Search results for "Embryonic Structures"

showing 10 items of 623 documents

A repetitive intracortical microstimulation pattern induces long-lasting synaptic depression in brain slices of the rat primary somatosensory cortex.

2000

Repetitive intracortical microstimulation (ICMS) applied to the rat primary somatosensory cortex (SI) in vivo was reported to induce reorganization of receptive fields and cortical maps. The present study was designed to exam- ine the effect of such an ICMS pattern applied to layer IV of brain slices containing SI on the efficacy of synaptic in- put to layer II/III. Effects of ICMS on the synaptic strength was quantified for the first synaptic component ( s1) of cor- tical field potentials (FPs) recorded from layer II/III of SI. FPs were evoked by stimulation in layer IV. The pattern of ICMS was identical to that used in vivo. However, stimula- tion intensity had to be raised to induce an a…

MaleLong-Term PotentiationNeurotransmissionIn Vitro TechniquesInhibitory postsynaptic potentialBicucullineReceptors N-Methyl-D-AspartateGABA AntagonistsRats Sprague-DawleymedicineAnimalsReceptors AMPASynaptic potentialNeuronal PlasticityChemistryGeneral NeuroscienceLong-term potentiationSomatosensory CortexBicucullineElectric StimulationRatsElectrophysiologyembryonic structuresSynaptic plasticitySynapsesExcitatory postsynaptic potentialNeuroscienceMicroelectrodesmedicine.drugExperimental brain research
researchProduct

NOTCH, a new signaling pathway implicated in holoprosencephaly.

2011

International audience; Genetics of Holoprosencephaly (HPE), a congenital malformation of the developing human forebrain, is due to multiple genetic defects. Most genes that have been implicated in HPE belong to the sonic hedgehog signaling pathway. Here we describe a new candidate gene isolated from array comparative genomic hybridization redundant 6qter deletions, DELTA Like 1 (DLL1), which is a ligand of NOTCH. We show that DLL1 is co-expressed in the developing chick forebrain with Fgf8. By treating chick embryos with a pharmacological inhibitor, we demonstrate that DLL1 interacts with FGF signaling pathway. Moreover, a mutation analysis of DLL1 in HPE patients revealed a three-nucleoti…

MaleMESH: Signal TransductionCandidate gene[SDV.GEN] Life Sciences [q-bio]/GeneticsChick EmbryoMESH: Amino Acid SequenceMESH: Base SequenceHoloprosencephalyMESH: Animals[SDV.BDD]Life Sciences [q-bio]/Development BiologyGenetics (clinical)Sequence DeletionGenetics0303 health sciencesReceptors NotchMESH: Androstenediols030305 genetics & heredityMESH: Infant NewbornIntracellular Signaling Peptides and ProteinsGeneral MedicineMESH: Sequence DeletionMESH: Chick EmbryoCell biologyembryonic structuresFemale[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]MESH: Membrane ProteinsSignal transductionMESH: HoloprosencephalySignal TransductionAdultmusculoskeletal diseasesCell signalingcongenital hereditary and neonatal diseases and abnormalitiesanimal structuresMolecular Sequence DataNotch signaling pathwayMESH: Sequence AlignmentBiologyArticle03 medical and health sciencesFGF8[SDV.BDD] Life Sciences [q-bio]/Development BiologyHoloprosencephalyAndrostenediolsGeneticsmedicineAnimalsHumans[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Amino Acid SequenceMolecular Biology030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsMESH: Molecular Sequence DataMESH: HumansBase SequenceInfant NewbornMembrane ProteinsMESH: Adultmedicine.diseaseMESH: MaleForebrainMutation testingMESH: Receptors NotchSequence AlignmentMESH: Female
researchProduct

The Genome of the Sea Urchin Strongylocentrotus purpuratus

2006

We report the sequence and analysis of the 814-megabase genome of the sea urchin Strongylocentrotus purpuratus , a model for developmental and systems biology. The sequencing strategy combined whole-genome shotgun and bacterial artificial chromosome (BAC) sequences. This use of BAC clones, aided by a pooling strategy, overcame difficulties associated with high heterozygosity of the genome. The genome encodes about 23,300 genes, including many previously thought to be vertebrate innovations or known only outside the deuterostomes. This echinoderm genome provides an evolutionary outgroup for the chordates and yields insights into the evolution of deuterostomes.

MaleMESH: Signal TransductionMESH: Sequence Analysis DNAMESH : Transcription FactorsMESH : Calcification PhysiologicGenomeMESH : Proteins0302 clinical medicineMESH : Embryonic DevelopmentMESH: Gene Expression Regulation DevelopmentalInnateMESH: Embryonic DevelopmentDevelopmentalNervous System Physiological PhenomenaMESH: AnimalsMESH: Proteins[SDV.BDD]Life Sciences [q-bio]/Development BiologyComplement ActivationComputingMilieux_MISCELLANEOUSMESH: Evolution MolecularMESH : Strongylocentrotus purpuratusGenetics0303 health sciencesMESH: Nervous System Physiological PhenomenaMultidisciplinaryGenomebiologyMedicine (all)MESH: Immunologic FactorsGene Expression Regulation DevelopmentalGenome projectMESH: Transcription FactorsMESH : Immunity InnateMESH : Complement ActivationMESH: GenesBacterial artificial chromosome (BAC)DeuterostomesStrongylocentrotus purpuratusVertebrate innovationsEchinodermMESH : Nervous System Physiological Phenomenaembryonic structuresMESH: Cell Adhesion MoleculesMESH : GenesMESH: Immunity InnateSequence AnalysisSignal TransductionMESH: Computational BiologyGenome evolutionMESH: Complement ActivationSequence analysisEvolutionMESH: Strongylocentrotus purpuratusMESH : MaleEmbryonic DevelopmentMESH : Immunologic FactorsArticleMESH: Calcification PhysiologicCalcificationMESH : Cell Adhesion MoleculesEvolution Molecular03 medical and health sciencesCalcification PhysiologicAnimalsImmunologic FactorsMESH: Genome[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH : Evolution MolecularPhysiologicGeneStrongylocentrotus purpuratus[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyMESH : Signal TransductionBacterial artificial chromosomeImmunityMolecularComputational BiologyProteinsAnimals; Calcification Physiologic; Cell Adhesion Molecules; Complement Activation; Computational Biology; Embryonic Development; Evolution Molecular; Gene Expression Regulation Developmental; Genes; Immunity Innate; Immunologic Factors; Male; Nervous System Physiological Phenomena; Proteins; Signal Transduction; Strongylocentrotus purpuratus; Transcription Factors; Genome; Sequence Analysis DNA; Medicine (all); MultidisciplinaryDNASequence Analysis DNAbiology.organism_classificationStrongylocentrotus purpuratusImmunity InnateMESH: MaleGene Expression RegulationGenesMESH : AnimalsMESH : Gene Expression Regulation DevelopmentalMESH : GenomeCell Adhesion Molecules030217 neurology & neurosurgeryMESH : Computational BiologyTranscription FactorsMESH : Sequence Analysis DNA
researchProduct

Bone morphogenetic protein-4 is required for mesoderm formation and patterning in the mouse.

1995

Bone morphogenetic protein-4 (BMP-4) is a member of the TGF-beta superfamily of polypeptide signaling molecules, closely related to BMP-2 and to Drosophila decapentaplegic (DPP). To elucidate the role of BMP-4 in mouse development the gene has been inactivated by homologous recombination in ES cells. Homozygous mutant Bmp-4tm1blh embryos die between 6.5 and 9.5 days p.c., with a variable phenotype. Most Bmp-4tm1blh embryos do not proceed beyond the egg cylinder stage, do not express the mesodermal marker T(Brachyury), and show little or no mesodermal differentiation. Some homozygous mutants develop to the head fold or beating heart/early somite stage or beyond. However, they are development…

MaleMesodermBrachyuryHeterozygoteanimal structuresMolecular Sequence DataBiologyCell LineMesodermEmbryonic and Fetal DevelopmentMiceGeneticsmedicineParaxial mesodermAnimalsCrosses GeneticDecapentaplegicBase SequenceChimeraStem CellsHomozygoteProteinsGastrulaCell biologyMice Inbred C57BLmedicine.anatomical_structureBone morphogenetic protein 5PhenotypeBone morphogenetic protein 4GDF6embryonic structuresMesoderm formationBone Morphogenetic ProteinsGene TargetingFemaleDevelopmental BiologyGenesdevelopment
researchProduct

Haploinsufficiency of the NOTCH1 receptor as a cause of Adams-Oliver syndrome with variable cardiac anomalies

2015

Background— Adams–Oliver syndrome (AOS) is a rare disorder characterized by congenital limb defects and scalp cutis aplasia. In a proportion of cases, notable cardiac involvement is also apparent. Despite recent advances in the understanding of the genetic basis of AOS, for the majority of affected subjects, the underlying molecular defect remains unresolved. This study aimed to identify novel genetic determinants of AOS. Methods and Results— Whole-exome sequencing was performed for 12 probands, each with a clinical diagnosis of AOS. Analyses led to the identification of novel heterozygous truncating NOTCH1 mutations (c.1649dupA and c.6049_6050delTC) in 2 kindreds in which AOS was segregat…

MaleModels MolecularProbandreceptorGene ExpressionHaploinsufficiencyNOTCH1Ectodermal DysplasiaMissense mutationExomeReceptor Notch1ChildExomeGenetics (clinical)GeneticsReverse Transcriptase Polymerase Chain ReactionAutosomal dominant traitMiddle AgedPedigreeembryonic structuresheart defectscardiovascular systemFemaleCardiology and Cardiovascular MedicineHaploinsufficiencySignal TransductionAdultHeart Defects CongenitalAdolescentLimb Deformities CongenitalNotch signaling pathwayBiologyArticleYoung AdultAdams-Oliver syndromeGeneticsmedicineHumansGenetic Predisposition to DiseaseGeneFamily HealthBase SequencecongenitalAdams-Oliver syndrome; genetics; haploinsufficiency; heart defects; congenital; receptor; NOTCH1; Cardiology and Cardiovascular Medicine; Genetics (clinical); GeneticsSequence Analysis DNAmedicine.diseaseProtein Structure TertiaryScalp DermatosesHuman medicineAdams–Oliver syndromeCirculation. Cardiovascular genetics
researchProduct

Stage-specific germ-cell marker genes are expressed in all mouse pluripotent cell types and emerge early during induced pluripotency.

2011

Embryonic stem cells (ESCs) generated from the in-vitro culture of blastocyst stage embryos are known as equivalent to blastocyst inner cell mass (ICM) in-vivo. Though several reports have shown the expression of germ cell/pre-meiotic (GC/PrM) markers in ESCs, their functional relevance for the pluripotency and germ line commitment are largely unknown. In the present study, we used mouse as a model system and systematically analyzed the RNA and protein expression of GC/PrM markers in ESCs and found them to be comparable to the expression of cultured pluripotent cells originated from the germ line. Further, siRNA knockdown experiments have demonstrated the parallel maintenance and independen…

MaleMouselcsh:MedicineGene ExpressionEmbryoid bodyCell Fate DeterminationMice0302 clinical medicineMolecular Cell BiologyNuclear Reprogramminglcsh:ScienceInduced pluripotent stem cellPromoter Regions Genetic0303 health sciencesMultidisciplinaryStem CellsGene Expression Regulation DevelopmentalAnimal ModelsCellular ReprogrammingChromatinChromatinMeiosismedicine.anatomical_structureBlastocyst Inner Cell Massembryonic structuresEpigeneticsBiological MarkersFemaleGerm cellResearch ArticleBivalent chromatinInduced Pluripotent Stem CellsBiologyCell Line03 medical and health sciencesModel OrganismsGeneticsmedicineAnimalsRNA MessengerGene NetworksEmbryonic stem cells (ESCs); germ layer cell typesBiology030304 developmental biologylcsh:RMolecular DevelopmentMolecular biologyEmbryonic stem cellGerm Cellslcsh:QGene FunctionChromatin immunoprecipitationBiomarkers030217 neurology & neurosurgeryDevelopmental Biology
researchProduct

Familial fatal fetal cardiomyopathy with isolated myocardial calcifications: A new syndrome?

2001

We describe three male sib fetuses with isolated myocardial calcifications resulting in intrauterine fetal death (IUFD) as early as the second trimester. No evidence for an underlying mitochondrial cytopathy, dystrophinopathy or myopathy was found. There were no signs of inflammation or a metabolic disorder, and the mother had no prenatal exposure of teratogenic drugs. Furthermore, no mutation in the Barth syndrome gene (G4.5) could be detected. Because isolated calcification of the heart and IUFD are not typical of any previously described inherited cardiomyopathy, it may represent a new familial fetal cardiomyopathy.

MaleMyocardial calcificationPathologymedicine.medical_specialtyHeart diseaseCardiomyopathyUltrasonography PrenatalFatal OutcomeFetusPregnancymedicineHumansMyopathyFetal DeathGenetics (clinical)Family HealthFetusbusiness.industryMyocardiumMetabolic disorderCalcinosisBarth syndromeSyndromemedicine.diseasePregnancy ComplicationsFetal DiseasesPregnancy Trimester Secondembryonic structuresFemalemedicine.symptomCardiomyopathiesbusinessCalcificationAmerican Journal of Medical Genetics
researchProduct

Bone morphogenetic protein 4 induces differentiation of colorectal cancer stem cells and increases their response to chemotherapy in mice.

2010

BACKGROUND & AIMS: The limited clinical response observed in many patients with colorectal cancer may be related to the presence of chemoresistant colorectal can- cer stem cells (CRC-SCs). Bone morphogenetic protein 4 (BMP4) promotes the differentiation of normal colonic stem cells. We investigated whether BMP4 might be used to induce differentiation of CRC-SCs and for therapeutic purposes. METHODS: CRC-SCs were isolated from 25 tumor samples based on expression of CD133 or using a selection culture medium. BMP4 expression and activity on CRC-SCs were evaluated in vitro; progeny of the stem cells were evaluated by immunofluorescence, immuno- blot, and flow cytometry analyses. The potential …

MaleOrganoplatinum CompoundsCellular differentiationDrug ResistanceApoptosisBone Morphogenetic Protein 4Colon Cancer; Drug Resistance; Neoplasia; Tumor Resistance to Chemotherapy; AC133 Antigen; Adenomatous Polyposis Coli; Aged; Aged 80 and over; Animals; Antigens CD; Antineoplastic Agents; Apoptosis; Bone Morphogenetic Protein 4; Cell Differentiation; Cells Cultured; Colorectal Neoplasms; Female; Fluorouracil; Glycoproteins; Humans; Male; Mice; Microsatellite Instability; Middle Aged; Mutation; Neoplastic Stem Cells; Organoplatinum Compounds; PTEN Phosphohydrolase; Peptides; Phosphatidylinositol 3-Kinase; Proto-Oncogene Proteins c-akt; Smad4 Protein; GastroenterologyMice80 and overBone morphogenetic protein receptorAC133 AntigenCells CulturedSmad4 ProteinAged 80 and overCulturedColon Cancerintegumentary systemGastroenterologyCell DifferentiationBMP4 colon stem cellsMiddle AgedCDOxaliplatinTumor Resistance to ChemotherapyBone morphogenetic protein 4Adenomatous Polyposis Coliembryonic structuresNeoplastic Stem CellsFemaleMicrosatellite InstabilityFluorouracilStem cellColorectal Neoplasmsanimal structuresCellsAntineoplastic AgentsBiologyBone morphogenetic proteinSettore MED/04 - PATOLOGIA GENERALECancer stem cellAntigens CDPTENAnimalsHumansAntigensneoplasmsPI3K/AKT/mTOR pathwayAgedGlycoproteinsNeoplasiaHepatologyPTEN Phosphohydrolasedigestive system diseasesMutationCancer researchbiology.proteinPhosphatidylinositol 3-KinasePeptidesProto-Oncogene Proteins c-aktGastroenterology
researchProduct

Sox-2 Positive Neural Progenitors in the Primate Striatum Undergo Dynamic Changes after Dopamine Denervation.

2013

The existence of endogenous neural progenitors in the nigrostriatal system could represent a powerful tool for restorative therapies in Parkinson's disease. Sox-2 is a transcription factor expressed in pluripotent and adult stem cells, including neural progenitors. In the adult brain Sox-2 is expressed in the neurogenic niches. There is also widespread expression of Sox-2 in other brain regions, although the neurogenic potential outside the niches is uncertain. Here, we analyzed the presence of Sox-2(+) cells in the adult primate (Macaca fascicularis) brain in naïve animals (N = 3) and in animals exposed to systemic administration of 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine to render th…

MalePathologyDopamineFluorescent Antibody Techniquelcsh:MedicineDopaminaStriatumchemistry.chemical_compoundNeural Stem CellsNeurobiology of Disease and RegenerationSox-2 PositiveNeurocièncieslcsh:Scienceeducation.field_of_studyMultidisciplinaryMPTPStem CellsCell DifferentiationNeurochemistryNeurodegenerative DiseasesParkinson DiseaseAnimal ModelsDopamine DenervationDenervationSubstantia NigraAdult Stem CellsNeurologyembryonic structuresMedicineNeural ProgenitorsCalretininNeurochemicalsMacaqueAdult stem cellmedicine.drugResearch Articlemedicine.medical_specialtyendocrine systemNeurogenesisPopulationSubstantia nigraModel OrganismsDevelopmental NeuroscienceDopamineInternal medicinemedicineAnimalsProgenitor celleducationBiologyurogenital systemSOXB1 Transcription Factorslcsh:RCorrectionCorpus StriatumMacaca fascicularisEndocrinologychemistrynervous systemlcsh:QDevelopmental BiologyNeurosciencePLoS ONE
researchProduct

Upregulation of activin-B and follistatin in pulmonary fibrosis: a translational study using human biopsies and a specific inhibitor in mouse fibrosi…

2014

Background: Activins are members of the TGF-ß superfamily of growth factors. First, we identified by expression array screening that activin-B and follistatin are upregulated in human idiopathic pulmonary fibrosis (IPF). Next, we wanted to clarify their specific role in lung fibrosis formation. Methods: We used specific antibodies for activin-A and -B subunits and follistatin to measure and localize their levels in idiopathic pulmonary fibrosis and control lung biopsies. To inhibit activin signaling, we used soluble activin type IIB receptor fused to the Fc portion of human IgG1 (sActRIIB-Fc) in two different mouse models of pulmonary fibrosis. Results: Activin-B and follistatin mRNA levels…

MalePathologyFollistatinPulmonary FibrosisPROTEINCell CountQuadriceps MuscleACTIVATIONIdiopathic pulmonary fibrosisMiceBMP-7FibrosisPulmonary fibrosisfollistatinInhibin-beta SubunitsGREMLINImmunity Cellularmedicine.diagnostic_testbiologyactivinsPIRFENIDONEPirfenidonerespiratory systemidiopathic pulmonary fibrosisMouse fibrosis model3. Good healthUp-RegulationActivinsmedicine.anatomical_structureACUTE EXACERBATIONmouse fibrosis modelembryonic structuresGROWTHBronchoalveolar Lavage Fluidhormones hormone substitutes and hormone antagonistsmedicine.drugResearch ArticleSignal TransductionPulmonary and Respiratory MedicineEXPRESSIONmedicine.medical_specialtyendocrine systemRecombinant Fusion ProteinseducationIdiopathic pulmonary fibrosisRespiratory MucosaAlveolar cellsINFLAMMATIONmedicineAnimalsHumansRNA MessengerLungbusiness.industrymedicine.diseaserespiratory tract diseasesMice Inbred C57BLPulmonary AlveoliDisease Models AnimalBronchoalveolar lavageProtein Biosynthesis3121 General medicine internal medicine and other clinical medicinebiology.proteinbusinessFollistatin
researchProduct