Search results for "RNA-BINDING PROTEINS"

showing 10 items of 149 documents

Quaking and miR-155 interactions in inflammation and leukemogenesis.

2015

Quaking (QKI) is a tumor-suppressor gene encoding a conserved RNA-binding protein, whose expression is downregulated in several solid tumors. Here we report that QKI plays an important role in the immune response and suppression of leukemogenesis. We show that the expression of Qki is reduced in lipopolysaccharide (LPS)-challenged macrophages, suggesting that Qki is a key regulator of LPS signaling pathway. Furthermore, LPS-induced downregulation of Qki expression is miR-155-dependent. Qki overexpression impairs LPS-induced phosphorylation of JNK and particularly p38 MAPKs, in addition to increasing the production of anti-inflammatory cytokine IL-10. In contrast, Qki ablation decreases Fas …

LipopolysaccharidesTime Factorsmedicine.medical_treatmentmedicine.disease_causeTransgenicMiceInnatePhosphorylationChronicB-LymphocytesLeukemiaRNA-Binding ProteinsU937 CellsLymphocyticCell biologyCytokineOncologyPhosphorylationCytokinesCLL; Glioblastoma; Inflammation; MiR-155; QKI; Animals; Apoptosis Regulatory Proteins; B-Lymphocytes; Case-Control Studies; Cytokines; Humans; Immunity Innate; Inflammation; Leukemia Lymphocytic Chronic B-Cell; Lipopolysaccharides; Macrophages; Mice; Mice Transgenic; MicroRNAs; Mitogen-Activated Protein Kinases; Phosphorylation; RAW 264.7 Cells; RNA-Binding Proteins; Signal Transduction; Time Factors; Transfection; U937 Cells; OncologySignal transductionMitogen-Activated Protein KinasesSignal Transductionp38 mitogen-activated protein kinasesOncology and CarcinogenesisMice TransgenicTransfectionNOmiR-155miR-155Downregulation and upregulationmicroRNAmedicineAnimalsHumansInflammationQKIbusiness.industryMacrophagesB-CellImmunityglioblastomaLeukemia Lymphocytic Chronic B-CellImmunity InnateMicroRNAsRAW 264.7 CellsCase-Control StudiesImmunologyCarcinogenesisbusinessApoptosis Regulatory ProteinsCLLPriority Research Paper
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pp32/PHAPI determines the apoptosis response of non-small-cell lung cancer

2007

During malignant transformation, cancer cells have to evade cell-intrinsic tumor suppressor mechanisms including apoptosis, thus acquiring a phenotype that is relatively resistant to clinically applied anticancer therapies. Molecular characterization of apoptotic signal transduction defects may help to identify prognostic markers and to develop novel therapeutic strategies. To this end we have undertaken functional analyses of drug-induced apoptosis in human non-small cell-lung cancer (NSCLC) cells. We found that primary drug resistance correlated with defects in apoptosome-dependent caspase activation in vitro. While cytochrome c-induced apoptosome formation was maintained, the subsequent …

Lung NeoplasmsTransplantation HeterologousAntineoplastic AgentsApoptosisMice SCIDBiologyMalignant transformationMiceProstate cancerIn vivoCarcinoma Non-Small-Cell LungmedicineAnimalsHumansLung cancerMolecular BiologyIntracellular Signaling Peptides and ProteinsNuclear ProteinsRNA-Binding ProteinsCancerCell Biologymedicine.diseaseCell biologyEnzyme ActivationApoptosisCaspasesCancer cellCancer researchSignal transductionNeoplasm TransplantationCell Death & Differentiation
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Caspase-8 prevents sustained activation of NF-kappaB in monocytes undergoing macrophagic differentiation.

2006

Abstract Caspases have demonstrated several nonapoptotic functions including a role in the differentiation of specific cell types. Here, we show that caspase-8 is the upstream enzyme in the proteolytic caspase cascade whose activation is required for the differentiation of peripheral-blood monocytes into macrophages. On macrophage colony-stimulating factor (M-CSF) exposure, caspase-8 associates with the adaptor protein Fas-associated death domain (FADD), the serine/threonine kinase receptor-interacting protein 1 (RIP1) and the long isoform of FLICE-inhibitory protein FLIP. Overexpression of FADD accelerates the differentiation process that does not involve any death receptor. Active caspase…

Macrophage colony-stimulating factorCellular differentiationFas-Associated Death Domain ProteinImmunologyCaspase 8BiochemistryMonocytesArticle03 medical and health sciences0302 clinical medicineCell Line TumormedicineHumansFADDCaspase030304 developmental biologyDeath domain0303 health sciencesCaspase 8biologyMonocyteMacrophage Colony-Stimulating FactorMacrophagesNF-kappa BSignal transducing adaptor proteinRNA-Binding ProteinsCell DifferentiationCell BiologyHematologyMolecular biologyNuclear Pore Complex Proteinsmedicine.anatomical_structure030220 oncology & carcinogenesisbiology.proteinBlood
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Transient structural ordering of the RNA-binding domain of carnation mottle virus p7 movement protein modulates nucleic acid binding.

2005

Plant viral movement proteins bind to RNA and participate in the intra- and intercellular movement of the RNAs from plant viruses. However, the role and magnitude of the conformational changes associated with the formation of RNA-protein complexes are not yet defined. Here we describe studies on the relevance of a preexisting nascent alpha-helix at the C terminus of the RNA-binding domain of p7, a movement protein from carnation mottle virus, to RNA binding. Synthetic peptide analogues and single amino acid mutation at the RNA-binding domain of recombinant p7 protein were used to correlate the transient structural order in aqueous solution with RNA-binding potential.

Magnetic Resonance SpectroscopyMolecular Sequence DataBiochemistryViral ProteinsPlant virusAmino Acid SequenceBinding siteMovement proteinMolecular BiologyBinding SitesbiologyC-terminusOrganic ChemistryRNARNA-Binding Proteinsbiology.organism_classificationRecombinant ProteinsProtein Structure TertiarySpectrometry FluorescenceBiochemistryCarnation mottle virusMutationNucleic acidMolecular MedicineRNAPeptidesBinding domainChembiochem : a European journal of chemical biology
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Protective effects of mirtazapine in mice lacking the Mbnl2 gene in forebrain glutamatergic neurons: Relevance for myotonic dystrophy 1

2019

Myotonic dystrophy type 1 (DM1) is a multisystemic disorder characterized by muscle weakness and wasting and by important central nervous system-related symptoms including impairments in executive functions, spatial abilities and increased anxiety and depression. The Mbnl2 gene has been implicated in several phenotypes consistent with DM1 neuropathology. In this study, we developed a tissue-specific knockout mouse model lacking the Mbnl2 gene in forebrain glutamatergic neurons to examine its specific contribution to the neurobiological perturbations related to DM1. We found that these mice exhibit long-term cognitive deficits and a depressive-like state associated with neuronal loss, increa…

Male0301 basic medicineMirtazapineGlutamic AcidHippocampusMice TransgenicMirtazapineMyotonic dystrophyAnimals Genetically ModifiedMice03 medical and health sciencesCellular and Molecular NeuroscienceGlutamatergicProsencephalon0302 clinical medicinemedicineAnimalsMyotonic DystrophyDentate gyrusInflammationMice KnockoutNeuronsPharmacologyDepressionbusiness.industryCognitive deficitsDentate gyrusNeurogenesisRNA-Binding Proteinsmedicine.disease3. Good healthMice Inbred C57BLNeuroprotective Agents030104 developmental biologynervous systemKnockout mouseForebrainNeuronal lossDrosophilaFemaleDM1businessNeuroscience030217 neurology & neurosurgerymedicine.drugNeuropharmacology
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Mutations in the Matrin 3 gene cause familial amyotrophic lateral sclerosis.

2013

MATR3 is an RNA- and DNA-binding protein that interacts with TDP-43, a disease protein linked to amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. Using exome sequencing, we identified mutations in MATR3 in ALS kindreds. We also observed MATR3 pathology in ALS-affected spinal cords with and without MATR3 mutations. Our data provide more evidence supporting the role of aberrant RNA processing in motor neuron degeneration. © 2014 Nature America, Inc. All rights reserved.

MaleAged Aged; 80 and over Amyotrophic Lateral Sclerosis; genetics/pathology Computational Biology DNA Mutational Analysis DNA-Binding Proteins; metabolism Family Health Female Genetic Predisposition to Disease; genetics Genotype Humans Male Middle Aged Muscle; Skeletal; metabolism/pathology Mutation; genetics Neurologic Examination Nuclear Matrix-Associated Proteins; genetics/metabolism RNA-Binding Proteins; genetics/metabolism Spinal Cord; metabolism/pathologyDNA Mutational Analysisgenetics/metabolismRNA-binding proteinSettore MED/03 - GENETICA MEDICAmedicine.disease_cause0302 clinical medicineNuclear Matrix-Associated ProteinsGenotype80 and overgeneticsAmyotrophic lateral sclerosisExome sequencingGeneticsAged 80 and overNeurologic Examination0303 health sciencesMutationGeneral NeuroscienceRNA-Binding ProteinsSkeletalMiddle AgedDNA-Binding ProteinsMATR3medicine.anatomical_structureSpinal Cordfamilial amyotrophic lateral sclerosisMuscleSettore MED/26 - NeurologiaFemaleFrontotemporal dementiametabolism/pathologyGenotypeArticle03 medical and health sciencesgenetics; familial amyotrophic lateral sclerosismental disordersmedicineHumansGenetic Predisposition to DiseaseMuscle Skeletal030304 developmental biologyAgedFamily Healthbusiness.industryAmyotrophic Lateral Sclerosisgenetics/pathologyRNAComputational BiologySpinal cordmedicine.diseaseMutationgeneticbusinessNeurosciencemetabolism030217 neurology & neurosurgery
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The ISWI chromatin remodeler organizes the hsrω ncRNA-containing omega speckle nuclear compartments.

2011

The complexity in composition and function of the eukaryotic nucleus is achieved through its organization in specialized nuclear compartments. The Drosophila chromatin remodeling ATPase ISWI plays evolutionarily conserved roles in chromatin organization. Interestingly, ISWI genetically interacts with the hsrω gene, encoding multiple non-coding RNAs (ncRNA) essential, among other functions, for the assembly and organization of the omega speckles. The nucleoplasmic omega speckles play important functions in RNA metabolism, in normal and stressed cells, by regulating availability of hnRNPs and some other RNA processing proteins. Chromatin remodelers, as well as nuclear speckles and their assoc…

MaleCancer ResearchRNA Untranslatedlcsh:QH426-470Gene ExpressionFluorescent Antibody TechniqueRNA-binding proteinBiologyEyeHeterogeneous ribonucleoprotein particleChromosomesHeterogeneous-Nuclear RibonucleoproteinsChromatin remodelingMolecular GeneticsGeneticsmedicineAnimalsDrosophila ProteinsOmega speckleBiologyMolecular BiologyTranscription factorAllelesGenetics (clinical)Ecology Evolution Behavior and SystematicsAdenosine TriphosphatasesCell NucleusGeneticsRNA-Binding ProteinsEpistasis GeneticChromatin Assembly and DisassemblyNon-coding RNAChromatinCell biologyCell nucleuslcsh:GeneticsPhenotypemedicine.anatomical_structureTandem Repeat SequencesChromatin remodeling non coding RNALarvaEpigeneticsDrosophilaRNA InterferenceResearch ArticleTranscription FactorsPLoS Genetics
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The genomic and clinical landscape of fetal akinesia

2020

International audience; Fetal akinesia has multiple clinical subtypes with over 160 gene associations, but the genetic etiology is not yet completely understood.Methods: In this study, 51 patients from 47 unrelated families were analyzed using next-generation sequencing (NGS) techniques aiming to decipher the genomic landscape of fetal akinesia (FA).Results: We have identified likely pathogenic gene variants in 37 cases and report 41 novel variants. Additionally, we report putative pathogenic variants in eight cases including nine novel variants. Our work identified 14 novel disease-gene associations for fetal akinesia: ADSSL1, ASAH1, ASPM, ATP2B3, EARS2, FBLN1, PRG4, PRICKLE1, ROR2, SETBP1…

MaleCandidate geneMyopathyVARIANTSFetal akinesiaMESH: Ryanodine Receptor Calcium Release Channel0302 clinical medicineMESH: ChildGuanine Nucleotide Exchange FactorsMESH: Guanine Nucleotide Exchange FactorsExomeCopy-number variationChildExomeMESH: High-Throughput Nucleotide SequencingGenetics (clinical)GeneticsArthrogryposisArthrogryposis0303 health sciencesMESH: Infant NewbornMESH: Genetic Predisposition to DiseaseHigh-Throughput Nucleotide SequencingRNA-Binding ProteinsMESH: Infant3. Good healthFetal DiseasesCopy-number variationMESH: Fetal DiseasesMESH: Young AdultChild PreschoolASAH1FemaleMESH: DNA Copy Number Variationsmedicine.symptomAdultGENETICSAdolescentDNA Copy Number VariationsMESH: Trans-ActivatorsMESH: ArthrogryposisBiologyASPMYoung Adult03 medical and health sciencesMuscular DiseasesmedicineHumansGenetic Predisposition to DiseaseGene030304 developmental biologyMESH: Adolescent[SDV.MHEP.PED]Life Sciences [q-bio]/Human health and pathology/PediatricsMESH: HumansMUTATIONSMESH: Child PreschoolInfant NewbornMESH: Muscular DiseasesInfantNEMALINE MYOPATHYRyanodine Receptor Calcium Release ChannelMESH: Adultmedicine.diseaseCongenital myopathyMESH: MaleMESH: RNA-Binding Proteins[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsDISTAL ARTHROGRYPOSISTrans-ActivatorsMESH: Female030217 neurology & neurosurgery
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Knockout of the KH-Type Splicing Regulatory Protein Drives Glomerulonephritis in MRL-Faslpr Mice

2021

KH-type splicing regulatory protein (KSRP) is an RNA-binding protein that promotes mRNA decay and thereby negatively regulates cytokine expression at the post-transcriptional level. Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by dysregulated cytokine expression causing multiple organ manifestations

MaleChemokineMice Inbred MRL lprQH301-705.5medicine.medical_treatmentLupus nephritisBiologyKidneyArticleImmune systemsystemic lupus erythematosusimmune system diseasesmedicinecytokineAnimalsCD11a AntigenRNA MessengerKSRPBiology (General)skin and connective tissue diseasesRegulation of gene expressionMice KnockoutSystemic lupus erythematosusFOXP3RNA-Binding ProteinsGlomerulonephritisGeneral Medicinemedicine.diseaseMice Inbred C57BLCytokineCancer researchbiology.proteinTrans-ActivatorsFemaleLymph NodesChemokinesBiomarkersglomerulonephritispost-transcriptional regulationCells
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Mitochondrial biogenesis fails in secondary biliary cirrhosis in rats leading to mitochondrial DNA depletion and deletions

2011

Chronic cholestasis is characterizedby mitochondrial dysfunction, associated with loss of mitochondrialmembrane potential, decreased activities of respiratory chaincomplexes, and ATP production. Our aim was to determine themolecular mechanisms that link long-term cholestasis to mitochondrialdysfunction. We studied a model of chronic cholestasis inducedby bile duct ligation in rats. Key sensors and regulators of theenergetic state and mitochondrial biogenesis, mitochondrial DNA(mtDNA)-to-nuclear DNA (nDNA) ratio (mtDNA/nDNA) relativecopy number, mtDNA deletions, and indexes of apoptosis (BAX,BCL-2, and cleaved caspase 3) and cell proliferation (PCNA) wereevaluated. Our results show that long…

MaleMitochondrial DNAPhysiologyMitochondrial TurnoverMitochondrial HepatopathyNF-E2-Related Factor 1Respiratory chainMitochondria LiverProtein Serine-Threonine KinasesMitochondrionBiologyDNA MitochondrialSirtuin 1CholestasisProliferating Cell Nuclear AntigenPhysiology (medical)medicineAnimalsRats Wistarbcl-2-Associated X ProteinCholestasisHepatologyCaspase 3Liver Cirrhosis BiliaryGastroenterologyPyruvate Dehydrogenase Acetyl-Transferring KinaseRNA-Binding ProteinsTFAMmedicine.diseaseGA-Binding Protein Transcription FactorPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMolecular biologyRatsGenes MitochondrialProto-Oncogene Proteins c-bcl-2Mitochondrial biogenesisChronic DiseaseBile DuctsGene DeletionTranscription FactorsAmerican Journal of Physiology-Gastrointestinal and Liver Physiology
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