Search results for "ras GTPase-Activating Proteins"

showing 3 items of 3 documents

Cigarette smoke affects the onco-suppressor DAB2IP expression in bronchial epithelial cells of COPD patients

2019

AbstractCigarette smoke is a risk factor for COPD and lung cancer. In cancer, epigenetic modifications affect the expression of Enhancer of Zester Homolog 2 (EZH2), and silenced disabled homolog 2 interacting protein gene (DAB2IP) (onco-suppressor gene) by Histone H3 tri-methylation in lysine 27 (H3K27me3). In“ex vivo”studies, we assessed EZH2, H3K27me3 and DAB2IP immunoreactivity in bronchial epithelial cells from COPD patients (smokers, ex-smokers), Smoker and control subjects. In“in vitro” experiments we studied the effect of cigarette smoke extract (CSE) on EZH2/H3K27me3/DAB2IP expression, apoptosis, invasiveness, and vimentin expression in 16HBE, primary cells, and lung cancer cell lin…

Jumonji Domain-Containing Histone DemethylasesLung NeoplasmsCigar SmokingCelllcsh:MedicineApoptosismacromolecular substancesArticlePulmonary Disease Chronic ObstructiveRisk FactorsmedicineHumansEnhancer of Zeste Homolog 2 ProteinNeoplasm Invasivenesslcsh:ScienceLung cancerA549 CellOncogenesisInflammationA549 cellRegulation of gene expressionCOPDMultidisciplinarybusiness.industrylcsh:REZH2ApoptosiJumonji Domain-Containing Histone DemethylaseCancerras GTPase-Activating Proteinmedicine.diseaseAlveolar Epithelial Cellrespiratory tract diseasesLung NeoplasmGene Expression Regulation NeoplasticNeoplasm Invasiveness Pulmonary Disease Chronic Obstructivemedicine.anatomical_structureA549 Cellsras GTPase-Activating ProteinsApoptosisAlveolar Epithelial CellsCancer researchlcsh:QbusinessHumanairway disease
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Htid-1, the human homolog of the Drosophila melanogaster l(2)tid tumor suppressor, defines a novel physiological role of APC.

2007

Htid-1, the human counterpart of the Drosophila tumor suppressor gene lethal(2)tumorous imaginal discs (l(2)tid) encodes three splice forms translated into three cytosolic - Tid50, Tid48 and Tid46 - and three mitochondrial - Tid43, Tid40 and Tid38 - proteins. Here we provide evidence for the association of the endogenous Tid50/Tid48 proteins with the adenomatous polyposis coli (APC) tumor suppressor in normal colon epithelium, colorectal cancer cells and mouse NIH3T3 fibroblasts. Using the Glutathione S-transferase binding assay we show that the N-terminal region including the Armadillo domain (ARM) of APC is sufficient to bind the Tid molecules. Using immunoprecipitation and confocal micro…

Patched ReceptorsBeta-cateninTumor suppressor geneAdenomatous polyposis coliAdenomatous Polyposis Coli ProteinReceptors Cell SurfacePlasma protein bindingLigandsMitochondrial ProteinsMiceCytosolCell Line TumorAnimalsDrosophila ProteinsGuanine Nucleotide Exchange FactorsHumansIntestinal MucosaActinHeat-Shock Proteinsbeta CateninPatched ReceptorsbiologySequence Homology Amino AcidGene Expression ProfilingTumor Suppressor ProteinsWnt signaling pathwayGene Expression Regulation DevelopmentalCell BiologyHSP40 Heat-Shock ProteinsActin cytoskeletonMolecular biologyCell biologyMitochondriaDrosophila melanogasterras GTPase-Activating ProteinsMultiprotein Complexesbiology.proteinNIH 3T3 CellsRho Guanine Nucleotide Exchange FactorsProtein BindingCellular signalling
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HMG-CoA reductase inhibitors (statins) as anticancer drugs (Review)

2005

Apart from their lipid lowering activity, HMG-CoA reductase inhibitors (statins) impair numerous cellular functions associated with metastasis, e.g. gene expression, angiogenesis, cell adhesion, cell motility and invasiveness. Furthermore, statins have impact on apoptotic cell death and modulate cellular susceptibility to cell killing by anticancer drugs and ionizing radiation. Part of the effects provoked by statins are due to the inhibition of the prenylation of low molecular weight GTPases, in particular Ras and Rho, which play key roles in signaling evoked by stimulation of cell surface receptors. C-terminal lipid modification of Ras/Rho GTPases is essential for their correct intracellu…

rho GTP-Binding ProteinsCancer ResearchCell DeathbiologyCell growthGTPaseCell killingOncologyBiochemistryPrenylationras GTPase-Activating ProteinsNeoplasmsRadiation IonizingHMG-CoA reductaseCell AdhesionCancer researchbiology.proteinHumansProtein prenylationHydroxymethylglutaryl-CoA Reductase InhibitorsNeoplasm MetastasisLipid modificationCell adhesionCell ProliferationInternational Journal of Oncology
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