Search results for "binding proteins"

showing 10 items of 911 documents

Phospholipase D in rat myocardium: formation of lipid messengers and synergistic activation by G-protein and protein kinase C.

1998

Activation of phospholipase D (PLD) and phosphoinositide-specific phospholipase C (PI-PLC) by fluoride, to stimulate heterotrimeric G-proteins, and by phorbol esters, to stimulate protein kinase C (PKC), was studied in rat atria. Fluoride and 4beta-phorbol-12beta,13alpha-dibutyrate (PDB), in contrast to 4beta-phorbol-13alpha-acetate (PAc), activated PLD, catalyzing the formation of [3H]-phosphatidylethanol ([3H]-PETH), [3H]-phosphatidic acid ([3H]-PA), choline and sn-1,2-diacylglycerol (DAG). Basal PLD activity was resistant to drastic changes in Ca2+ and to Ro 31-8220, a PKC inhibitor, but was decreased by genistein, an inhibitor of tyrosine kinase, and increased by vanadate, a tyrosine ph…

MaleG proteinProtein tyrosine phosphataseBiologyBiochemistrySecond Messenger Systemschemistry.chemical_compoundPhosphoinositide Phospholipase CGTP-Binding ProteinsPhorbol EstersPhospholipase DAnimalsRats WistarProtein kinase CPhorbol 1213-DibutyrateProtein Kinase CDiacylglycerol kinasePharmacologyPhospholipase CPhospholipase DMyocardiumPhosphatidylinositol Diacylglycerol-LyaseTyrosine phosphorylationDrug SynergismLipid MetabolismLipidsRatsEnzyme ActivationBiochemistrychemistryType C PhospholipasesSecond messenger systemlipids (amino acids peptides and proteins)Biochemical pharmacology
researchProduct

Mechanisms of Ca2+ liberation at fertilization

2005

The mechanisms underlying the Ca2+ release at fertilization of several animal organisms are reported. Four main classical theories are described, i.e., that of Ca2+ release following simple sperm contact and a G protein stimulation; that of simple sperm contact followed by a tyrosine kinase receptor activation; that of the necessity of introduction by sperm into the egg of molecules for Ca2+ release; and that the molecule introduced into the marine eggs for Ca2+ release is the same Ca2+. Two other mechanisms for Ca2+ release are also illustrated: that of ryanodine receptor stimulation and that of NAADP formation.

MaleG proteinXenopusBiophysicsStimulationChick EmbryoFERTILIZATION CALCIUM RELEASEBiologyModels BiologicalBiochemistryReceptor tyrosine kinaseMiceHuman fertilizationGTP-Binding ProteinsAnimalsMolecular BiologySperm-Ovum InteractionsAdenine NucleotidesRyanodine receptorCell BiologySpermatozoaSpermCell biologyBiochemistryFertilizationbiology.proteinLiberationCalciumBiochemical and Biophysical Research Communications
researchProduct

Nuclear localization of the protein encoded by the Wilms’ tumor gene WT1 in embryonic and adult tissues

1993

ABSTRACT The human Wilms’ tumor gene WT1 encodes a putative transcription factor implicated in tumorigenesis and in specifying normal urogenital development. We have studied the distribution of WT1 protein and mRNA using immunohistochemistry and in situ hybridization. Monoclonal antibodies were raised against a peptide specific to the first alternative splice site of WT1. Two antibodies specifically reacted on Western blot to this WT1 isoform. Immunofluorescence localized WT1 protein to podocytes during mesonephric and metanephric development. In situ hybridization revealed a similar pattern of expression except that WT1 mRNA was also present in metanephric blastema and renal vesicles. Mess…

MaleGene isoformcongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyBlotting WesternFluorescent Antibody TechniqueGene ExpressionUrogenital SystemIn situ hybridizationBiologyKidneyurologic and male genital diseasesPolymerase Chain ReactionInternal medicineGene expressionmedicineHumansRNA MessengerWT1 ProteinsMolecular BiologyTranscription factorIn Situ HybridizationCell NucleusMessenger RNAGranulosa CellsSertoli Cellsurogenital systemfungiZinc FingersWilms' tumormedicine.diseasefemale genital diseases and pregnancy complicationsWilms Tumor ProteinCell biologyDNA-Binding ProteinsCell nucleusmedicine.anatomical_structureEndocrinologyMesonephrosFemaleTranscription FactorsDevelopmental BiologyDevelopment
researchProduct

Genetic elimination of known pheromones reveals the fundamental chemical bases of mating and isolation in Drosophila

1999

Overexpression of the UAS-tra transgene in Drosophila melanogaster females led to the complete elimination of their cuticular pheromones. According to current models of Drosophila behavior, these flies should induce no courtship. In fact, they are still attractive to conspecific males. Three classes of stimuli are shown to induce courtship, with different effects on male behavior: ( i ) known pheromones produced by control females, ( ii ) stimuli produced by living control and transgenic flies, and ( iii ) as-yet-undetermined pheromones present on both control and transgenic flies. Only the latter class of pheromones are required for mating. They appear to represent a layer of ancestral at…

MaleHot TemperaturePheromones/genetics/*physiologyPheromonesAnimals Genetically ModifiedCourtshipSexual Behavior AnimalAnimal/*physiologyMelanogasterMatingreproductive and urinary physiologymedia_commonGeneticsMultidisciplinarybiologyBiological SciencesDNA-Binding ProteinsDrosophila melanogasterSocial IsolationSex pheromonebehavior and behavior mechanismsDrosophilaFemaleDrosophila melanogasteranimal structuresSaccharomyces cerevisiae ProteinsGenotypeRecombinant Fusion ProteinsRecombinant Fusion Proteins/biosynthesisSexual BehaviorTransgenemedia_common.quotation_subjectGenetically ModifiedCrossesHSP70 Heat-Shock Proteins/biosynthesis/genetics/physiologyFungal ProteinsGeneticSibling speciesAnimalsHSP70 Heat-Shock ProteinsDrosophilaCrosses Geneticfungibiology.organism_classificationHeatTranscription Factors/biosynthesis/geneticsFungal Proteins/biosynthesis/geneticsHydrocarbonsDrosophila melanogaster/genetics/*physiologyEvolutionary biologyDrosophila/genetics/*physiologyTranscription FactorsProceedings of the National Academy of Sciences
researchProduct

Stage-specific chromosomal association of Drosophila dMBD2/3 during genome activation.

2002

The Drosophila gene dMBD2/3 encodes a protein with significant homologies to the mammalian methyl-DNA binding proteins MBD2 and MBD3. These proteins are essential components of chromatin complexes involved in epigenetic gene regulation. Because the available in vitro data on dMBD2/3 are conflicting we have started an in vivo characterization of dMBD2/3. We detected expression of two isoforms specifically during embryonic development. Staining of whole embryos combined with high-resolution confocal microscopy revealed a highly regulated spatial distribution. During the syncytial blastoderm stage, dMBD2/3 formed speckles that localized to the cytoplasm. Shortly after, during the cellular blas…

MaleImmunoblottingBiologyY chromosomeGenomeChromosomesSpermatocytesY ChromosomeGeneticsAnimalsDrosophila ProteinsEpigeneticsGeneGenetics (clinical)Regulation of gene expressionMicroscopy ConfocalGene Expression Regulation DevelopmentalMolecular biologyChromatinCell biologyDNA-Binding ProteinsCytoplasmDrosophilaFemaleBlastodermProtein BindingChromosoma
researchProduct

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
researchProduct

High-sensitivity troponin assay improves prediction of cardiovascular risk in patients with cerebral ischaemia

2013

Background and purpose Clinical scores are recommended for predicting cardiovascular risk in patients with cerebral ischaemia to inform secondary prevention. Blood biomarkers may improve prediction beyond clinical scores. Methods Within the observational Find-AF trial (ISRCTN46104198), 197 patients >18 years of age with cerebral ischaemia and without atrial fibrillation had blood sampled at baseline. The predictive value of five biomarkers for a combined vascular endpoint (acute coronary syndrome, stroke, cardiovascular death) and all-cause mortality was determined, alone and in addition to the Essen Stroke Risk Score (ESRS), Stroke Prognostic Instrument 2 (SPI-2) and National Institutes of…

MaleKaplan-Meier Estimate030204 cardiovascular system & hematologyBrain IschemiaCohort Studies0302 clinical medicineNatriuretic Peptide BrainMedicine1506Prospective StudiesProspective cohort studyStrokeTroponin TAtrial fibrillationMiddle AgedPrognosisTroponin3. Good healthStrokePsychiatry and Mental healthCardiovascular DiseasesIschemic Attack TransientPredictive value of testsCardiologyFemaleFatty Acid Binding Protein 3Atrial Natriuretic Factormedicine.medical_specialtyAcute coronary syndromeGrowth Differentiation Factor 15Endpoint DeterminationCardiologyFatty Acid-Binding ProteinsRisk Assessment03 medical and health sciencesTroponin TPredictive Value of TestsInternal medicineHumansSurvival analysisAgedbusiness.industryProportional hazards modelmedicine.diseaseSurvival AnalysisPeptide FragmentsSurgeryCerebrovascular DiseaseSurgeryNeurology (clinical)businessBiomarkers030217 neurology & neurosurgeryFollow-Up StudiesJournal of Neurology, Neurosurgery & Psychiatry
researchProduct

Evolution of chromatin-remodeling complexes: comparative genomics reveals the ancient origin of "novel" compensasome genes.

2003

Dosage compensation in Drosophila is mediated by a complex, called compensasome, com- posed of at least five proteins and two noncoding RNAs. Genes encoding compensasome proteins have been collectively named male-specific lethals or msls. Recent work showed that three of the Drosophila msls (msl-3, mof, and mle) have an ancient origin. In this study, I describe likely orthologues of the two re- maining msls, msl-1 and msl-2, in several inverte- brates and vertebrates. The MSL-2 protein is the only one found in Drosophila and vertebrate genomes that contains both a RING finger and a peculiar type of CXC domain, related to the one present in Enhancer of Zeste proteins. MSL-1 also contains two…

MaleLeucine zipperAmino Acid MotifsMolecular Sequence DataBiologyGenomeChromatin remodelingEvolution MolecularDosage Compensation GeneticGeneticsRing fingermedicineAnimalsDrosophila ProteinsHumansAmino Acid SequenceEnhancerMolecular BiologyEcology Evolution Behavior and SystematicsCaenorhabditis elegansPhylogenyComparative genomicsGeneticsDosage compensationfungiNuclear ProteinsGenomicsbiology.organism_classificationChromatin Assembly and DisassemblyProtein Structure TertiaryDNA-Binding Proteinsmedicine.anatomical_structureVertebratesDrosophilaSequence AlignmentTranscription FactorsJournal of molecular evolution
researchProduct

Plasticity-related gene-1 inhibits lysophosphatidic acid-induced vascular smooth muscle cell migration and proliferation and prevents neointima forma…

2012

International audience; Plasticity-related gene-1 (PRG-1) protects neuronal cells from lysophosphatidic acid (LPA) effects. In vascular smooth muscle cells (VSMCs), LPA was shown to induce phenotypic modulation in vitro and vascular remodeling in vivo. Thus we explored the role of PRG-1 in modulating VSMC response to LPA. PCR, Western blot, and immunofluorescence experiments showed that PRG-1 is expressed in rat and human vascular media. PRG-1 expression was strongly inhibited in proliferating compared with quiescent VSMCs both in vitro and in vivo (medial vs. neointimal VSMCs), suggesting that PRG-1 expression is dependent on the cell phenotype. In vitro, adenovirus-mediated overexpression…

MaleMAPK/ERK pathwayNeointimaVascular smooth musclePhysiologyPhenotypic modulation[SDV]Life Sciences [q-bio]Genetic VectorsBiologyPlasticityMuscle Smooth VascularAdenoviridaechemistry.chemical_compoundCell MovementNeointimaLysophosphatidic acidAnimalsHumansRats WistarCells CulturedCell ProliferationCell BiologyLipid-phosphate phosphatasePhosphoric Monoester HydrolasesIn vitroRatsCell biologyGene Expression RegulationchemistryBiochemistryCalmodulin-Binding ProteinsLysophospholipidsAmerican Journal of Physiology-Cell Physiology
researchProduct

A role for the peroxisomal 3-ketoacyl-CoA thiolase B enzyme in the control of PPARα-mediated upregulation of SREBP-2 target genes in the liver.: ThB …

2011

International audience; Peroxisomal 3-ketoacyl-CoA thiolase B (Thb) catalyzes the final step in the peroxisomal β-oxidation of straight-chain acyl-CoAs and is under the transcription control of the nuclear hormone receptor PPARα. PPARα binds to and is activated by the synthetic compound Wy14,643 (Wy). Here, we show that the magnitude of Wy-mediated induction of peroxisomal β-oxidation of radiolabeled (1-(14)C) palmitate was significantly reduced in mice deficient for Thb. In contrast, mitochondrial β-oxidation was unaltered in Thb(-/-) mice. Given that Wy-treatment induced Acox1 and MFP-1/-2 activity at a similar level in both genotypes, we concluded that the thiolase step alone was respons…

MaleMESH: HepatomegalyPalmitatesMESH : PyrimidinesMESH : Gene DeletionBiochemistryelement-binding proteinsMESH : Acetyl-CoA C-AcyltransferaseMiceMESH: Up-RegulationMESH: AnimalsMESH : Up-RegulationMESH: Lipid Metabolism0303 health sciencesMESH : Gene Expression RegulationThiolase030302 biochemistry & molecular biologyGeneral MedicineMESH : HepatomegalyUp-Regulationzellweger-syndromePeroxisome ProliferatorsMESH: Peroxisome ProliferatorsHepatomegalySterol Regulatory Element Binding Protein 2peroxisomal 3-ketoacyl-CoA thiolase BMESH: Mitochondria3-oxoacyl-coa thiolaseLathosterolfatty-acid oxidationrat-liverMESH: Sterol Regulatory Element Binding Protein 203 medical and health sciencesMESH : Sterol Regulatory Element Binding Protein 2HumansPPAR alphaMESH : Peroxisome Proliferators[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyPPARaVLAGMESH : Oxidation-ReductionFatty Acid Oxidation.MESH: HumansCholesterolMESH : HumanscholesterolLipid MetabolismMESH: PeroxisomesSterol regulatory element-binding proteinchemistryMESH: PyrimidinesCholesterol; Micro-array analysis; Peroxisomal 3-ketoacyl-CoA thiolase B; PPARα and SREBP-2; Wy14643Fatty Acid OxidationGene DeletionMESH: LiverMESH: Oxidation-ReductionMESH: Signal TransductionMESH: Mice KnockoutVoeding Metabolisme en Genomicachemistry.chemical_compoundMESH: CholesterolMESH : Lipid MetabolismWy14MESH : PalmitatesMESH: PPAR alphaMESH : CholesterolMice Knockoutneuronal migration643PeroxisomeAcetyl-CoA C-AcyltransferaseMESH: Gene Expression RegulationMetabolism and GenomicsMitochondriaLiverBiochemistryMicro-array analysisMetabolisme en GenomicaACOX1Nutrition Metabolism and GenomicsMESH : MitochondriaOxidation-ReductionSignal Transductionacyl-coa oxidasecholesterol-synthesisMESH : MaleMESH : PPAR alphaPeroxisome ProliferationPPARα and SREBP-2Biologybeta-oxidationVoedingproliferator-activated receptorsMESH : MicePeroxisomesAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Mice030304 developmental biologySCP2NutritionMESH : Signal TransductionMESH : LiverMESH: PalmitatesMESH: MalePyrimidinesMESH: Acetyl-CoA C-AcyltransferaseGene Expression RegulationMESH: Gene DeletionMESH : Mice KnockoutMESH : AnimalsMESH : Peroxisomes
researchProduct