Search results for "GENI"

showing 10 items of 6843 documents

rbFOX1/MBNL1 competition for CCUG RNA repeats binding contributes to myotonic dystrophy type 1/type 2 differences

2018

Myotonic dystrophy type 1 and type 2 (DM1, DM2) are caused by expansions of CTG and CCTG repeats, respectively. RNAs containing expanded CUG or CCUG repeats interfere with the metabolism of other RNAs through titration of the Muscleblind-like (MBNL) RNA binding proteins. DM2 follows a more favorable clinical course than DM1, suggesting that specific modifiers may modulate DM severity. Here, we report that the rbFOX1 RNA binding protein binds to expanded CCUG RNA repeats, but not to expanded CUG RNA repeats. Interestingly, rbFOX1 competes with MBNL1 for binding to CCUG expanded repeats and overexpression of rbFOX1 partly releases MBNL1 from sequestration within CCUG RNA foci in DM2 muscle ce…

0301 basic medicineModels MolecularProtein Conformation alpha-Helical[SDV]Life Sciences [q-bio]General Physics and AstronomyGene ExpressionRNA-binding proteinCrystallography X-Raychemistry.chemical_compoundMOLECULAR-BASISGene expressionMBNL1Myotonic DystrophyComputingMilieux_MISCELLANEOUSMultidisciplinaryCHLORIDE CHANNELQRNA-Binding ProteinsRecombinant Proteins3. Good healthCell biologyCONGENITAL HEART-DISEASEDrosophila melanogasterThermodynamicsSKELETAL-MUSCLERNA Splicing FactorsCUG REPEATSProtein BindingRNA Splicing Factorsmusculoskeletal diseasesSTEADY-STATEcongenital hereditary and neonatal diseases and abnormalitiesScienceRBFOX1BiologyMyotonic dystrophyBinding CompetitiveGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesmedicineEscherichia coliAnimalsHumansProtein Interaction Domains and MotifsBinding siteNucleotide MotifsMuscle SkeletalSPLICING REGULATOR RBFOX2MUSCLEBLIND PROTEINSBinding SitesPRE-MESSENGER-RNARNAGeneral Chemistrymedicine.diseaseDisease Models AnimalKinetics030104 developmental biologychemistryTRIPLET REPEATRNAProtein Conformation beta-Strand3111 Biomedicine
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Immunmodulatory and Antiproliferative Properties of Rhodiola Species.

2016

The traditional medicines of Asia and Europe have long used various Rhodiola species, which are endemic to the subarctic areas of the northern hemisphere, as tonic, adaptogen, antidepressant, and anti-inflammatory drugs. In order to establish the therapeutic uses of these plants in modern medicine, the pharmacological effects of Rhodiola sp. have been widely studied. Indeed, the most amply researched species, Rhodiola rosea, has been shown to possess antioxidant, adaptogenic, antistress, antimicrobial, immunomodulatory, angiomodulatory, and antitumoral effects. Salidroside (p-hydroxyphenethyl-β-D-glucoside), a major compound in Rhodiola, seems to be responsible for many of the effects obser…

0301 basic medicineModern medicineRhodiola algidaImmunologic Factorsmedicine.medical_treatmentPharmaceutical SciencePharmacologyAnalytical Chemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineGlucosidesPhenolsSpecies SpecificityDrug DiscoveryAdaptogenRhodiolamedicineAnimalsHumansImmunologic FactorsRhodiola crenulataCell ProliferationPharmacologybiologyTraditional medicinePlant ExtractsOrganic ChemistrySalidrosidebiology.organism_classificationAntineoplastic Agents Phytogenic030104 developmental biologyRhodiola roseaComplementary and alternative medicinechemistry030220 oncology & carcinogenesisMolecular MedicineRhodiolaPlanta medica
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In silico discovery of substituted pyrido[2,3-d]pyrimidines and pentamidine-like compounds with biological activity in myotonic dystrophy models

2016

Myotonic dystrophy type 1 (DM1) is a rare multisystemic disorder associated with an expansion of CUG repeats in mutant DMPK (dystrophia myotonica protein kinase) transcripts; the main effect of these expansions is the induction of pre-mRNA splicing defects by sequestering muscleblind-like family proteins (e.g. MBNL1). Disruption of the CUG repeats and the MBNL1 protein complex has been established as the best therapeutic approach for DM1, hence two main strategies have been proposed: targeted degradation of mutant DMPK transcripts and the development of CUG-binding molecules that prevent MBNL1 sequestration. Herein, suitable CUG-binding small molecules were selected using in silico approach…

0301 basic medicineMolecular biologyPhysiologyMutantMyotonic dystrophyDruggabilitylcsh:Medicine01 natural sciencesBiochemistryPhysical ChemistryMyoblastschemistry.chemical_compoundAnabolic AgentsMedicaments--InteraccióAnimal CellsDrug DiscoveryMedicine and Health SciencesMBNL1Drosophila ProteinsMyotonic Dystrophylcsh:ScienceRNA structureConnective Tissue CellsMultidisciplinaryMolecular StructureOrganic CompoundsStem CellsPhysicsRNA-Binding ProteinsBiological activityPhenotypeClimbingMolecular Docking SimulationNucleic acidsChemistryDrosophila melanogasterBiochemistryGenetic DiseasesConnective TissueRNA splicingPhysical SciencesCellular TypesAnatomyLocomotion57 - BiologiaSignal TransductionResearch ArticleBiotechnologyHydrogen bondingcongenital hereditary and neonatal diseases and abnormalitiesIn silicoPrimary Cell CultureComputational biologyBiology010402 general chemistryMyotonic dystrophyMyotonin-Protein KinaseDrug interactionsSmall Molecule Libraries03 medical and health sciencesStructure-Activity RelationshipmedicineAnimalsHumansRNA MessengerEnllaços d'hidrogenClinical GeneticsChemical PhysicsBiology and life sciencesChemical BondingBiological Locomotionlcsh:ROrganic ChemistryEstructura molecularChemical CompoundsHydrogen BondingCell BiologyFibroblastsmedicine.disease0104 chemical sciencesBenzamidinesAlternative SplicingDisease Models AnimalMacromolecular structure analysis030104 developmental biologyPyrimidinesBiological TissuechemistrySmall MoleculesRNAlcsh:QTrinucleotide Repeat ExpansionMolecular structure
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Inhibition of human monoamine oxidase A and B by flavonoids isolated from two Algerian medicinal plants

2017

Abstract Background Monoamine oxidases (MAOs) are outer mitochondrial membrane flavoenzymes. They catalyze the oxidative deamination of a variety of neurotransmitters. MAO-A and MAO-B may be considered as targets for inhibitors to treat neurodegenerative diseases and depression and for managing symptoms associated with Parkinson's and Alzheimer's diseases. Purpose The objective was to evaluate the inhibitory effect of Hypericum afrum and Cytisus villosus against MAO-A and B and to isolate the compounds responsible for the MAO-inhibitory activity. Methods The inhibitory effect of extracts and purified constituents of H. afrum and C. villosus were investigated in vitro using recombinant human…

0301 basic medicineMonoamine Oxidase InhibitorsMonoamine oxidaseDrug Evaluation PreclinicalPharmaceutical ScienceGenisteinMixed inhibitionArticleMass SpectrometryInhibitory Concentration 5003 medical and health scienceschemistry.chemical_compoundDrug DiscoveryHumansChrysinMonoamine OxidaseIC50CytisusFlavonoidsPharmacologyPlants MedicinalMolecular Docking Simulation030104 developmental biologyComplementary and alternative medicinechemistryBiochemistryDocking (molecular)AlgeriaMolecular MedicineQuercetinMyricetinQuercetinHypericumPhytomedicine
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Murine cytomegalovirus (CMV) infection via the intranasal route offers a robust model of immunity upon mucosal CMV infection

2016

Cytomegalovirus (CMV) is a ubiquitous virus, causing the most common congenital infection in humans, yet a vaccine against this virus is not available. Experimental studies of immunity against CMV in animal models of infection, such as the infection of mice with mouse CMV (MCMV), have relied mainly on parenteral infection protocols, although the virus naturally transmits by mucosal routes via body fluids. To characterize the biology of infections by mucosal routes, we compared the kinetics of virus replication, latent viral load and CD8 T-cell responses in lymphoid organs upon experimental intranasal (targeting the respiratory tract) and intragastric (targeting the digestive tract) infectio…

0301 basic medicineMuromegalovirusMice 129 StrainCongenital cytomegalovirus infectionSpleenCD8-Positive T-LymphocytesBiologyVirus ReplicationVirus03 medical and health sciencesImmunityVirologyVirus latencymedicineAnimalsImmunity MucosalMice Inbred BALB CAnimal StructuresViral Loadmedicine.diseaseVirologyVirus Latency030104 developmental biologymedicine.anatomical_structureLymphatic systemViral replicationModels AnimalImmunologyFemaleViral load
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The shared frameshift mutation landscape of microsatellite-unstable cancers suggests immunoediting during tumor evolution

2020

The immune system can recognize and attack cancer cells, especially those with a high load of mutation-induced neoantigens. Such neoantigens are abundant in DNA mismatch repair (MMR)-deficient, microsatellite-unstable (MSI) cancers. MMR deficiency leads to insertion/deletion (indel) mutations at coding microsatellites (cMS) and to neoantigen-inducing translational frameshifts. Here, we develop a tool to quantify frameshift mutations in MSI colorectal and endometrial cancer. Our results show that frameshift mutation frequency is negatively correlated to the predicted immunogenicity of the resulting peptides, suggesting counterselection of cell clones with highly immunogenic frameshift peptid…

0301 basic medicineMutation rateGeneral Physics and Astronomymedicine.disease_causeCOLORECTAL-CANCER0302 clinical medicineINDEL MutationMutation RateimmunologiaHLA AntigensNeoplasmsFrameshift Mutationlcsh:ScienceImmunologic SurveillanceGeneticsMutationMultidisciplinaryMISMATCH REPAIR DEFICIENCYQPEPTIDES3. Good healthkohdunrungon syöpäsyöpäsolutimmuunivaste030220 oncology & carcinogenesisTumour immunologyMicrosatellite InstabilityDNA mismatch repairINDEL MutationEXPRESSIONcongenital hereditary and neonatal diseases and abnormalitieskasvaimetDATABASESciencegastrointestinal cancerINSTABILITY3122 CancerssuolistosyövätBiologycomplex mixturesArticleGeneral Biochemistry Genetics and Molecular BiologyFrameshift mutationGastrointestinal cancer03 medical and health sciencesAntigens NeoplasmCOLONmedicineHumansCELLSelection GeneticIndelSIGNATUREStumour immunologyMicrosatellite instabilityGeneral ChemistryDNAmedicine.disease3126 Surgery anesthesiology intensive care radiologydigestive system diseases030104 developmental biologyImmunoeditinglcsh:Qmutaatiotbeta 2-MicroglobulinMicrosatellite Repeats
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One NF1 Mutation may Conceal Another

2019

Neurofibromatosis type 1 (NF1) is an autosomal dominant disease with complete penetrance but high variable expressivity. NF1 is caused by loss-of-function mutations in the NF1 gene, a negative regulator of the RAS-MAPK pathway. The NF1 gene has one of the highest mutation rates in human disorders, which may explain the outbreak of independent de novo variants in the same family. Here, we report the co-occurrence of pathogenic variants in the NF1 and SPRED1 genes in six families with NF1 and Legius syndrome, using next-generation sequencing. In five of these families, we observed the co-occurrence of two independent NF1 variants. All NF1 variants were classified as pathogenic, according to t…

0301 basic medicineMutation ratemedicine.medical_specialtySPRED1congenital hereditary and neonatal diseases and abnormalities<i>SPRED1</i>lcsh:QH426-470[SDV]Life Sciences [q-bio]030105 genetics & heredityBiologyneurofibromatosis type 103 medical and health sciencesGeneticsmedicineNeurofibromatosisneoplasmsGenetics (clinical)Legius syndromeGeneticsMolecular pathologyAutosomal dominant traitmedicine.diseasePenetrance<i>NF1</i>eye diseases3. Good healthnervous system diseases[SDV] Life Sciences [q-bio]Legius syndromelcsh:Genetics030104 developmental biologyNF1Medical geneticsSPRED1 Genede novo variantGenes
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Local adaptation in populations of Mycobacterium tuberculosis endemic to the Indian Ocean Rim

2021

24 páginas, 3 figuras, 1 tabla. The sequence data generated by this study has been deposited on SRA (https://www.ncbi.nlm.nih.gov/sra) under the accession number PRJNA670836. Extended data is available here: https://github.com/fmenardo/MTBC_L1_L3. DOI: https://doi.org/10.5281/zenodo.4609804 (Menardo, 2021).

0301 basic medicineMycobacterium tuberculosis / patogenicidadeTuberculosisGenotypevirusesLineage (evolution)030106 microbiologyLocus (genetics)adaptationBiologyGenomeGeneral Biochemistry Genetics and Molecular BiologyMycobacterium tuberculosis03 medical and health sciencesAdapta??oGenoma BacterianomedicineHumansOceano ?ndico / epidemiologiaGeneral Pharmacology Toxicology and PharmaceuticsAdaptationIndian OceanLocal adaptationGenetic diversityGeneral Immunology and Microbiologyvirus diseasesTuberculose / patologiaGeneral MedicineArticlesMycobacterium tuberculosisbiochemical phenomena metabolism and nutritionbiology.organism_classificationmedicine.diseasedigestive system diseases3. Good health030104 developmental biologyMycobacterium tuberculosis complexEvolutionary biologycoevolutionLinhagemCoevolutionResearch ArticleF1000Research
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Myeloid leukemia with transdifferentiation plasticity developing from T-cell progenitors

2016

Unfavorable patient survival coincides with lineage plasticity observed in human acute leukemias. These cases are assumed to arise from hematopoietic stem cells, which have stable multipotent differentiation potential. However, here we report that plasticity in leukemia can result from instable lineage identity states inherited from differentiating progenitor cells. Using mice with enhanced c-Myc expression, we show, at the single-cell level, that T-lymphoid progenitors retain broad malignant lineage potential with a high capacity to differentiate into myeloid leukemia. These T-cell-derived myeloid blasts retain expression of a defined set of T-cell transcription factors, creating a lymphoi…

0301 basic medicineMyeloidBone Marrow CellsBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health scienceshemic and lymphatic diseasesmedicineCell LineageProgenitor cellMolecular BiologyGeneral Immunology and MicrobiologyGeneral NeuroscienceTransdifferentiationMyeloid leukemiaCell DifferentiationArticlesmedicine.diseaseHematopoietic Stem CellsHaematopoiesisLeukemia030104 developmental biologymedicine.anatomical_structureImmunologyCancer researchLymphoid Progenitor CellsStem cell
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Mesenchymal Transition of High-Grade Breast Carcinomas Depends on Extracellular Matrix Control of Myeloid Suppressor Cell Activity

2016

SummaryThe extracellular matrix (ECM) contributes to the biological and clinical heterogeneity of breast cancer, and different prognostic groups can be identified according to specific ECM signatures. In high-grade, but not low-grade, tumors, an ECM signature characterized by high SPARC expression (ECM3) identifies tumors with increased epithelial-to-mesenchymal transition (EMT), reduced treatment response, and poor prognosis. To better understand how this ECM3 signature is contributing to tumorigenesis, we expressed SPARC in isogenic cell lines and found that SPARC overexpression in tumor cells reduces their growth rate and induces EMT. SPARC expression also results in the formation of a h…

0301 basic medicineMyeloidMDSCGene Expressionmedicine.disease_causeT-Lymphocytes RegulatoryPolyethylene GlycolsExtracellular matrixMiceBreast cancerMyeloid CellsOsteonectinMast Cellslcsh:QH301-705.5Mice KnockoutAntigen PresentationMice Inbred BALB CEMTepithelial to mesenchymal transitionBreast cancer; COX-2; CXCL12; ECM; EMT; G-CSF; GM-CSF; MDSC; SPARC; aminobisphosphonates; cyclooxygenase-2; epithelial to mesenchymal transition; extracellular matrix; granulocyte colony-stimulating factor; granulocyte-macrophage colony-stimulating factor; myeloid-derived suppressor cellsCXCL12Granulocyte macrophage colony-stimulating factormedicine.anatomical_structurecyclooxygenase-2granulocyte-macrophage colony-stimulating factorFemalegranulocyte colony-stimulating factormedicine.drugEpithelial-Mesenchymal Transitionextracellular matrixAntineoplastic AgentsBreast NeoplasmsBiologySettore MED/08 - Anatomia PatologicaG-CSFGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesCell Line TumormedicineAnimalsHumansEpithelial–mesenchymal transitionECMMesenchymal stem cellSPARCGM-CSFCOX-2myeloid-derived suppressor cellsXenograft Model Antitumor AssaysIsogenic human disease modelsaminobisphosphonates030104 developmental biologylcsh:Biology (General)CelecoxibDoxorubicinImmunologyCancer researchMyeloid-derived Suppressor CellaminobisphosphonateNeoplasm GradingCarcinogenesisCell Reports
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