Search results for "ERK1"

showing 10 items of 17 documents

Characteristic ERK1/2 signaling dynamics distinguishes necroptosis from apoptosis

2021

International audience; ERK1/2 involvement in cell death remains unclear, although many studies have demonstrated the importance of ERK1/2 dynamics in determining cellular re- sponses. To untangle how ERK1/2 contributes to two cell death programs, we investigated ERK1/2 signaling dynamics during hFasL-induced apoptosis and TNF-induced necroptosis in L929 cells. We observed that ERK1/2 inhibition sensi- tizes cells to apoptosis while delaying necroptosis. By monitoring ERK1/2 activity by live-cell imaging using an improved ERK1/2 biosensor (EKAR4.0), we reported differential ERK1/2 signaling dynamics between cell survival, apoptosis, and nec- roptosis. We also decrypted a temporally shifted …

Cell biologyProgrammed cell deathScience[SDV]Life Sciences [q-bio]Necroptosis[SDV.BBM.BP] Life Sciences [q-bio]/Biochemistry Molecular Biology/BiophysicsPROTEINMECHANISMSESCRTACTIVATION03 medical and health sciences0302 clinical medicineINFLAMMATIONGene expressionMedicine and Health SciencesKINASEBiology030304 developmental biology0303 health sciencesMultidisciplinaryIDENTIFICATIONChemistryNECROSISQDynamics (mechanics)Biology and Life SciencesErk1 2 signalingCell biology[SDV.BBM.BP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biophysics[SDV] Life Sciences [q-bio]Biological sciencesBiomolecular engineeringCELL-DEATHApoptosisCell culture030220 oncology & carcinogenesisTumor necrosis factor alphaBIOSENSORSHuman medicineiScience
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Intestinal CD36 : A long chain fatty acid receptor which controls post prandial hypertriglyceridemia, endotoxemia and intestinal epithelium integrity

2014

Post prandial hypertriglyceridemia represents a risk factor for cardio-vascular diseases and it is associated with metabolic syndrom, obesity, and insulino-resistance. The intestine influences lipid bioavailibility and post prandial hypertriglyceridemia. It controls the quantity and the quality of secreted chylomicrons by adapting its metabolism according to the lipid content of the diet. Nevertheless, the mechanism of dietary lipid detection by the enterocyte is not understood. Our work demonstrates that the transmembrane glycoprotein CD36 is a Long Chain Fatty Acid (LCFA) receptor which triggers ERK1/2 activation. This activation is responsible for the induction of mRNA rate of 3 key prot…

InflammationDietary lipidsIntestin grêle[SDV.AEN] Life Sciences [q-bio]/Food and NutritionERK1/2ChylomicronsEndotoxémieLipides alimentairesCD36EndotoxemiaIntestine
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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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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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Biphasic Erk1/2 activation sequentially involving Gs and Gi signaling is required in beta3-adrenergic receptor-induced primary smooth muscle cell pro…

2013

Abstract The beta3 adrenergic receptor (B3-AR) reportedly induces cell proliferation, but the signaling pathways that were proposed, involving either Gs or Gi coupling, remain controversial. To further investigate the role of G protein coupling in B3-AR induced proliferation, we stimulated primary human myometrial smooth muscle cells with SAR150640 (B3-AR agonist) in the absence or presence of variable G-protein inhibitors. Specific B3-AR stimulation led to an Erk1/2 induced proliferation. We observed that the proliferative effects of B3-AR require two Erk1/2 activation peaks (the first after 3 min, the second at 8 h). Erk1/2 activation at 3 min was mimicked by forskolin (adenylyl-cyclase a…

Beta-3 adrenergic receptorGs alpha subunitMAP Kinase Signaling SystemMyocytes Smooth MuscleProliferationG protein coupled receptorBiologyGTP-Binding Protein alpha Subunits Gi-GoPertussis toxinchemistry.chemical_compoundErk1/2Protein kinasesCyclinsReceptors Adrenergic betaGTP-Binding Protein alpha Subunits GsHumansMolecular BiologyPI3K/AKT/mTOR pathwayCells CulturedG protein-coupled receptorCell ProliferationForskolinColforsinBeta-3 adrenergic receptorCell BiologyCell biologychemistryGene Expression RegulationPertussis ToxinMyometriumFemaleSignal transductionProto-oncogene tyrosine-protein kinase SrcBiochimica et Biophysica Acta (BBA) - Molecular Cell Research
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HSP60 activity on human bronchial epithelial cells

2017

HSP60 has been implicated in chronic inflammatory disease pathogenesis, including chronic obstructive pulmonary disease (COPD), but the mechanisms by which this chaperonin would act are poorly understood. A number of studies suggest a role for extracellular HSP60, since it can be secreted from cells and bind Toll-like receptors; however, the effects of this stimulation have never been extensively studied. We investigated the effects (pro- or anti-inflammatory) of HSP60 in human bronchial epithelial cells (16-HBE) alone and in comparison with oxidative, inflammatory, or bacterial challenges. 16-HBE cells were cultured for 1–4 h in the absence or presence of HSP60, H2O2, lipopolysaccharide (…

0301 basic medicinep38αSettore BIO/17 - IstologiaLipopolysaccharidep38 mitogen-activated protein kinasesImmunologyStimulationBronchip38 Mitogen-Activated Protein KinasesERK1Cell LinePathogenesisMitochondrial Proteins03 medical and health scienceschemistry.chemical_compound0302 clinical medicineOriginal Research ArticlesHumansImmunology and AllergyCOPDInterleukin 8Protein kinase AReceptor16-HBE; COPD; CREB1; ERK1; HSP60; IL-10; IL-8; JNK1; MyD88; NF-κB p65 subunit; TLR-4; p38αPharmacologyIL-8Settore BIO/16 - Anatomia UmanaInterleukin-8JNK1NF-κB p65 subunitEpithelial CellsTLR-4Chaperonin 60MyD88Interleukin-1016-HBEToll-Like Receptor 416-HBE; COPD; CREB1; ERK1; HSP60; IL-10; IL-8; JNK1; MyD88; NF-κB p65 subunit; p38α; TLR-4; Immunology and Allergy; Immunology; PharmacologyInterleukin 10030104 developmental biologychemistry030220 oncology & carcinogenesisIL-10Cancer researchCREB1NF-κB p65 subunitHSP60p38α
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Regulation of the effects of CYP2E1-induced oxidative stress by JNK signaling

2014

The generation of excessive amounts of reactive oxygen species (ROS) leads to cellular oxidative stress that underlies a variety of forms of hepatocyte injury and death including that from alcohol. Although ROS can induce cell damage through direct effects on cellular macromolecules, the injurious effects of ROS are mediated largely through changes in signal transduction pathways such as the mitogen-activated protein kinase c-Jun N-terminal kinase (JNK). In response to alcohol, hepatocytes have increased levels of the enzyme cytochrome P450 2E1 (CYP2E1) which generates an oxidant stress that promotes the development of alcoholic steatosis and liver injury. These effects are mediated in larg…

Alcoholic liver diseaseClinical BiochemistryReview ArticleMitogen-activated protein kinase kinasemedicine.disease_causeBiochemistryCytochrome P450 2E10302 clinical medicineMolecular Targeted TherapyMitogen-activated protein kinaseslcsh:QH301-705.5c-Jun N-terminal kinasechemistry.chemical_classificationTNF tumor necrosis factorlcsh:R5-9200303 health sciencesCell DeathCYP2E1 cytochrome P450 2E1Cytochrome P-450 CYP2E13. Good healthCell biologyPKD protein kinase DLiverJNK c-Jun N-terminal kinaseSab SH3 homology associated BTK binding protein030211 gastroenterology & hepatologySignal transductionlcsh:Medicine (General)MAP Kinase Signaling SystemAPAP acetaminophenMKK MAPK kinaseBiology03 medical and health sciencesROS reactive oxygen speciesPKC protein kinase CmedicineAnimalsHumansMAPKKK MAPK kinase kinaseProtein kinase ACell damage030304 developmental biologyReactive oxygen speciesMAP kinase kinase kinaseOrganic ChemistryJNK Mitogen-Activated Protein KinasesAlcoholic liver diseasemedicine.diseaseERK1/2 extracellular signal-regulated kinase 1/2Fatty Liverlcsh:Biology (General)chemistryOxidative stressNAFLD nonalcoholic fatty liver diseaseReactive Oxygen SpeciesMAPK mitogen-activated protein kinaseOxidative stressRedox Biology
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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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The PDGFRβ/ERK1/2 pathway regulates CDCP1 expression in triple-negative breast cancer

2018

Background CDCP1, a transmembrane protein with tumor pro-metastatic activity, was recently identified as a prognostic marker in TNBC, the most aggressive breast cancer subtype still lacking an effective molecular targeted therapy. The mechanisms driving CDCP1 over-expression are not fully understood, although several stimuli derived from tumor microenvironment, such as factors present in Wound Healing Fluids (WHFs), reportedly increase CDCP1 levels. Methods The expression of CDCP1, PDGFRβ and ERK1/2cell was tested by Western blot after stimulation of MDA-MB-231 cells with PDGF-BB and, similarly, in presence or not of ERK1/2 inhibitor in a panel of TNBC cell lines. Knock-down of PDGFRβ was e…

0301 basic medicineCancer ResearchMAP Kinase Signaling SystemCDCP1medicine.medical_treatmentPDGFRβPDGF-BBBecaplerminTriple Negative Breast NeoplasmsBiologylcsh:RC254-282Targeted therapyReceptor Platelet-Derived Growth Factor beta03 medical and health sciences0302 clinical medicineFISHDownregulation and upregulationWestern blotAntigens CDAntigens NeoplasmCell Line TumorGeneticsmedicineHumansRNA Small InterferingReceptorTriple-negative breast cancerMitogen-Activated Protein Kinase 1Tumor microenvironmentMitogen-Activated Protein Kinase 3ERK1/2medicine.diagnostic_testMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensNeoplasm ProteinsUp-RegulationGene Expression Regulation Neoplastic030104 developmental biologyOncologyGene Knockdown Techniques030220 oncology & carcinogenesisCDCP1Cancer researchImmunohistochemistryFemaleCell Adhesion MoleculesTNBCResearch ArticleIHCBMC Cancer
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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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