Search results for "expression"

showing 10 items of 5168 documents

Transcription of genes in the biosynthetic pathway for fumonisin mycotoxins is epigenetically and differentially regulated in the fungal maize pathog…

2012

ABSTRACT When the fungal pathogen Gibberella moniliformis (anamorph, Fusarium verticillioides ) colonizes maize and maize-based products, it produces class B fumonisin (FB) mycotoxins, which are a significant threat to human and animal health. FB biosynthetic enzymes and accessory proteins are encoded by a set of clustered and cotranscribed genes collectively named FUM, whose molecular regulation is beginning to be unraveled by researchers. FB accumulation correlates with the amount of transcripts from the key FUM genes, FUM1 , FUM21 , and FUM8 . In fungi in general, gene expression is often partially controlled at the chromatin level in secondary metabolism; when this is the case, the deac…

DISRUPTIONTranscription GeneticFUM21[SDV]Life Sciences [q-bio]DIVERSITYPROTEINFusarium verticillioidesmaizeSECONDARY METABOLISMgene clusterEpigenesis GeneticHistonesFUM8FusariumGene Expression Regulation FungalASPERGILLUSPromoter Regions Genetic2. Zero hungerGenetics0303 health sciencesHistone deacetylase inhibitorhistone acetylationAcetylationArticlesGeneral MedicineChromatinChromatinGENOMEHistoneMultigene Family[SDE]Environmental SciencesTrichostatin AEpigenetics; Fusarium verticillioides; fmonisin synthesismedicine.drugCONIDIATIONChromatin Immunoprecipitationmedicine.drug_classGenes FungalChIPBiologyGFPZea maysMicrobiologyFumonisinsChromatin remodeling03 medical and health sciencesmedicineEpigeneticsMolecular Biology030304 developmental biologyepigenetics030306 microbiologyCLUSTERFumonisins; epigenetics; Fusarium verticillioides; maize; histone acetylation; histone deacetylases; ChIP; Trichostatin A; FUM1; FUM21; FUM8; GFP; gene clusterMycotoxinsChromatin Assembly and DisassemblyFUM1Histone Deacetylase InhibitorsTrichostatin AAcetylationbiology.proteinChromatin immunoprecipitationhistone deacetylases
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Corrigendum: Dissection of DLBCL microenvironment provides a gene expression-based predictor of survival applicable to formalin-fixed paraffin-embedd…

2019

The affiliations of authors T. Venesio and A. Sapino were originally incorrect. These have now been corrected as per the author listing above.

DLBCL microenvironment gene expression DLBCL
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A loop involving NRF2, miR‐29b‐1‐5p and AKT, regulates cell fate of MDA‐MB‐231 triple‐negative breast cancer cells

2019

The present study shows that nuclear factor erythroid 2-related factor 2 (NRF2) and miR-29b-1-5p are two opposite forces which could regulate the fate of MDA-MB-231 cells, the most studied triple-negative breast cancer (TNBC) cell line. We show that NRF2 activation stimulates cell growth and markedly reduces reactive oxygen species (ROS) generation, whereas miR-29b-1-5p overexpression increases ROS generation and reduces cell proliferation. Moreover, NRF2 downregulates miR-29b-1-5p expression, whereas miR-29b-1-5p overexpression decreases p-AKT and p-NRF2. Furthermore, miR-29b-1-5p overexpression induces both inhibition of DNA N-methyltransferases (DNMT1, DNMT3A, and DNMT3B) expression and …

DNA (Cytosine-5-)-Methyltransferase 10301 basic medicineNF-E2-Related Factor 2PhysiologyClinical BiochemistryTriple Negative Breast NeoplasmsAKT DNMTs miR‐29b‐1‐5p NRF2 parthenolide tumor suppressor genesCell fate determinationenvironment and public healthDNA Methyltransferase 3A03 medical and health scienceschemistry.chemical_compound0302 clinical medicineSettore BIO/10 - BiochimicaCell Line TumorCyclin D2HumansParthenolideDNA (Cytosine-5-)-MethyltransferasesProtein kinase BTriple-negative breast cancerCell Proliferationchemistry.chemical_classificationReactive oxygen speciesCell growthTumor Suppressor ProteinsCell BiologyDNA Methylationrespiratory systemCell biologyGene Expression Regulation NeoplasticMicroRNAs030104 developmental biologychemistryCell culture030220 oncology & carcinogenesisDNMT1FemaleReactive Oxygen SpeciesProto-Oncogene Proteins c-aktSesquiterpenesSignal TransductionJournal of Cellular Physiology
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Aneuploid IMR90 cells induced by depletion of pRB, DNMT1 and MAD2 show a common gene expression signature

2019

Chromosome segregation defects lead to aneuploidy which is a major feature of solid tumors. How diploid cells face chromosome mis-segregation and how aneuploidy is tolerated in tumor cells are not completely defined yet. Thus, an important goal of cancer genetics is to identify gene networks that underlie aneuploidy and are involved in its tolerance. To this aim, we induced aneuploidy in IMR90 human primary cells by depleting pRB, DNMT1 and MAD2 and analyzed their gene expression profiles by microarray analysis. Bioinformatic analysis revealed a common gene expression profile of IMR90 cells that became aneuploid. Gene Set Enrichment Analysis (GSEA) also revealed gene-sets/pathways that are …

DNA (Cytosine-5-)-Methyltransferase 1AneuploidyBiologyMicroarrayReal-Time Polymerase Chain ReactionRetinoblastoma ProteinCell LineRNA interferenceGene expressionProtein Interaction MappingGeneticsmedicineHumansGeneOligonucleotide Array Sequence AnalysisMicroarray analysis techniquesGene Expression ProfilingBioinformatics analysiChromosomeFibroblastsmedicine.diseaseAneuploidyGene Expression RegulationRNAiMad2 ProteinsDNMT1Cancer researchKIF4ARNA InterferenceTranscriptomeIMR90 human fibroblast
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Sex-specific windows for high mRNA expression of DNA methyltransferases 1 and 3A and methyl-CpG-binding domain proteins 2 and 4 in human fetal gonads

2006

DNA methyltransferases (DNMTs) and 5-methyl-CpG-binding domain proteins (MBDs) are involved in the acquisition of parent-specific epigenetic modifications in human male and female germ cells. Reverse Northern blot analyses demonstrated sex-specific differences in mRNA expression for the maintenance DNMT1 and the de novo DNMT3A in developing testis and ovary. In fetal testis DNMT1 and DNMT3A expression peaked in mitotically arrested spermatogonia around 21 weeks gestation. In fetal ovary transcriptional upregulation of DNMT1 and DNMT3A occurred during a very brief period at 16 weeks gestation, when the oocytes proceeded through meiotic prophase. Fetal gonads showed several fold higher DNMT3A…

DNA (Cytosine-5-)-Methyltransferase 1MaleMethyltransferaseEmbryonic DevelopmentGestational AgeOvaryBiologyGene Expression Regulation EnzymologicChromatin remodelingDNA Methyltransferase 3AFetal DevelopmentPregnancyTestisGeneticsmedicineHumansDNA (Cytosine-5-)-MethyltransferasesRNA MessengerEpigeneticsRegulation of gene expressionFetusReverse Transcriptase Polymerase Chain Reactionurogenital systemOvaryGene Expression Regulation DevelopmentalCell BiologyReverse northern blotMolecular biologyMethyl-CpG-binding domainCell biologyDNA-Binding Proteinsmedicine.anatomical_structureembryonic structuresFemaleTranscription FactorsDevelopmental BiologyMolecular Reproduction and Development
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Antitumor Effects of a Combined 5-Aza-2′Deoxycytidine and Valproic Acid Treatment on Rhabdomyosarcoma and Medulloblastoma in Ptch Mutant Mice

2009

Abstract Patched (Ptch) heterozygous mice develop medulloblastoma (MB) and rhabdomyosarcoma (RMS) resembling the corresponding human tumors. We have previously shown that epigenetic silencing of the intact Ptch allele contributes to tumor formation in this model. Here, we investigated whether targeting of epigenetic silencing mechanisms could be useful in the treatment of Ptch-associated cancers. A reduction of endogenous DNA methyltransferase1 (Dnmt1) activity significantly reduced tumor incidence in heterozygous Ptch knockout mice. A combined treatment with the Dnmt inhibitor 5-aza-2′deoxycytidine (5-aza-dC) and the histone deacetlyase (HDAC) inhibitor valproic acid (VPA) efficiently prev…

DNA (Cytosine-5-)-Methyltransferase 1Patched ReceptorsPatchedCancer Researchmedicine.drug_classGene ExpressionDecitabineReceptors Cell SurfaceBiologyDecitabineHistone DeacetylasesHistonesMice03 medical and health sciences0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsRhabdomyosarcomamedicineAnimalsDNA (Cytosine-5-)-MethyltransferasesGene SilencingMuscle SkeletalRhabdomyosarcoma030304 developmental biologyMedulloblastomaMice Inbred BALB C0303 health sciencesValproic AcidHistone deacetylase inhibitorCancerAcetylationDNA Methylationmedicine.disease3. Good healthHistone Deacetylase InhibitorsMice Inbred C57BLPatched-1 Receptorstomatognathic diseasesOncology030220 oncology & carcinogenesisAzacitidineCancer researchDNMT1Epigenetic therapyMedulloblastomamedicine.drugCancer Research
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APE/Ref-1 and the mammalian response to genotoxic stress.

2003

Human apurinic/apyrimidinic endonuclease/redox factor-1 (hAPE/Ref-1) is a multifunctional protein involved in the repair of DNA damaged by oxidative or alkylating compounds as well as in the regulation of stress inducible transcription factors such as AP-1, NF-kappaB, HIF-1 and p53. With respect to transcriptional regulation, both redox dependent and independent mechanisms have been described. APE/Ref-1 also acts as a transcriptional repressor. Recent data indicate that APE/Ref-1 negatively regulates the activity of the Ras-related GTPase Rac1. How these different physiological activities of APE/Ref-1 are coordinated is poorly understood. So far, convincing evidence is available that the ex…

DNA RepairDNA repairRAC1Genotoxic StressTransfectionBiologyToxicologymedicine.disease_causeMolecular biologyCell biologyCell killingDNA Repair EnzymesGene Expression RegulationNeoplasmsmedicineTranscriptional regulationDNA-(Apurinic or Apyrimidinic Site) LyaseAnimalsHumansAmino Acid SequenceTranscription factorOxidative stressMutagensToxicology
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Cockayne syndrome: varied requirement of transcription-coupled nucleotide excision repair for the removal of three structurally different adducts fro…

2014

Hereditary defects in the transcription-coupled nucleotide excision repair (TC-NER) pathway of damaged DNA cause severe neurodegenerative disease Cockayne syndrome (CS), however the origin and chemical nature of the underlying DNA damage had remained unknown. To find out, to which degree the structural properties of DNA lesions determine the extent of transcription arrest in human CS cells, we performed quantitative host cell reactivation analyses of expression vectors containing various synthetic adducts. We found that a single 3-(deoxyguanosin-N 2-yl)-2-acetylaminofluorene adduct (dG(N 2)-AAF) constitutes an unsurmountable obstacle to transcription in both CS-A and CS-B cells and is remov…

DNA RepairTranscription GeneticGenetic ToxicologyDNA damagelcsh:MedicineBiologyToxicologyHost-Cell ReactivationBiochemistryCockayne syndromeCell LineDNA Adductschemistry.chemical_compoundGenes ReporterTranscription (biology)Nucleic AcidsMolecular Cell BiologyGene expressionmedicineHumansGene SilencingCockayne SyndromePoly-ADP-Ribose Binding Proteinslcsh:ScienceFluorenesMultidisciplinaryBiology and life sciencesOligonucleotidelcsh:RDNA HelicasesDeoxyguanosineDNACell Biologymedicine.diseaseMolecular biologyDNA Repair EnzymesGene Expression RegulationchemistryBiochemistrylcsh:QDNAResearch ArticleNucleotide excision repairPLoS ONE
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Excision of Uracil from Transcribed DNA Negatively Affects Gene Expression

2014

Uracil is an unavoidable aberrant base in DNA, the repair of which takes place by a highly efficient base excision repair mechanism. The removal of uracil from the genome requires a succession of intermediate products, including an abasic site and a single strand break, before the original DNA structure can be reconstituted. These repair intermediates are harmful for DNA replication and also interfere with transcription under cell-free conditions. However, their relevance for cellular transcription has not been proved. Here we investigated the influence of uracil incorporated into a reporter vector on gene expression in human cells. The expression constructs contained a single uracil opposi…

DNA RepairTranscription GeneticGreen Fluorescent ProteinsGene ExpressionDNA and ChromosomesBiologyBiochemistryCell LineDNA Glycosylaseschemistry.chemical_compoundGenes ReporterActivation-induced (cytidine) deaminaseHumansheterocyclic compoundsProtein–DNA interactionAP siteUracilUracil-DNA GlycosidaseMolecular BiologyUracilDNACell BiologyBase excision repairMolecular biologyThymine DNA GlycosylasechemistryDNA glycosylaseGene Knockdown TechniquesUracil-DNA glycosylasebiology.proteinHeLa CellsNucleotide excision repairJournal of Biological Chemistry
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c-Fos is required for excision repair of UV-light induced DNA lesions by triggering the re-synthesis of XPF

2006

Cells deficient in c-Fos are hypersensitive to ultraviolet (UV-C) light. Here we demonstrate that mouse embryonic fibroblasts lacking c-Fos (fos-/-) are defective in the repair of UV-C induced DNA lesions. They show a decreased rate of sealing of repair-mediated DNA strand breaks and are unable to remove cyclobutane pyrimidine dimers from DNA. A search for genes responsible for the DNA repair defect revealed that upon UV-C treatment the level of xpf and xpg mRNA declined but, in contrast to the wild type (wt), did not recover in fos-/- cells. The observed decline in xpf and xpg mRNA is due to impaired re-synthesis, as shown by experiments using actinomycin D. Block of xpf transcription resu…

DNA RepairUltraviolet RaysDNA repairDNA damageRNA StabilityGene ExpressionPyrimidine dimerBiologyCell LineMicechemistry.chemical_compoundTranscription (biology)Gene expressionGeneticsAnimalsDNA Breaks Single-StrandedRNA MessengerMolecular BiologyTranscription factorMice KnockoutGenetic Complementation TestGenes fosNuclear ProteinsDNAEndonucleasesMolecular biologyDNA-Binding ProteinsTranscription Factor AP-1chemistryPyrimidine DimersDNADNA DamageTranscription FactorsNucleotide excision repairNucleic Acids Research
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