Search results for " DNA Primers"

showing 7 items of 7 documents

Glycogen synthase 2 is a novel target gene of peroxisome proliferator-activated receptors.

2007

International audience; Glycogen synthase 2 (Gys-2) is the ratelimiting enzyme in the storage of glycogen in liver and adipose tissue, yet little is known about regulation of Gys-2 transcription. The peroxisome proliferator-activated receptors (PPARs) are transcription factors involved in the regulation of lipid and glucose metabolism and might be hypothesized to govern glycogen synthesis as well. Here, we show that Gys-2 is a direct target gene of PPARalpha, PPARbeta/delta and PPARgamma. Expression of Gys-2 is significantly reduced in adipose tissue of PPARalpha-/-, PPARbeta/delta-/- and PPARgamma+/- mice. Furthermore, synthetic PPARbeta/delta, and gamma agonists markedly up-regulate Gys-2…

Animals; Chromatin/ultrastructure; DNA Primers; Gene Expression Regulation Enzymologic; Glycogen Synthase/genetics; Hepatocytes/enzymology; Hepatocytes/physiology; Mice; Mice Knockout; Peroxisome Proliferator-Activated Receptors/deficiency; Peroxisome Proliferator-Activated Receptors/genetics; Polymerase Chain Reaction; RNA/genetics; RNA/isolation & purification; Rats; Transcription GeneticTranscription GeneticPeroxisome proliferator-activated receptorMESH : HepatocytesPPREPolymerase Chain Reactionadipose-tissuePPARMESH: HepatocytesMice0302 clinical medicineMESH: Animals610 Medicine & healthchemistry.chemical_classificationRegulation of gene expression0303 health sciencesGlycogenglycogen-synthaseChromatinGlycogen Synthase030220 oncology & carcinogenesisMESH : DNA PrimersmicroarrayMESH: DNA Primersmedicine.medical_specialtyHealth aging / healthy living [IGMD 5]fatty-acid oxidationliverGene Expression Regulation EnzymologicMESH: Chromatin03 medical and health sciencesskeletal-muscleGlycogen synthaseMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyHNF4αVLAGPharmacologybeta/deltaMESH: Polymerase Chain Reactionresponse elementsMESH : Peroxisome Proliferator-Activated ReceptorsEndocrinologychemistryMicrobial pathogenesis and host defense [UMCN 4.1]Response elementPeroxisome Proliferator-Activated ReceptorsAdipose tissueMESH: Peroxisome Proliferator-Activated Receptorsin-vivoMESH: Mice KnockoutTransactivationchemistry.chemical_compoundVoeding Metabolisme en GenomicaMESH : RNAMESH : Polymerase Chain ReactionMice KnockoutMESH : ChromatinMESH : RatsMESH: Gene Expression Regulation EnzymologicMetabolism and Genomicsadipose tissueMetabolisme en GenomicaMolecular MedicineNutrition Metabolism and GenomicsMESH : Glycogen SynthaseResearch ArticleMESH: Ratsglycogen synthase 2610 Medicine & healthBiologyMESH : Gene Expression Regulation EnzymologicCellular and Molecular NeuroscienceVoedingMESH: RNAInternal medicineMESH : MicemedicineAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyTranscription factorMESH: Micealpha ppar-alpha030304 developmental biologyNutritionDNA PrimersMESH: Glycogen SynthaseMESH: Transcription GeneticMESH : Transcription GeneticCell BiologyRatsgene transcriptionbiology.proteinHepatocytesRNAMESH : Mice KnockoutgammaMESH : Animalsmetabolism
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A Mutation With Major Effects on Drosophila melanogaster Sex Pheromones

2005

0016-6731 (Print) Comparative Study Journal Article Research Support, Non-U.S. Gov't; Sex pheromones are intraspecific chemical signals that are crucial for mate attraction and discrimination. In Drosophila melanogaster, the predominant hydrocarbons on the cuticle of mature female and male flies are radically different and tend to stimulate or inhibit male courtship, respectively. This sexual difference depends largely upon the number of double bonds (one in males and two in females) added by desaturase enzymes. A mutation was caused by a PGal4 transposon inserted in the desat1 gene that codes for the desaturase crucial for setting these double bonds. Homozygous mutant flies produced 70-90%…

Fatty Acid DesaturasesMaleChromatography GasPeriod (gene)Analysis of Variance Animals Chromatography Gas DNA Primers DNA Transposable Elements/genetics Drosophila Proteins/*genetics/metabolism Drosophila melanogaster/enzymology/*genetics Fatty Acid Desaturases/*genetics/metabolism Female Gene Components Hexanes/chemistry Hydrocarbons/chemistry/isolation & purification Male Mutation/*genetics Reverse Transcriptase Polymerase Chain Reaction Sex Attractants/analysis/*biosynthesis Sex Factors Species SpecificityMutation/*geneticsMutantHexanes/chemistryInvestigationsDrosophila Proteins/*genetics/metabolismHydrocarbons/chemistry/isolation & purificationSex FactorsFatty Acid Desaturases/*genetics/metabolismSpecies SpecificityGeneticsDrosophila ProteinsHexanesAnimalsSex Attractants/analysis/*biosynthesis[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Sex AttractantsAlleleDrosophila melanogaster/enzymology/*geneticsGeneComputingMilieux_MISCELLANEOUSDNA PrimersGeneticsAnalysis of VarianceChromatographybiologyReverse Transcriptase Polymerase Chain Reactionfungibiology.organism_classificationMolecular biologyHydrocarbonsDNA Transposable Elements/geneticsSexual dimorphismDrosophila melanogasterGene ComponentsGas[ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Sex pheromoneMutationDNA Transposable ElementsSex AttractantsFemaleDrosophila melanogasterGenetics
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Gallium modulates osteoclastic bone resorption in vitro without affecting osteoblasts.

2010

Gallium (Ga) has been shown to be effective in the treatment of disorders associated with accelerated bone loss, including cancer-related hypercalcemia and Paget's disease. These clinical applications suggest that Ga could reduce bone resorption. However, few studies have studied the effects of Ga on osteoclastic resorption. Here, we have explored the effects of Ga on bone cells in vitro.In different osteoclastic models [osteoclasts isolated from long bones of neonatal rabbits (RBC), murine RAW 264.7 cells and human CD14-positive cells], we have performed resorption activity tests, staining for tartrate resistant acid phosphatase (TRAP), real-time polymerase chain reaction analysis, viabili…

MESH: Bone ResorptionMESH: RabbitsGallium[SDV.BC.IC] Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB]MESH: Base Sequence[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMiceMESH: Alkaline PhosphataseMESH: Reverse Transcriptase Polymerase Chain Reaction[SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB]MESH: Animals[SDV.BBM.BC] Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM]Cells Cultured[SDV.MHEP.RSOA] Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal systemReverse Transcriptase Polymerase Chain ReactionCell DifferentiationMESH: GalliumResearch Papers[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM]Isoenzymes[SDV.MHEP.RSOA]Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal systemMESH: Isoenzymes[SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]RabbitsMESH: Cells Culturedmusculoskeletal diseasesMESH: Cell DifferentiationMESH: DNA PrimersAcid Phosphatase[SDV.CAN]Life Sciences [q-bio]/CancerIn Vitro TechniquesMESH: Acid Phosphatase[SDV.CAN] Life Sciences [q-bio]/Cancer[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]AnimalsHumansBone Resorption[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM]MESH: Tartrate-Resistant Acid Phosphatase[SDV.IB.BIO]Life Sciences [q-bio]/Bioengineering/BiomaterialsMESH: MiceDNA PrimersMESH: In Vitro TechniquesMESH: OsteoblastsOsteoblastsMESH: HumansBase SequenceTartrate-Resistant Acid Phosphatase[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyAlkaline Phosphatase[SDV.IB.BIO] Life Sciences [q-bio]/Bioengineering/Biomaterials
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A novel mutation of gene CBFA1/RUNX2 in cleidocranial dysplasia.

2007

Cleidocranial dysplasia (CCD) is an autosomal dominant skeletal dysplasia characterised by abnormal clavicles, patent sutures and fontanelles, supernumerary teeth, short stature, and a variety of other skeletal changes. The disease gene is CBFA1/RUNX2, which is mapped to chromosome 6p21. Inactivation of the CBFA1/RUNX2 gene by mutations is involved in the skeletal defects that occur in patients with CCD. CBFA1/RUNX2 controls the differentiation of precursor cells into osteoblasts and is essential for membranous as well as endochondral bone formation. In this study of a 14-yr-old boy with typical CCD phenotype, the authors found a novel CBFA1/RUNX2 gene mutation. All of the amplified segment…

MaleHeterozygoteAdolescentDNA Mutational AnalysisCore Binding Factor Alpha 1 SubunitPolymerase Chain ReactionPedigreeAdolescent Chromosomes Human Pair 6 Cleidocranial Dysplasia/genetics* Cleidocranial Dysplasia/pathology Codon Nonsense/genetics* Core Binding Factor Alpha 1 Subunit/genetics* DNA Mutational Analysis DNA Primers/chemistry Female Gene Silencing Heterozygote Humans Male Pedigree Point Mutation* Polymerase Chain Reactioncleidocranial dysplasiaCodon NonsenseCBFA1/RUNX2HumansPoint MutationChromosomes Human Pair 6Femalegene mutationGene SilencingCleidocranial DysplasiaDNA Primers
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Friedreich's Ataxia: Autosomal Recessive Disease Caused by an Intronic GAA Triplet Repeat Expansion

1996

International audience; Friedreich's ataxia (FRDA) is an autosomal recessive, degenerative disease that involves the central and peripheral nervous systems and the heart. A gene, X25, was identified in the critical region for the FRDA locus on chromosome 9q13. This gene encodes a 210-amino acid protein, frataxin, that has homologs in distant species such as Caenorhabditis elegans and yeast. A few FRDA patients were found to have point mutations in X25, but the majority were homozygous for an unstable GAA trinucleotide expansion in the first X25 intron.

MaleIron-sulfur cluster assemblyPolymerase Chain Reaction0302 clinical medicineTrinucleotide RepeatsIron-Binding ProteinsGenetics0303 health sciencesMultidisciplinaryAutosomal recessive cerebellar ataxiaPedigree3. Good healthFemalemedicine.symptomChromosomes Human Pair 9HumanPair 9Heterozygotecongenital hereditary and neonatal diseases and abnormalitiesAtaxiaMolecular Sequence DataGenes RecessiveLocus (genetics)BiologyChromosomes03 medical and health sciencesGene mappingAlleles; Amino Acid Sequence; Base Sequence; Chromosomes Human Pair 9; DNA Primers; Female; Friedreich Ataxia; Genes Recessive; Heterozygote; Humans; Male; Molecular Sequence Data; Pedigree; Point Mutation; Polymerase Chain Reaction; Proteins; Sequence Alignment; Introns; Iron-Binding Proteins; Trinucleotide RepeatsmedicineRecessiveHumansPoint MutationAmino Acid SequenceAlleleAllelesDNA Primers030304 developmental biologyBase SequencePoint mutationProteins[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologymedicine.diseaseMolecular biologyIntronsGenes[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsFriedreich AtaxiaFrataxinbiology.proteinSequence Alignment030217 neurology & neurosurgeryScience
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The abrogation of the HOXB7/PBX2 complex induces apoptosis in melanoma through the miR-221&222-c-FOS pathway.

2013

Cutaneous melanoma is the fastest increasing cancer worldwide. Although several molecular abnormalities have been associated with melanoma progression, the underlying mechanisms are still largely unknown and few targeted therapies are under evaluation. Here we show that the HOXB7/PBX2 dimer acts as a positive transcriptional regulator of the oncogenic microRNA-221 and -222. In addition, demonstrating c-FOS as a direct target of miR-221&222, we identify a HOXB7/PBX2→miR-221&222 →c-FOS regulatory link, whereby the abrogation of functional HOXB7/PBX2 dimers leads to reduced miR-221&222 transcription and elevated c-FOS expression with consequent cell death. Taking advantage of the treatment wit…

Programmed cell deathCancer ResearchSkin NeoplasmsTranscription GeneticApoptosisSmall Interferingc-FosPolymerase Chain ReactionCell LineGeneticCell Line TumorProto-Oncogene ProteinsHOXB7/PBX2 complexmicroRNATranscriptional regulationmedicinemelanomaHumansPBXRNA Small InterferingDNA PrimersHomeodomain Proteinsc-FOS pathwayTumorbiologymicroRNABase SequenceMelanomaHOXB7; HXR9 peptide; melanoma; microRNA; PBX; Apoptosis; Base Sequence; Cell Line Tumor; DNA Primers; Dimerization; Homeodomain Proteins; Humans; Melanoma; MicroRNAs; Polymerase Chain Reaction; Proto-Oncogene Proteins; Proto-Oncogene Proteins c-fos; RNA Small Interfering; Skin Neoplasms; Transcription Genetic; Cancer Research; Oncologymedicine.diseaseMicroRNAsHXR9 peptideOncologyApoptosisCell cultureCutaneous melanomaHOXB7/PBX2 complex ;melanoma ;c-FOS pathwayCancer researchbiology.proteinHOXB7RNATranscriptionDimerizationProto-Oncogene Proteins c-fosCancer Cell Biology
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Two Patients With History of STEC-HUS, Posttransplant Recurrence and Complement Gene Mutations

2013

Hemolytic uremic syndrome (HUS) is a disease of microangiopathic hemolytic anemia, thrombocytopenia and acute renal failure. About 90% of cases are secondary to infections by Escherichia coli strains producing Shiga-like toxins (STEC-HUS), while 10% are associated with mutations in genes encoding proteins of complement system (aHUS). We describe two patients with a clinical history of STEC-HUS, who developed end-stage renal disease (ESRD) soon after disease onset. They received a kidney transplant but lost the graft for HUS recurrence, a complication more commonly observed in aHUS. Before planning a second renal transplantation, the two patients underwent genetic screening for aHUS-associat…

Shiga-toxinGraft RejectionMaleDNA Primer030232 urology & nephrologyEscherichia coli InfectionGene mutationurologic and male genital diseasesGastroenterology0302 clinical medicineRecurrenceRisk Factorshemic and lymphatic diseasesImmunology and AllergyPharmacology (medical)gene mutationKidney transplantationEscherichia coli Infections0303 health sciencesKidneymedicine.diagnostic_testShiga-Toxigenic Escherichia coliAntigens CD46Microangiopathic hemolytic anemiaMiddle AgedPrognosisfemale genital diseases and pregnancy complications3. Good healthPedigreemedicine.anatomical_structureComplement Factor IComplement factor I; gene mutation; hemolytic uremic syndrome; kidney transplantation; membrane cofactor protein; Shiga-toxin; Adult; Antigens CD46; Case-Control Studies; Complement Factor I; DNA Primers; Escherichia coli Infections; Female; Genetic Testing; Graft Rejection; Hemolytic-Uremic Syndrome; Heterozygote; Humans; Kidney Failure Chronic; Kidney Transplantation; Male; Middle Aged; Mutation; Pedigree; Prognosis; Recurrence; Risk Factors; Shiga-Toxigenic Escherichia coli; Thrombocytopenia; Young Adult; Transplantation; Immunology and Allergy; Pharmacology (medical)FemaleCase-Control StudieHumanAdultmedicine.medical_specialtyHeterozygotePrognosiComplement factor IMembrane Cofactor Protein03 medical and health sciencesYoung AdultInternal medicinemedicineHumansGenetic Testing030304 developmental biologyGenetic testingDNA PrimersTransplantationbusiness.industryCD46Risk Factormedicine.diseaseKidney TransplantationThrombocytopeniaTransplantationCase-Control StudiesImmunologyHemolytic-Uremic SyndromeMutationhemolytic uremic syndromeKidney Failure ChronicbusinessAmerican Journal of Transplantation
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