Search results for "knockdown"

showing 10 items of 178 documents

Targeting Aberrant Ncam (neural cell adhesion molecule; CD56) Expression in Acute Myeloid Leukemia

2015

Abstract Background Acute myeloid leukemia (AML) is a heterogeneous disease of the hematopoietic progenitor cell driven by the subsequent acquisition of genetic alterations. Approximately 20% of AML patients show strong expression of CD56 (neural cell adhesion molecule; NCAM). Expression of NCAM is associated with poor overall survival; however, the functional role of aberrant NCAM expression has not been investigated to date. The goal of this study is to examine the biological role of NCAM in AML and to explore whether NCAM represents a potential therapeutic target. Results In order to evaluate the clinical significance of elevated NCAM expression in AML, we screened a panel of human cell …

Gene knockdownChemistryCell growthImmunologyCellMyeloid leukemiaCell BiologyHematologymedicine.diseaseBiochemistryLeukemiamedicine.anatomical_structurenervous systemCell cultureCancer researchmedicineNeural cell adhesion moleculeK562 cellsBlood
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Expression Of FLT3-ITD Dysregulates The DBC1-Sirt1-p53 Signaling and Promotes Therapy Resistance

2013

Abstract Background SIRT1 is a NAD+ dependent histone deacetylase, which has been shown to act as an important regulator of apoptosis, DNA-repair and is involved in the maintenance of genetic integrity under conditions of cellular stress. Beside deacetylation of histones H4K16, SIRT1 has numeral other substrates including KU70, FOXO1 or p53. SIRT1 deacetylates p53 at lysine 382 thereby reducing its transcriptional activity followed by loss of p53 dependent apoptosis in response to cell damage. The activity of SIRT1 is negatively regulated by DBC1 (Deleted in Breast Cancer 1) and involves protein–protein interaction (Kim et al., Nature 2008). Recent reports have demonstrated increased expres…

Gene knockdownImmunologyMyeloid leukemiaCell BiologyHematologyBiologyBiochemistryMolecular biologychemistry.chemical_compoundchemistryhemic and lymphatic diseasesCancer cellCancer researchMidostaurinStem cellSignal transductionKinase activityTyrosine kinaseBlood
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Hsp70 is required for optimal cell proliferation in mouse A6 mesoangioblast stem cells.

2009

Mouse Hsp70 (70 kDa heat shock protein) is preferentially induced by heat or stress stimuli. We previously found that Hsp70 is constitutively expressed in A6 mouse mesoangioblast stem cells, but its possible role in these cells and the control of its basal transcription remained unexplored. Here we report that in the absence of stress, Ku factor is able to bind the HSE (heat shock element) consensus sequence in vitro, and in vivo it is bound to the proximal hsp70 promoter. In addition, we show that constitutive hsp70 transcription depends on the co-operative interaction of different factors such as Sp1 (specificity protein 1) and GAGA-binding protein with Ku factor, which binds the HSE cons…

Gene knockdownMesoangioblastBinding SitesGeneral transcription factorCell growthStem CellsCell BiologyBiologyFlow CytometryBiochemistryMolecular biologyHsp70MiceTranscription (biology)Heat shock proteinAnimalsBlood VesselsHSP70 Heat-Shock ProteinsRNA InterferenceStem cellmesoangioblast RNAi doubling timePromoter Regions GeneticMolecular BiologyCell ProliferationTranscription FactorsThe Biochemical journal
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BRAF mutation influences hypoxia-inducible factor-1α expression levels in papillary thyroid cancer

2010

Hypoxia-inducible factor-1α is found frequently overexpressed in solid tumors cells, exerting an important role in angiogenesis, glucose metabolism, cell proliferation, survival and invasion. In thyroid carcinomas, hypoxia-inducible factor-1α expression was found increased in differentiated, poorly differentiated, medullary and anaplastic variants. Hypoxia represents the principal stimulus responsible for hypoxia-inducible factor-1α induction. Other nonhypoxic stimuli increase hypoxia-inducible factor-1α synthesis through the activation of phosphatidylinositol 3-kinase and mitogen-activated protein kinase pathways in a cell-type-specific manner. We have previously shown the role of BRAFV600…

Gene knockdownPathologymedicine.medical_specialtyMutationCell growthAngiogenesisBiologymedicine.diseasemedicine.disease_causePathology and Forensic MedicinePapillary thyroid cancerThyroid carcinomaCancer researchmedicineSignal transductionPAX8Modern Pathology
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The Evolutionary Conserved Transmembrane BAX Inhibitor Motif (TMBIM) Containing Protein Family Members 5 and 6 Are Essential for the Development and …

2021

Frontiers in cell and developmental biology 9, 666484 (2021). doi:10.3389/fcell.2021.666484 special issue: "Cell Death and Survival / You-Wen He, Speciality Chief Editor; Craig Michael Walsh, Speciality Chief Editor; Arm Ruhul Amin, Associate Editor; Gustavo P. Amarante-Mendes, Associate Editor"

Gene knockdowncalciumProtein familylifeguardQH301-705.5Cell BiologyBiologyMitochondrionbiology.organism_classificationTransmembrane proteinGHITMCell biologymitochondriaMICS1RNA interferenceGRINAUnfolded protein responseDrosophila melanogasterBiology (General)ER stressDevelopmental Biology
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MUC4 overexpression correlates corticoid resistance in chronic rhinosinusitis with nasal polyps

2015

Background: Some patients with chronic rhinosinusitis with nasal polyps (CRSwNP) are resistant to corticoids. Mucin 4 (MUC4) is a membrane anchored protein with a nuclear translocation domain which is modulated by corticoids. Because glucocorticoid receptor (GR) nuclear translocation is key to the anti-inflammatory effect of corticoids, we hypothesized that MUC4 is involved in the effectiveness of these drugs Objective: To analyze the role of MUC4 in corticoid effectiveness in different cohorts of patients with CRSwNP and elucidate the possible mechanisms involved Methods: 73 patients with CRSwNP took oral corticoids for 15 days. Corticoid resistance was evaluated by nasal endoscopy. The ex…

Gene knockdownmedicine.medical_specialtybusiness.industryMucinmedicine.diseaseBlotGlucocorticoid receptorEndocrinologyDownregulation and upregulationInternal medicineImmunologymedicineImmunohistochemistryNasal polypssense organsbusinessDexamethasonemedicine.drug5.1 Airway Pharmacology and Treatment
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Polycystin-1 downregulation induces ERK-dependent mTOR pathway activation in a cellular model of psoriasis

2018

Psoriatic plaques tend to localize to the knees and elbows, areas that are particularly subject to mechanical stress resulting from bending and friction. Moreover, plaques often develop at sites of mechanical trauma or injury (Koebner phenomenon). Nevertheless, mechanotransduction has never been linked to psoriasis. Polycystins (polycystin-1, PC1; polycystin-2, PC2) are mechanosensitive molecules that function as key regulators of cellular mechanosensitivity and mechanotransduction. The aim of this in vitro study was to investigate the role of polycystins in the development of psoriasis. We showed that PC1 knockdown in HaCaT cells led to an elevated mRNA expression of psoriasis-related biom…

Genetic Markers0301 basic medicineMAPK/ERK pathwayendocrine systemTRPP Cation ChannelsMAP Kinase Signaling SystemDown-RegulationModels BiologicalCell Line03 medical and health sciences0302 clinical medicineDownregulation and upregulationCell MovementPsoriasismedicineHumansPsoriasisMechanotransductionMolecular BiologyPI3K/AKT/mTOR pathwayCell ProliferationGene knockdownCell growthChemistryTOR Serine-Threonine Kinasesmedicine.diseaseCell biologyHaCaT030104 developmental biologyGene Knockdown Techniques030220 oncology & carcinogenesisMolecular MedicineBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
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Identification of ELF3 as an early transcriptional regulator of human urothelium

2014

AbstractDespite major advances in high-throughput and computational modelling techniques, understanding of the mechanisms regulating tissue specification and differentiation in higher eukaryotes, particularly man, remains limited. Microarray technology has been explored exhaustively in recent years and several standard approaches have been established to analyse the resultant datasets on a genome-wide scale. Gene expression time series offer a valuable opportunity to define temporal hierarchies and gain insight into the regulatory relationships of biological processes. However, unless datasets are exactly synchronous, time points cannot be compared directly.Here we present a data-driven ana…

Hepatocyte Nuclear Factor 3-alphaTime seriesTime FactorsPPARγMicroarrayNormal Human UrotheliumComputational biologyBiologyReal-Time Polymerase Chain ReactionBioinformaticsProto-Oncogene ProteinsGene expressionElectric ImpedanceTranscriptional regulationHumansRNA Small InterferingGeneTranscription factorMolecular BiologyDNA PrimersGene knockdownProto-Oncogene Proteins c-etsReverse Transcriptase Polymerase Chain ReactionMicroarray analysis techniquesGene Expression Regulation DevelopmentalCell DifferentiationCell BiologyMicroarray AnalysisImmunohistochemistryELF3DNA-Binding ProteinsDifferentiationGene Knockdown TechniquesGene chip analysisGene expressionUrotheliumTranscription FactorsDevelopmental BiologyDevelopmental Biology
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Mutant p53 gain of function can be at the root of dedifferentiation of human osteosarcoma MG63 cells into 3AB-OS cancer stem cells

2014

Osteosarcoma is a highly metastatic tumor affecting adolescents, for which there is no second-line chemotherapy. As suggested for most tumors, its capability to overgrow is probably driven by cancer stem cells (CSCs), and finding new targets to kill CSCs may be critical for improving patient survival. TP53 is the most frequently mutated tumor suppressor gene in cancers and mutant p53 protein (mutp53) can acquire gain of function (GOF) strongly contributing to malignancy. Studies thus far have not shown p53-GOF in osteosarcoma. Here, we investigated TP53 gene status/role in 3AB-OS cells-a highly aggressive CSC line previously selected from human osteosarcoma MG63 cells-to evaluate its involv…

HistologyTumor suppressor genePhysiologyEndocrinology Diabetes and MetabolismApoptosisIn situ hybridizationBiologyTNF-Related Apoptosis-Inducing LigandCell MovementCancer stem cellCell Line TumorSettore BIO/10 - BiochimicaBiomarkers TumormedicineHumansNeoplasm Invasiveness3AB-OS cells CSCs Cancer cell dedifferentiation Cancer stem cells FISH Fluorescent in situ hybridization GOF Gain of function Human osteosarcoma MMPs Matrix metalloproteinases Mutant p53 Mutant p53 gain of function Mutp53 OS OsteosarcomaClonogenic assayTumor Stem Cell AssayCell ProliferationMembrane Potential MitochondrialOsteosarcomaCancerReceptors Death DomainCell DedifferentiationCell cyclemedicine.diseaseMolecular biologyAmino Acid SubstitutionProto-Oncogene Proteins c-bcl-2Gene Knockdown TechniquesMutationNeoplastic Stem CellsCancer researchOsteosarcomaEctopic expressionTumor Suppressor Protein p53Bone
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AAV Vector–mediated RNAi of Mutant Huntingtin Expression Is Neuroprotective in a Novel Genetic Rat Model of Huntington's Disease

2008

We report the characterization of a new rapid-onset model of Huntington's disease (HD) generated by adeno-associated virus (AAV) vector–mediated gene transfer of N-terminal huntingtin (htt) constructs into the rat striatum. Expression of exon 1 of mutant htt containing 70 CAG repeats rapidly led to neuropathological features associated with HD. In addition, we report novel data relating to neuronal transduction of AAV vectors that modulated the phenotype observed in this model. Quantitative reverse transcriptase–polymerase chain reaction (RT–PCR) revealed that AAV vector–mediated expression in the striatum increased by >100-fold as compared to the endogenous htt level. Moreover, AAV vectors…

HuntingtinvirusesGenetic VectorsNerve Tissue ProteinsSubstantia nigraBiologyArticleViral vectorHuntington's diseaseRNA interferenceDrug DiscoverymedicineHuntingtin ProteinGeneticsAnimalsHumansMolecular BiologyNeuronsPharmacologyHuntingtin ProteinGene knockdownReverse Transcriptase Polymerase Chain ReactionNeurodegenerationNuclear ProteinsExonsGenetic TherapyDependovirusmedicine.diseaseMolecular biologyCorpus StriatumRatsHuntington DiseaseNeuroprotective AgentsPhenotypenervous systemMolecular MedicineRNA InterferenceMolecular Therapy
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