Search results for "Gene Expression"

showing 10 items of 4085 documents

Postnatal alterations of the inhibitory synaptic responses recorded from cortical pyramidal neurons in the Lis1/sLis1 mutant mouse

2006

Mutations in the mouse Lis1 gene produce severe alterations in the developing cortex. We have examined some electrophysiological responses of cortical pyramidal neurons during the early postnatal development of Lis/sLis1 mutant mice. In P7 and P30 Lis1/sLis1 neurons we detected a lower frequency and slower decay phase of mIPSCs, and at P30 the mIPSCs amplitude and the action potential duration were reduced. Zolpidem (an agonist of GABAA receptors containing the alpha1 subunit) neither modified the amplitude nor the decay time of mIPSCs at P7 in Lis1/sLis1 neurons, whereas it increased the decay time at P30. The levels of GABAA receptor alpha1 subunit mRNA were reduced in the Lis1/sLis1 brai…

Agonistmedicine.medical_specialtyZolpidemPyridinesmedicine.drug_classAction PotentialsIn Vitro TechniquesBiologyInhibitory postsynaptic potentialMiceCellular and Molecular NeuroscienceInternal medicinemedicineAnimalsReceptorGABA AgonistsMolecular BiologyCerebral CortexReverse Transcriptase Polymerase Chain ReactionGABAA receptorPyramidal CellsAge FactorsGene Expression Regulation DevelopmentalCell BiologyElectric StimulationMice Mutant StrainsCortex (botany)ZolpidemElectrophysiologymedicine.anatomical_structureEndocrinologyAnimals NewbornInhibitory Postsynaptic Potentialsnervous systemCerebral cortex1-Alkyl-2-acetylglycerophosphocholine EsteraseMicrotubule-Associated Proteinsmedicine.drugMolecular and Cellular Neuroscience
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LXR antagonists induce ABCD2 expression

2014

X-linked adrenoleukodystrophy (X-ALD) is a rare neurodegenerative disorder characterized by the accumulation of very-long-chain fatty acids resulting from a beta-oxidation defect. Oxidative stress and inflammation are also key components of the pathogenesis. X-ALD is caused by mutations in the ABCDI gene, which encodes for a peroxisomal half ABC transporter predicted to participate in the entry of VLCFA-CoA into the peroxisome, the unique site of their beta-oxidation. Two homologous peroxisomal ABC transporters, ABCD2 and ABCD3 have been proven to compensate for ABCD1 deficiency when overexpressed. Pharmacological induction of these target genes could therefore represent an alternative ther…

Agonistx-ald;very-long-chain fatty acid;lxr;hydroxycholesterol;abcd2medicine.medical_specialtymedicine.drug_classx-aldEndogenyContext (language use)ATP-binding cassette transporterBiologyATP Binding Cassette Transporter Subfamily DInternal medicinemedicineHumanslxr[ SDV.BDD ] Life Sciences [q-bio]/Development BiologyhydroxycholesterolLiver X receptorAdrenoleukodystrophyMolecular Biology[SDV.BDD]Life Sciences [q-bio]/Development BiologyLiver X ReceptorsFatty AcidsBiologie du développementNeurosciencesCell BiologyHep G2 CellsPeroxisomemedicine.diseaseOrphan Nuclear ReceptorsDevelopment BiologyHydroxycholesterolsvery-long-chain fatty acidOxidative StressEndocrinologyGene Expression RegulationCell cultureabcd2Neurons and Cognition[ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Cancer researchlipids (amino acids peptides and proteins)AdrenoleukodystrophyATP-Binding Cassette Transporters[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]
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RNA2-encoded VP37 protein of Broad bean wilt virus 1 is a determinant of pathogenicity, host susceptibility, and a suppressor of post-transcriptional…

2020

Abstract Broad bean wilt virus 1 (BBWV‐1, genus Fabavirus, family Secoviridae) is a bipartite, single‐stranded positive‐sense RNA virus infecting many horticultural and ornamental crops worldwide. RNA1 encodes proteins involved in viral replication whereas RNA2 encodes two coat proteins (the large and small coat proteins) and two putative movement proteins (MPs) of different sizes with overlapping C‐terminal regions. In this work, we determined the role played by the small putative BBWV‐1 MP (VP37) on virus pathogenicity, host specificity, and suppression of post‐transcriptional gene silencing (PTGS). We engineered a BBWV‐1 35S‐driven full‐length cDNA infectious clone corresponding to BBWV‐…

AgroinfiltrationInfectious cloneDeterminant of pathogenicityvirusesdeterminant of pathogenicityGene ExpressionSoil ScienceNicotiana benthamianaPlant ScienceBBWV-1 determinant of pathogenicity Fabavirus infectious clone Secoviridae VSRBBWV‐1Host SpecificityBBWV-1VirusViral ProteinsBroad bean wilt virusSolanum lycopersicumTobaccoH20 Plant diseasesMolecular BiologyPlant DiseasesVirulencebiologySecoviridaeTurnip crinkle virusfungiinfectious cloneVSRfood and beveragesSettore AGR/12 - Patologia VegetaleRNA virusOriginal ArticlesDeteminant of Pathogenicitybiology.organism_classificationPotato virus XVirologyFabavirusVicia fabaRNA silencingSettore AGR/11 - Entomologia Generale E ApplicataRNA ViralOriginal ArticleRNA InterferenceCapsicumAgronomy and Crop Science
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Regulation of microRNAs and their role in liver development, regeneration and disease

2013

Abstract Since their discovery more than a decade ago microRNAs have been demonstrated to have profound effects on almost every aspect of biology. Numerous studies in recent years have shown that microRNAs have important roles in development and in the etiology and progression of disease. This review is focused on microRNAs and the roles they play in liver development, regeneration and liver disease; particularly chronic liver diseases such as alcoholic liver disease, non-alcoholic fatty liver disease, non-alcoholic steatohepatitis, viral hepatitis and primary liver cancer. The key microRNAs identified in liver development and chronic liver disease will be discussed together with, where pos…

Alcoholic liver diseaseLiver DiseasesFatty liverCell BiologyDiseaseBiologyBioinformaticsmedicine.diseaseChronic liver diseaseBiochemistryLiver RegenerationMicroRNAsLiver diseaseGene Expression RegulationLivermicroRNAmedicineAnimalsHumansSteatohepatitisViral hepatitisThe International Journal of Biochemistry & Cell Biology
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Aldehyde dehydrogenase and HSP90 co-localize in human glioblastoma biopsy cells.

2013

The concept of a stem cell subpopulation as understood from normal epithelial tissue or bone marrow function has been extended to our understanding of cancer tissue and is now the target of treatment efforts specifically directed to this subpopulation. In glioblastoma, as well as in other cancers, increased expression of aldehyde dehydrogenase (ALDH) has been found localized within a minority sub-population of tumor cells which demonstrate stem cell properties. A separate body of research associated increased expression of heat-shock protein-90 (HSP90) with stem cell attributes. We present here results from our initial immunohistochemistry study of human glioblastoma biopsy tissue where bot…

Aldehyde dehydrogenasePharmacologyBiochemistryAldehyde dehydrogenase; Disulfiram; Glioblastoma; HSP90; Ritonavir; Stem cell; TemozolomideCancer stem cellBiopsyDisulfirammedicineTemozolomideHSP90HumansHSP90 Heat-Shock ProteinsTemozolomideRitonavirStem cellmedicine.diagnostic_testbiologyCancerGeneral MedicineAldehyde Dehydrogenasemedicine.diseaseGene Expression Regulation NeoplasticProtein Transportmedicine.anatomical_structurebiology.proteinCancer researchImmunohistochemistryBone marrowStem cellGlioblastomamedicine.drugBiochimie
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Change in expression of MGMT during maturation of human monocytes into dendritic cells.

2005

Dendritic cells (DCs) maturated from monocytes play an important role in the immune system, not only in defense against conventional infections but also in cancer rejection. Because of the central role of DCs in tumor host defense it is highly important that DCs as well as the progenitor cell population are protected during cancer therapy. Since most anticancer drugs target DNA, the DNA repair capacity is most importance for the response of DCs and their precursor cells. Here, we studied the expression of the DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT) in monocytes obtained from peripheral blood of healthy donors and DCs maturated from monocytes (moDCs). We show that MG…

Alkylating AgentsDNA RepairDNA repairPopulationAntigens CD34ApoptosisBiologyBiochemistryMonocytesO(6)-Methylguanine-DNA MethyltransferaseImmune systemmedicineGene silencingHumansLymphocytesProgenitor celleducationPromoter Regions GeneticneoplasmsMolecular BiologyCells CulturedRegulation of gene expressioneducation.field_of_studyReverse Transcriptase Polymerase Chain ReactionMonocyteCell DifferentiationCell BiologyDendritic CellsDNA MethylationFlow Cytometrydigestive system diseasesmedicine.anatomical_structureImmunologyCytokinesStem cellDNA repair
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MGMT: Key node in the battle against genotoxicity, carcinogenicity and apoptosis induced by alkylating agents

2007

O(6)-methylguanine-DNA methyltransferase (MGMT) plays a crucial role in the defense against alkylating agents that generate, among other lesions, O(6)-alkylguanine in DNA (collectively termed O(6)-alkylating agents [O(6)AA]). The defense is highly important, since O(6)AA are common environmental carcinogens, are formed endogenously during normal cellular metabolism and possibly inflammation, and are being used in cancer therapy. O(6)AA induced DNA damage is subject to repair, which is executed by MGMT, AlkB homologous proteins (ABH) and base excision repair (BER). Although this review focuses on MGMT, the mechanism of repair by ABH and BER will also be discussed. Experimental systems, in wh…

Alkylating AgentsMethyltransferaseAlkylationDNA RepairDNA repairDNA damageGene ExpressionApoptosisIn Vitro TechniquesBiologyDNA Mismatch RepairModels BiologicalBiochemistryNecrosisO(6)-Methylguanine-DNA MethyltransferaseNeoplasmsAnimalsHumansDNA Modification MethylasesneoplasmsMolecular BiologyCarcinogenChromosome AberrationsGeneticsTumor Suppressor ProteinsO-6-methylguanine-DNA methyltransferaseDNACell BiologyBase excision repairdigestive system diseasesDNA Repair EnzymesMutationCancer researchDNA mismatch repairSister Chromatid ExchangeDNA DamageAlkyltransferaseDNA Repair
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Activation of c-Jun N-terminal kinase 1 by UV irradiation is inhibited by wortmannin without affecting c-iun expression.

1999

Activation of c-Jun N-terminal kinases (JNKs)/stress-activated protein kinases is an early response of cells upon exposure to DNA-damaging agents. JNK-mediated phosphorylation of c-Jun is currently understood to stimulate the transactivating potency of AP-1 (e.g., c-Jun/c-Fos; c-Jun/ATF-2), thereby increasing the expression of AP-1 target genes. Here we show that stimulation of JNK1 activity is not a general early response of cells exposed to genotoxic agents. Treatment of NIH 3T3 cells with UV light (UV-C) as well as with methyl methanesulfonate (MMS) caused activation of JNK1 and an increase in c-Jun protein and AP-1 binding activity, whereas antineoplastic drugs such as mafosfamide, mito…

Alkylating AgentsProto-Oncogene Proteins c-junUltraviolet RaysStimulationBiologyenvironment and public healthWortmanninTransactivationchemistry.chemical_compoundMiceAnimalsPhosphatidylinositolCollagenasesProtein kinase AMolecular BiologyCell Growth and DevelopmentMitogen-Activated Protein Kinase 1Kinasec-junJNK Mitogen-Activated Protein KinasesCell Biology3T3 CellsMethyl MethanesulfonateMolecular biologyAndrostadienesEnzyme ActivationGene Expression Regulation NeoplasticTranscription Factor AP-1chemistryCalcium-Calmodulin-Dependent Protein KinasesPhosphorylationMitogen-Activated Protein KinasesWortmanninMolecular and cellular biology
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Regulation of IgE production and airway reactivity by CD4(-)CD8(-) regulatory T cells

2015

The mechanisms of tolerance induction occurring in the course of allergen-specific immunotherapy have not been elucidated in full detail. Our study aimed to characterize high zone tolerance in mouse models of type I allergy and of allergic airway inflammation induced by subcutaneous sensitization of mice with high doses of the model allergen ovalbumin (OVA) without the use of adjuvant. Mice were immunized by subcutaneous injection of high doses (HD) of OVA or, for comparison, low doses (LD) of OVA in saline. HD-mice showed lower specific IgE, but augmented IgG in sera than LD-mice. Pre-treatment of mice with HD-OVA antigen-specifically inhibited IgE production subsequently induced by LD-OVA…

AllergyAdoptive cell transferAllergyOvalbuminImmunologyGene ExpressionCD4-CD8-double-negative T cellsLymphocyte ActivationImmunoglobulin EAirway hyperreactivityT-Lymphocytes RegulatoryImmunophenotypingMouse modelImmunomodulationMiceSubcutaneous injectionAntibody SpecificityT-Lymphocyte SubsetsRespiratory HypersensitivitymedicineAnimalsImmunology and AllergyAntigen doseSensitizationbiologymedicine.diagnostic_testbusiness.industryReceptors Antigen T-Cell gamma-deltaHematologyImmunoglobulin Erespiratory systemmedicine.diseaseAdoptive TransferTolerance inductionOvalbuminImmunoglobulin (Ig)EBronchoalveolar lavagemedicine.anatomical_structureAntibody FormationImmunologybiology.proteinCytokinesFemaleImmunizationbusinessBronchoalveolar Lavage Fluid
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Cellular stress induces cap-independent alpha-enolase/MBP-1 translation.

2015

AbstractMyc promoter-binding protein-1 (MBP-1) is a shorter protein variant of the glycolytic enzyme alpha-enolase. Although several lines of evidence indicate that MBP-1 acts as a tumor suppressor, the cellular mechanisms and signaling pathways underlying MBP-1 expression still remain largely elusive. To dissect these pathways, we used the SkBr3 breast cancer cell line and non-tumorigenic HEK293T cells ectopically overexpressing alpha-enolase/MBP-1. Here, we demonstrate that induced cell stresses promote MBP-1 expression through the AKT/PERK/eIF2α signaling axis. Our results contribute to shedding light on the molecular mechanisms underlying MBP-1 expression in non-tumorigenic and cancer c…

Alpha-enolaseCellEukaryotic Initiation Factor-2Alternative translationBiochemistryeIF-2 KinaseBreast cancerHEK293 CellStructural BiologyProtein IsoformsbiologyMedicine (all)Translation (biology)Recombinant ProteinEndoplasmic Reticulum StressRecombinant ProteinsNeoplasm ProteinsDNA-Binding ProteinsGene Expression Regulation Neoplasticmedicine.anatomical_structureFemaleSignal transductionMyc promoter-binding protein-1Breast NeoplasmHumanSignal TransductionCell SurvivalDNA-Binding ProteinRecombinant Fusion ProteinsBiophysicsBreast NeoplasmsNeoplasm ProteinGeneticCell Line TumorEndoplasmic reticulum streGeneticsmedicineBiomarkers TumorHumansGene SilencingMolecular BiologyProtein kinase BTumor Suppressor ProteinTumor Suppressor ProteinsHEK 293 cellsProtein IsoformCell BiologySettore BIO/18 - GeneticaHEK293 CellsBiophysicGene Expression RegulationPhosphopyruvate HydrataseCancer cellbiology.proteinUnfolded protein responseCancer researchProto-Oncogene Proteins c-aktRecombinant Fusion ProteinFEBS letters
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