Search results for " Mammalia"

showing 10 items of 126 documents

The histone deacetylase Rpd3 regulates the heterochromatin structure of Drosophila telomeres

2011

Telomeres are specialized structures at the end of eukaryotic chromosomes that are required to preserve genome integrity, chromosome stability and nuclear architecture. Telomere maintenance and function are established epigenetically in several eukaryotes. However, the exact chromatin enzymatic modifications regulating telomere homeostasis are poorly understood. In Drosophila melanogaster, telomere length and stability are maintained through the retrotransposition of specialized telomeric sequences and by the specific loading of protecting capping proteins, respectively. Here, we show that the loss of the essential and evolutionarily conserved histone deacetylase Rpd3, the homolog of mammal…

Telomere-binding proteinGeneticsEpigenomicsMaleHistone deacetylase 5Histone deacetylase 2HDAC11Histone Deacetylase 1Cell BiologyBiologyTelomereHistone H4Telomere HomeostasisDrosophila melanogasterHeterochromatinHistone H2Ahistone deacetylaseHistone codeAnimalsDrosophila Proteinsanimals; article; chromosome aberration; chromosome structure; drosophila; drosophila melanogaster; drosophila proteins; enzyme activity; epigenetics; epigenomics; eukaryota; heterochromatin; histone acetylation; histone deacetylase 1; histone deacetylase rpd 3; histone methylation; male; mammalia; nonhuman; polytene chromosome; priority journal; regulatory mechanism; telomere; unclassified drugPolytene Chromosomes
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Fluctuation Methods To Study Protein Aggregation in Live Cells: Concanavalin A Oligomers Formation

2011

Prefibrillar oligomers of proteins are suspected to be the primary pathogenic agents in several neurodegenerative diseases. A key approach for elucidating the pathogenic mechanisms is to probe the existence of oligomers directly in living cells. In this work, we were able to monitor the process of aggregation of Concanavalin A in live cells. We used number and brightness analysis, two-color cross number and brightness analysis, and Raster image correlation spectroscopy to obtain the number of molecules, aggregation state, and diffusion coefficient as a function of time and cell location. We observed that binding of Concanavalin A to the membrane and the formation of small aggregates paralle…

Time FactorsCell SurvivalCellSpectroscopy Imaging and Other TechniquesBiophysicsProtein aggregationCell morphologyCell membraneDiffusion03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineProtein structure2-NaphthylaminemedicineConcanavalin AAnimalsconfocal microscopy super resolution protein aggregation kinetics in live cells amyloid related pathologiesAnnexin A5Protein Structure QuaternaryCell Shape030304 developmental biology0303 health sciencesbiologySpectrum AnalysisCell MembraneFibroblastsEmbryo MammalianCell biologyMembranemedicine.anatomical_structurechemistryConcanavalin Abiology.proteinLaurdan030217 neurology & neurosurgeryFluorescein-5-isothiocyanateLaurates
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Triclosan induces Fas receptor-dependent apoptosis in mouse neocortical neurons in vitro

2014

Triclosan (TCS) is a commonly used antimicrobial agent in personal care and sanitizing products, as well as in household items. Numerous studies have demonstrated the presence of TCS in various human tissues. Several studies have reported the accumulation of TCS in fish and human brain tissue. The aim of the present study was to investigate the effect of TCS on apoptosis in mouse neocortical neurons after 7 days of culture in vitro following 3, 6 and 24 h of exposure. To explore the mechanism underlying the effects of TCS in neurons, we studied the activation and protein expression of the Fas receptor (FasR) and caspase- 8, caspase-9 and caspase-3, as well as DNA fragmentation in TCS-treate…

Time FactorsExtrinsic apoptotic signaling pathwayApoptosisNeocortexDNA fragmentation.DNA FragmentationCaspase 8caspase-8FasRMicePregnancyAnimalsfas ReceptorFADDEnzyme InhibitorsCells CulturedNeuronsDose-Response Relationship DrugL-Lactate DehydrogenasebiologyGeneral NeurosciencefungiEmbryo MammalianStaurosporineFas receptorApoptotic bodyTriclosanIn vitroCell biologyBiochemistryApoptosisCaspasesbiology.proteinFatty Acid Synthesis InhibitorsDNA fragmentationFemaleNeuroscience
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Tbx1 regulates Vegfr3 and is required for lymphatic vessel development

2010

Defects in lymphangiogenesis are added to the broad clinical manifestations of DiGeorge syndrome, caused by deletion of the T box transcription factor Tbx1.

Vascular Endothelial Growth Factor ATBX1Cellular differentiationBiologyMice03 medical and health sciences0302 clinical medicinestomatognathic systemReportLymphatic vesselmedicineAnimalsHumansLymphangiogenesisEnhancerCells CulturedResearch ArticlesLymphatic Vessels030304 developmental biology0303 health sciencesABNORMAL CAROTID ARTERIES; TRANSGENIC MICE; VELOCARDIOFACIAL SYNDROME; CARDIOVASCULAR DEFECTS; LYMPHANGIOGENESIS; LYMPHEDEMA; MOUSE; RECEPTOR-3; MUTATION; SYSTEMEndothelial CellsGene Expression Regulation DevelopmentalCell DifferentiationCell BiologyEmbryo Mammalian3. Good healthLymphangiogenesisCell biologyVascular endothelial growth factor ALymphatic systemmedicine.anatomical_structureVascular endothelial growth factor Cembryonic structuresImmunologyT-Box Domain Proteins030217 neurology & neurosurgeryJournal of Cell Biology
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Microphthalmia, persistent hyperplastic hyaloid vasculature and lens anomalies following overexpression of VEGF-A188 from the αA-crystallin promoter

2007

Purpose During growth of the embryonic eye, dose- and site-specific expression of heparin-binding growth factors is critical for the formation of an appropriate vascular supply. Overexpression of vascular endothelial growth factor-A188 (VEGF-A188), a strongly heparin-binding, endothelial-specific mitogen, leads to severe disturbance of vascular and overall ocular morphology. This study aimed to evaluate the effects of VEGF-A188 overexpression on growth of ocular tissue components. Methods Stereological and immunohistochemical methods were employed to identify the vascular profiles, ocular tissue proportions, and cell types in VEGF-A188 transgenic mice and compare them with wild-type mice. R…

Vascular Endothelial Growth Factor Agenetic structuresMyocytes Smooth MuscleCell CountMice TransgenicEyealpha-Crystallin A ChainCongenital AbnormalitiesCorneaMiceLens CrystallineAnimalsMicrophthalmosVascular DiseasesPromoter Regions GeneticHyperplasiaEndothelial CellsHypertrophyEmbryo MammalianAntigens DifferentiationImmunohistochemistryeye diseasesActinsDisease Models AnimalAnimals NewbornBlood Vesselssense organsPericytesHeparan Sulfate ProteoglycansResearch ArticleMolecular Vision
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Anti-inflammatory Function of High-Density Lipoproteins via Autophagy of IκB Kinase

2015

Background & Aims: Plasma levels of high-density lipoprotein (HDL) cholesterol are frequently found decreased in patients with inflammatory bowel disease (IBD). Therefore, and because HDL exerts anti-inflammatory activities, we investigated whether HDL and its major protein component apolipoprotein A-I (apoA-I) modulate mucosal inflammatory responses in vitro and in vivo. Methods: The human intestinal epithelial cell line T84 was used as the in vitro model for measuring the effects of HDL on the expression and secretion of tumor necrosis factor (TNF), interleukin-8 (IL-8), and intracellular adhesion molecule (ICAM). Nuclear factor-κB (NF-κB)-responsive promoter activity was studied by …

WT wild typeApolipoprotein BEMSA electrophoretic mobility shift assayMPO myeloperoxidaseIκB kinaseDSS dextran sodium sulphatemTOR the mammalian target of rapamycinRT-PCR real-time polymerase chain reactionNF-κBchemistry.chemical_compound540 ChemistryApoA-I apolipoprotein A-I10038 Institute of Clinical ChemistryOriginal ResearchTNF tumor necrosis factorbiologyIBD inflammatory bowel diseaseChemistryGastroenterologyMyeloperoxidase10076 Center for Integrative Human PhysiologyMEICS murine endoscopic index of colitis severityTumor necrosis factor alphalipids (amino acids peptides and proteins)3-MA 3-methyl adenineNF-κB nuclear factor κBHDL high-density lipoproteinLC3II light chain 3 IIPBS phosphate-buffered salinep-IKK phosphorylated IκB kinase610 Medicine & healthICAM intracellular adhesion molecule246-Trinitrobenzenesulfonic acidTg transgenicmedicineAutophagyCD Crohn’s disease2715 GastroenterologyColitislcsh:RC799-869KO knockoutHepatologyApolipoprotein A-IAutophagyInflammatory Bowel DiseaseTNBS 246-trinitrobenzenesulfonic acidmedicine.diseaseMolecular biologyIL interleukinsiRNA small interfering RNAPI-3 phosphatidylinositol-3Immunologybiology.protein2721 Hepatologylcsh:Diseases of the digestive system. GastroenterologyPFA paraformaldehydeLipoproteinDAPI 4′6-diamidino-2-phenylindoleCMGH Cellular and Molecular Gastroenterology and Hepatology
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Regulation of the alpha-secretase ADAM10 by its prodomain and proprotein convertases.

2001

SPECIFIC AIMSTo identify the proprotein convertases responsible for maturation of the α-secretase ADAM10, we investigated the influence of PC7 and furin on ADAM10 processing and the resulting effect on amyloid precursor protein cleavage. We also examined the functional role of the ADAM10 prodomain by coexpression of a prodomain-deleted ADAM10 mutant together with its prodomain in trans.PRINCIPAL FINDINGS1. ADAM10 is proteolytically processed by PC7 and furinThe disintegrin metalloproteinase ADAM10 possesses α-secretase activity as well as a potential proprotein convertase recognition sequence (RKKR) after its prodomain. By amino-terminal sequencing of ADAM10 purified from bovine kidney plas…

animal structuresADAM10Blotting WesternKidneyTransfectionBiochemistryCell LineAmyloid beta-Protein PrecursorStructure-Activity RelationshipZymogenEndopeptidasesGeneticsAmyloid precursor proteinAnimalsAspartic Acid EndopeptidasesHumansSubtilisinsProtein PrecursorsMolecular BiologyFurinFurinbiologyChemistryProprotein convertaseEmbryo MammalianRecombinant ProteinsEnzyme ActivationBiochemistryAlpha secretaseMutagenesisbiology.proteinCattleAmyloid Precursor Protein SecretasesProprotein ConvertasesAmyloid precursor protein secretaseBiotechnologyFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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Intraflagellar transport protein 172 is essential for primary cilia formation and plays a vital role in patterning the mammalian brain

2008

AbstractIFT172, also known as Selective Lim-domain Binding protein (SLB), is a component of the intraflagellar transport (IFT) complex. In order to evaluate the biological role of the Ift172 gene, we generated a loss-of-function mutation in the mouse. The resulting Slb mutant embryos die between E12.5 and 13.0, and exhibit severe cranio-facial malformations, failure to close the cranial neural tube, holoprosencephaly, heart edema and extensive hemorrhages. Cilia outgrowth in cells of the neuroepithelium is initiated but the axonemes are severely truncated and do not contain visible microtubules. Morphological and molecular analyses revealed a global brain-patterning defect along the dorsal–…

animal structuresBody PatterningNodal ProteinSlbNodalBiologyArticleMiceFGF8Intraflagellar transportHoloprosencephalymedicineMHB boundaryAnimalsHedgehog ProteinsRNA MessengerCiliaNodeMolecular BiologyAdaptor Proteins Signal TransducingBody PatterningGeneticsMammalsCell DeathCiliumEndodermNeural tubeIntracellular Signaling Peptides and ProteinsBrainGene Expression Regulation DevelopmentalCell BiologyEmbryo MammalianCell biologyNeuroepithelial cellGastrulationCytoskeletal Proteinsmedicine.anatomical_structurePhenotypeIFT172Gene Targetingembryonic structuresNODALBiomarkersGene DeletionDevelopmental BiologySignal TransductionDevelopmental Biology
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Distinct 5' SCL enhancers direct transcription to developing brain, spinal cord, and endothelium: neural expression is mediated by GATA factor bindin…

1999

The SCL gene encodes a basic helix-loop-helix transcription factor with a pivotal role in the development of endothelium and of all hematopoietic lineages. SCL is also expressed in the central nervous system, although its expression pattern has not been examined in detail and its function in neural development is unknown. In this article we present the first analysis of SCL transcriptional regulation in vivo. We have identified three spatially distinct regulatory modules, each of which was both necessary and sufficient to direct reporter gene expression in vivo to three different regions within the normal SCL expression domain, namely, developing endothelium, midbrain, and hindbrain/spinal …

animal structuresEmbryo NonmammalianTranscription GeneticHindbrainMice TransgenicChick EmbryoBiologybehavioral disciplines and activities03 medical and health sciencesMice0302 clinical medicineTranscription (biology)Genes Reporterhemic and lymphatic diseasesProto-Oncogene ProteinsBasic Helix-Loop-Helix Transcription FactorsAnimalsTissue DistributionEndotheliumEnhancerMolecular BiologyTranscription factorGeneIn Situ HybridizationT-Cell Acute Lymphocytic Leukemia Protein 1Zebrafish030304 developmental biologyRegulation of gene expressionGenetics0303 health sciencesReporter geneModels GeneticfungiBrainCell BiologyZebrafish ProteinsEmbryo MammalianCell biologyDNA-Binding ProteinsLac OperonSpinal CordNeural development030217 neurology & neurosurgeryDevelopmental BiologyTranscription FactorsDevelopmental biology
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Hyperplastic Conotruncal Endocardial Cushions and Transposition of Great Arteries in Perlecan-Null Mice

2002

Perlecan is a heparan-sulfate proteoglycan abundantly expressed in pericellular matrices and basement membranes during development. Inactivation of the perlecan gene in mice is lethal at two developmental stages: around E10 and around birth. We report a high incidence of malformations of the cardiac outflow tract in perlecan-deficient embryos. Complete transposition of great arteries was diagnosed in 11 out of 15 late embryos studied (73%). Three of these 11 embryos also showed malformations of semilunar valves. Mesenchymal cells in the outflow tract were abnormally abundant in mutant embryos by E9.5, when the endocardial-mesenchymal transformation starts in wild-type embryos. At E10.5, mut…

animal structuresPhysiologyTransposition of Great VesselsMesenchymeMorphogenesisPerlecanBiologyMesodermExtracellular matrixMiceCoronary CirculationmedicineAnimalsEndocardiumMice KnockoutHyperplasiaMyocardiumEmbryogenesisMesenchymal stem cellNeural crestHeartArteriesAnatomyEmbryo MammalianImmunohistochemistryCell biologyKineticsPhenotypemedicine.anatomical_structureembryonic structuresbiology.proteinCardiology and Cardiovascular MedicineHeparan Sulfate ProteoglycansEndocardial Cushion DefectsCirculation Research
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