Search results for "Mitogen-Activated Protein Kinase"

showing 10 items of 353 documents

Unjamming overcomes kinetic and proliferation arrest in terminally differentiated cells and promotes collective motility of carcinoma.

2019

During wound repair, branching morphogenesis and carcinoma dissemination, cellular rearrangements are fostered by a solid-to-liquid transition, known as unjamming. The biomolecular machinery behind unjamming and its pathophysiological relevance remain, however, unclear. Here, we study unjamming in a variety of normal and tumorigenic epithelial two-dimensional (2D) and 3D collectives. Biologically, the increased level of the small GTPase RAB5A sparks unjamming by promoting non-clathrin-dependent internalization of epidermal growth factor receptor that leads to hyperactivation of the kinase ERK1/2 and phosphorylation of the actin nucleator WAVE2. This cascade triggers collective motility effe…

EndosomeCellular differentiationmedia_common.quotation_subjectMotility02 engineering and technologySettore MED/08 - Anatomia Patologica010402 general chemistry01 natural sciencesExtracellular matrixCell MovementCell Line TumorHumansGeneral Materials ScienceSmall GTPaseEpidermal growth factor receptorInternalizationActinmedia_commonCell Proliferationrab5 GTP-Binding ProteinsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3biologyChemistryMechanical EngineeringCell DifferentiationGeneral Chemistry021001 nanoscience & nanotechnologyCondensed Matter Physics0104 chemical sciencesCell biologyErbB ReceptorsKineticscarcinoma differentiated neoplastic cellsMechanics of Materialsbiology.protein0210 nano-technologyNature materials
researchProduct

Influence ofKi-ras-driven oncogenic transformation on the protein network of murine fibroblasts

2007

Ki-ras gene mutations that specifically occur in codons 12, 13 and 61 are involved in the carcinogenesis of acute myeloid leukemia, melanoma and different carcinomas. In order to define potential mutation-specific therapeutic targets, stable transfectants of NIH3T3 cells carrying different Ki-ras4B gene mutations were generated. Wild type Ki-ras transformants, mock transfectants and parental cells served as controls. These in vitro model systems were systematically analyzed for their protein expression pattern using two-dimensional gel electrophoresis followed by mass spectrometry and/or protein sequencing. Using this approach, a number of target molecules that are differentially but coordi…

Gel electrophoresismedicine.diagnostic_testWild typeFibroblastsBiologyGene mutationTransfectionmedicine.disease_causeProteomicsBiochemistryMolecular biologyMiceCell Transformation NeoplasticWestern blotHeat shock proteinNIH 3T3 Cellsras ProteinsmedicineAnimalsMitogen-Activated Protein KinasesCarcinogenesisMolecular BiologyGeneSignal TransductionPROTEOMICS
researchProduct

Akt induces enhanced myocardial contractility and cell size in vivo in transgenic mice

2002

The serine-threonine kinase Akt seems to be central in mediating stimuli from different classes of receptors. In fact, both IGF-1 and IL6-like cytokines induce hypertrophic and antiapoptotic signals in cardiomyocytes through PI3K-dependent Akt activation. More recently, it was shown that Akt is involved also in the hypertrophic and antiapoptotic effects of β-adrenergic stimulation. Thus, to determine the effects of Akt on cardiac function in vivo, we generated a model of cardiac-specific Akt overexpression in mice. Transgenic mice were generated by using the E40K, constitutively active mutant of Akt linked to the rat α-myosin heavy chain promoter. The effects of cardiac-selective Akt overex…

Gene ExpressionTransgenicGlycogen Synthase Kinase 3MiceGSK-3Receptorsgenetics/physiologycytology/metabolismMultidisciplinaryBiological SciencesProtein-Serine-Threonine KinasesDNA-Binding Proteinsenzymology/genetics/pathologyAdrenergicPhosphorylationSignal transductionMitogen-Activated Protein KinasesSignal Transductionmedicine.medical_specialtyCardiomyopathyAnimals; Calcium-Calmodulin-Dependent Protein Kinases; metabolism; Cardiomyopathy; Hypertrophic; enzymology/genetics/pathology; Cell Size; physiology; DNA-Binding Proteins; GATA4 Transcription Factor; Gene Expression; Glycogen Synthase Kinase 3; Mice; Transgenic; Mitogen-Activated Protein Kinases; Myocardial Contraction; Myocardium; cytology/metabolism; Point Mutation; Protein-Serine-Threonine Kinases; Proto-Oncogene Proteins c-akt; Proto-Oncogene Proteins; genetics/physiology; Rats; Receptors; Adrenergic; beta; Signal Transduction; Transcription FactorsMice TransgenicBiologyProtein Serine-Threonine KinasesContractilityIn vivoInternal medicineProto-Oncogene ProteinsReceptors Adrenergic betamedicineAnimalsPoint MutationGlycogen synthaseProtein kinase BPI3K/AKT/mTOR pathwayCell SizeMyocardiumCardiomyopathy HypertrophicMyocardial ContractionGATA4 Transcription FactorRatsEndocrinologyHypertrophicphysiologyCalcium-Calmodulin-Dependent Protein Kinasesbiology.proteinbetametabolismProto-Oncogene Proteins c-aktTranscription Factors
researchProduct

Role of Gadd45a in Wip1-dependent regulation of intestinal tumorigenesis.

2012

Conversion of intestinal stem cells into tumor-initiating cells is an early step in Apc(Min)-induced polyposis. Wild-type p53-induced phosphatase 1 (Wip1)-dependent activation of a DNA damage response and p53 has a permanent role in suppression of stem cell conversion, and deletion of Wip1 lowers the tumor burden in Apc(Min) mice. Here we show that cyclin-dependent kinase inhibitor 2a, checkpoint kinase 2, and growth arrest and DNA damage gene 45a (Gadd45a) exert critical functions in the tumor-resistant phenotype of Wip1-deficient mice. We further identified Gadd45a as a haploinsufficient gene in the regulation of Wip1-dependent tumor resistance in mice. Gadd45a appears to function through…

Genes APCDNA RepairDNA repairDNA damageApoptosisCell Cycle ProteinsBiologyProtein Serine-Threonine KinasesReceptors G-Protein-CoupledMicePhosphoprotein PhosphatasesGene silencingAnimalsMolecular BiologyCheckpoint Kinase 2Cyclin-Dependent Kinase Inhibitor p16beta CateninMice KnockoutOriginal PaperKinaseIntestinal PolyposisStem CellsJNK Mitogen-Activated Protein KinasesNuclear ProteinsCell BiologyCell biologyProtein Phosphatase 2CCheckpoint Kinase 2Cell Transformation NeoplasticCancer researchSignal transductionStem cellTumor Suppressor Protein p53GADD45ASignal TransductionCell death and differentiation
researchProduct

Aβ and tau toxicities in Alzheimer’s are linked via oxidative stress-induced p38 activation: Protective role of vitamin E

2014

AbstractOxidative stress is a hallmark of Alzheimer’s disease (AD). We propose that rather than causing damage because of the action of free radicals, oxidative stress deranges signaling pathways leading to tau hyperphosphorylation, a hallmark of the disease. Indeed, incubation of neurons in culture with 5 µM beta-amyloid peptide (Aβ) causes an activation of p38 MAPK (p38) that leads to tau hyperphosphorylation. Inhibition of p38 prevents Aβ-induced tau phosphorylation. Aβ-induced effects are prevented when neurons are co-incubated with trolox (the water-soluble analog of vitamin E).We have confirmed these results in vivo, in APP/PS1 double transgenic mice of AD. We have found that APP/PS1 …

Genetically modified mouseMalemedicine.medical_specialtyCell signalingAntioxidantP-p38p38 mitogen-activated protein kinasesmedicine.medical_treatmentClinical BiochemistryMice Transgenictau ProteinsBiologyBeta-amyloidmedicine.disease_causeProtective AgentsBiochemistryHippocampusp38 Mitogen-Activated Protein KinasesArticlechemistry.chemical_compoundMiceAlzheimer DiseaseInternal medicinemental disordersmedicineVitamin EAnimalsPhosphorylationlcsh:QH301-705.5Cells CulturedNeuronslcsh:R5-920Amyloid beta-PeptidesVitamin EOrganic Chemistrymedicine.diseaseRatsDisease Models AnimalOxidative StressEndocrinologylcsh:Biology (General)chemistryTroloxAlzheimer's diseaseAntioxidantlcsh:Medicine (General)Oxidative stressRedox Biology
researchProduct

Combination of the novel farnesyltransferase inhibitor RPR130401 and the geranylgeranyltransferase-1 inhibitor GGTI-298 disrupts MAP kinase activatio…

1999

To test the Kirsten-Ras (Ki-Ras) alternative prenylation hypothesis in malignant transformation, we used a novel farnesyltransferase inhibitor competitive to farnesyl-pyrophosphate, RPR130401, and a CaaX peptidomimetic geranylgeranyltransferase-1 inhibitor GGTI-298. In Ki-Ras-overexpressing transformed adrenocortical cells, RPR130401 at 1-10 microM inhibited very efficiently the [(3)H]farnesyl but not [(3)H]geranylgeranyl transfer to Ras. However, proliferation of these cells was only slightly sensitive to RPR130401 (IC(50)=30 microM). GGTI-298 inhibited the growth of these cells with an IC(50) of 11 microM but cell lysis was observed at 15 microM. The combination of 10 microM RPR130401 and…

GeranylgeranyltransferaseFarnesyltransferaseSimvastatinIndolesTime FactorsFarnesyltransferaseBiophysicsProtein PrenylationAntineoplastic AgentsKirsten-RasBiochemistryAnti-proliferative effectS PhasePrenylationStructural BiologyAlternative pathwayAdrenal GlandsGeneticsAnimalsFarnesyltranstransferaseLovastatinBinding siteEnzyme InhibitorsMolecular BiologyCells CulturedCell Line TransformedPrenylationAlkyl and Aryl TransferasesbiologyDose-Response Relationship DrugCell growthFarnesyltransferase inhibitorG1 PhaseG1/S transitionDrug SynergismCell BiologyCell cycleFlow CytometryCell biologyRatsGenes rasBiochemistryMitogen-activated protein kinaseBenzamidesbiology.proteinras ProteinsMitogen-Activated Protein KinasesCell DivisionFEBS letters
researchProduct

Effect of hypoosmotic stress by low salinity acclimation of Mediterranean mussels Mytilus galloprovincialis on biological parameters used for polluti…

2008

In the present study, we investigated the progressive acclimation of the mussel Mytilus galloprovincialis to different reduced seawater (SW) salinities and its effect on several biochemical markers and biotests. Mussels were purchased from a local mariculture facility during summer (SW temperature 27 degrees C, salinity 37.5 psu) and winter (13 degrees C, 37 psu) seasons, and transferred to the laboratory for acclimation to reduced SW salinities (37, 28, 18.5 and 11 psu). At the beginning and at the end of acclimation processes tests of mussel survival in air were provided. After 14 days of acclimation the DNA integrity, p38-MAPK activation, metallothionein induction, oxygen consumption rat…

GillGillsSalinityanimal structuresHealth Toxicology and MutagenesisMuscle ProteinsAquatic ScienceAcclimatizationp38 Mitogen-Activated Protein KinasesCondition indexAnimal scienceOxygen ConsumptionOsmotic PressureAnimalsMaricultureFluorometrySeawaterPhosphorylationMytilusPrincipal Component AnalysisbiologyEcologyfungiMusselMytilus galloprovincialis; biomarkers; salinity; temperature; environmental condition variations; hypoosmotic stressbiology.organism_classificationBivalviaMytilusSalinityElectrophoresis Polyacrylamide GelMetallothioneinSeasonsDNA DamageEnvironmental Monitoring
researchProduct

Specific stress-induced storage of trehalose, glycerol and D-arabitol in response to oxidative and osmotic stress in Candida albicans.

2012

Candida albicans exponential yeast cells are able to face environmental challenges by mounting a rapid and efficient "general stress response". Here we show that one of the main components of this response consists of the intracellular protective accumulation of the non-reducing disaccharide trehalose and two polyols, glycerol and D-arabitol, an accumulation that occurs in a stress-specific dependent manner. Thus, oxidative exposures promoted a marked increase in both trehalose and D-arabitol in the wild type strain, RM-100, whereas the glycerol content remained virtually unaffected with respect to basal levels. In contrast, osmotic challenges induced the significant storage of glycerol acc…

GlycerolOsmotic shockBiophysicsOxidative phosphorylationBiologyBiochemistrychemistry.chemical_compoundSugar AlcoholsOsmotic PressureCandida albicansGlycerolCandida albicansMolecular BiologyTrehaloseCell Biologybiology.organism_classificationTrehaloseYeastOxidative StresschemistryBiochemistryMitogen-activated protein kinasebiology.proteinMitogen-Activated Protein KinasesOxidation-ReductionIntracellularBiochemical and biophysical research communications
researchProduct

Apoptosis induced by (E)-5-(2-bromovinyl)-2'-deoxyuridine in varicella zoster virus thymidine kinase-expressing cells is driven by activation of c-Ju…

2003

The molecular mode of cell killing by the antiviral drug (E)-5-(2-bromovinyl-2'-deoxyuridine (BVDU) was studied in Chinese hamster ovary (CHO) cells stably transfected with the thymidine kinase gene (tk) of varicella zoster virus (CHO-VZVtk). The colony-forming ability of the cells was reduced to <1% at a concentration of approximately 1 microM BVDU, whereas for nontransfected cells or cells transfected with tk gene of herpes simplex virus type 1 (CHO-HSVtk), a 1000-fold higher dose was required to achieve the same response. BVDU inhibited thymidylate synthase in CHO-VZVtk but not in CHO-HSVtk and control cells. On the other hand, the drug was incorporated into DNA of VZVtk- and HSVtk-expre…

Herpesvirus 3 HumanFas Ligand ProteinFas-Associated Death Domain ProteinApoptosisCHO CellsBiologyTransfectionAntiviral AgentsThymidine KinaseFas ligandchemistry.chemical_compoundNecrosisCricetinaeCytotoxic T cellAnimalsSimplexvirusAdaptor Proteins Signal TransducingPharmacologyCaspase 8GenomeMembrane GlycoproteinsChinese hamster ovary cellCell CycleJNK Mitogen-Activated Protein KinasesTransfectionDNAThymidylate SynthaseMolecular biologyCaspase 9Transcription Factor AP-1Cell killingchemistryBromodeoxyuridineApoptosisThymidine kinaseCaspasesMolecular MedicineMitogen-Activated Protein KinasesCarrier ProteinsBromodeoxyuridineMolecular pharmacology
researchProduct

Atypical Phacomatosis Pigmentokeratotica as the Expression of a Mosaic RASopathy With the BRAF-Glu586Lys Mutation

2016

Histologybusiness.industryDermatologyMitogen-activated protein kinase kinaseRASopathymedicine.diseaseMolecular biologyPathology and Forensic MedicinePhacomatosis pigmentokeratoticaProto-Oncogene Proteins B-raf030207 dermatology & venereal diseases03 medical and health sciences0302 clinical medicine030220 oncology & carcinogenesisMutation (genetic algorithm)medicinebusinessActas Dermo-Sifiliográficas (English Edition)
researchProduct