2NitrilesButadienesTumor Cells CulturedHumansCyclooxygenase InhibitorsSulfonesEnzyme InhibitorsPhosphorylationProtein kinase ACell ProliferationPharmacologychemistry.chemical_classificationMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase KinasesMitogen-Activated Protein Kinase 3biologyDose-Response Relationship DrugLiver NeoplasmsCytochromes cLong-term potentiationDrug SynergismIsoxazolesFlow CytometryEnzymeOncologychemistryCyclooxygenase 2CaspasesCancer cellbiology.proteinCyclooxygenase 1Molecular MedicineMEK-ERK PathwayPyrazolesDrug Therapy CombinationCyclooxygenaseHepatoma cellCancer biologytherapy
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Trastuzumab therapy vs tetracycline controlled ERBB2 downregulation: influence on tumour development in an ERBB2-dependent mouse tumour model

2008

Trastuzumab (Herceptin) has improved therapy of breast cancer. Only patients overexpressing ERBB2 are treated with trastuzumab, whereas its use in tumours without ERBB2 expression is useless. This led to the concept that the subgroup of trastuzumab-sensitive tumours is ‘ERBB2-dependent', meaning that ERBB2 signalling is indispensable for growth of these tumours. We used a mouse model that allows anhydrotetracycline (ATc)-controlled downregulation of ERBB2 in tumour tissue. ERBB2 mRNA and protein expression were downregulated below detection limit leading to a macroscopically complete tumour remission within 14 days. Tumour remission was accompanied by a strong decrease in proliferation, a m…

MaleCancer ResearchReceptor ErbB-2AKT1AKT2ApoptosisMiceTrastuzumabPKBskin and connective tissue diseasesERBB2Mitogen-Activated Protein Kinase 3biologyERK1/2herceptinAntibodies MonoclonalCytochromes cImmunohistochemistrynude miceGene Expression Regulation NeoplasticOncologyTetracyclinesKi-67Ki-67Femalemedicine.drugmedicine.medical_specialtyBlotting WesternDown-RegulationMice NudeAntineoplastic AgentsProtein Serine-Threonine KinasesAntibodies Monoclonal Humanizedresistance3-Phosphoinositide-Dependent Protein Kinasesbreast cancerDownregulation and upregulationresponse to therapyInternal medicineHER2medicineAnimalsRNA Messengercytochrome c releaseProtein kinase Bneoplasmstumour developmentCell Proliferationhumanised monoclonal antibodyAktCancerMammary Neoplasms ExperimentalTrastuzumabmedicine.diseaseEndocrinologyKi-67 AntigenApoptosisDrug Resistance Neoplasmbiology.proteinCancer researchreceptor tyrosine kinaseTranslational TherapeuticsProto-Oncogene Proteins c-aktBritish Journal of Cancer
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Dephosphorylation of p-ERK1/2 in relation to tumor remission after HER-2 and Raf1 blocking therapy in a conditional mouse tumor model

2006

Several studies have shown that HER-2/neu (erbB-2) blocking therapy strategies can cause tumor remission. However, the responsible molecular mechanisms are not yet known. Both ERK1/2 and Akt/PKB are critical for HER-2-mediated signal transduction. Therefore, we used a mouse tumor model that allows downregulation of HER-2 in tumor tissue by administration of anhydrotetracycline (ATc). Switching-off HER-2 caused a rapid tumor remission by more than 95% within 7 d of ATc administration compared to the volume before switching-off HER-2. Interestingly, HER-2 downregulation caused a dephosphorylation of p-ERK1/2 by more than 80% already before tumor remission occurred. Levels of total ERK protein…

MaleMAPK/ERK pathwayCancer Researchmedicine.medical_specialtyReceptor ErbB-2Blotting WesternDown-RegulationMice NudeP erk1 2BiologyTransfectionDephosphorylationMiceDownregulation and upregulationInternal medicinemedicineAnimalsHumansMouse tumorPhosphorylationMolecular BiologyProtein kinase BMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Remission InductionNeoplasms ExperimentalTumor tissueGene Expression Regulation NeoplasticProto-Oncogene Proteins c-rafDisease Models AnimalEndocrinologyTetracyclinesNIH 3T3 CellsCancer researchSignal transductionSignal TransductionMolecular Carcinogenesis
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Identification et caractérisation du récepteur à la flagelline (VvFLS2) et recherche du récepteur aux chito-oligosaccharides chez la vigne

2014

Pattern-recognition receptors (PRRs) play a key role in plant immunity by assuring recognition of microbe-associated molecular patterns (MAMPs), signature of microbial presence. MAMP perception constitutes the first layer of pathogen detection and activates defense mechanisms that aim to block the intruder. This study brings an insight into how grapevine (Vitis vinifera) perceives two MAMPs: the flagellin-derived flg22 peptide and chitin, which are conserved motifs occurring over the whole bacterial and fungal classes, respectively. This study analyzed MAMP-triggered early signaling events, defense gene expression and also the efficiency of elicited defense against gray mold and downy milde…

[SDE] Environmental SciencesPRRChitin[ SDV.BBM.BM ] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biology[SDV.BC]Life Sciences [q-bio]/Cellular BiologyChitine[ SDV.BBM.BC ] Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM]RécepteursReceptors[SDV.BV] Life Sciences [q-bio]/Vegetal BiologyVigneSDV:BCSDV:BBM:BCFlg22[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyÉliciteursfungiImmunity[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biology[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM][SDV] Life Sciences [q-bio]Grapevine;Immunity;MAMP;Receptors;PRR;FLS2;Flg22;CERK1;Chitin;Vitis vinifera;Vigne;Immunité;Éliciteurs;Récepteurs;ChitineCERK1MAMPVitis viniferaImmunitéGrapevineSDV:BBM:BMFLS2
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Silencing of C3G increases cardiomyocyte survival inhibition and apoptosis via regulation of p-ERK1/2 and Bax

2019

Experimental studies have shown that overexpression of Rap guanine nucleotide exchange factor 1 (C3G) plays pro‐survival and anti‐apoptotic roles through molecule phosphorylated extracellular signal‐regulated kinase1/2 (p‐ERK1/2) in cardiomyocytes. However, it is still unclear if silencing of C3G may increase cell survival inhibition and apoptosis in cardiomyocytes, and whether C3G silence induced injuries are reduced by the overexpression of C3G through regulation of p‐ERK1/2 and pro‐apoptotic molecule Bax. In this study, the rat‐derived H9C2 cardiomyocytes were infected with C3G small hairpin RNA interference recombinant lentiviruses, which silenced the endogenous C3G expression in the ca…

ohjelmoitunut solukuolemaBaxsydänapoptosiscardiac myocyteRap guanine nucleotide exchange factor 1proteiinithenkiinjääminenH9C2 cell linep-ERK1/2lihassolut
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