Search results for "MESH: Phenotype"

showing 10 items of 13 documents

Reverse-engineering the Arabidopsis thaliana transcriptional network under changing environmental conditions

2009

46 pages, 4 tables, 6 figures, 3 additinoal files.

0106 biological sciencesMESH: Genome PlantArabidopsis thalianaGene regulatory networkArabidopsis01 natural sciencesTranscriptomeGene Expression Regulation PlantArabidopsisMESH: Gene Expression Regulation DevelopmentalCluster AnalysisGene Regulatory NetworksMESH: ArabidopsisMESH: EcosystemMESH: Models GeneticOligonucleotide Array Sequence AnalysisMESH: Gene Regulatory NetworksGenetics0303 health sciencesMESH: Stress MechanicalbiologyMESH: Genomicsfood and beveragesGene Expression Regulation DevelopmentalGenomicsPhenotypeAlgorithmsGenome PlantMESH: MutationSystems biologyGenomicsMESH: AlgorithmsComputational biologyMESH: Arabidopsis ProteinsMESH: Phenotype03 medical and health sciencesMESH: Gene Expression Profiling[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Gene Expression Regulation PlantEcosystem030304 developmental biologyModels GeneticMicroarray analysis techniquesArabidopsis ProteinsGene Expression ProfilingResearchfungiRobustness (evolution)biology.organism_classificationMESH: Cluster AnalysisGene expression profilingMutationMESH: Oligonucleotide Array Sequence AnalysisStress Mechanical010606 plant biology & botany
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Arabidopsis thaliana nicotianamine synthase 4 is required for proper response to iron deficiency and to cadmium exposure.

2013

International audience; The nicotianamine synthase (NAS) enzymes catalyze the formation of nicotianamine (NA), a non-proteinogenic amino acid involved in iron homeostasis. We undertook the functional characterization of AtNAS4, the fourth member of the Arabidopsis thaliana NAS gene family. A mutant carrying a T-DNA insertion in AtNAS4 (atnas4), as well as lines overexpressing AtNAS4 both in the atnas4 and the wild-type genetic backgrounds, were used to decipher the role of AtNAS4 in NA synthesis, iron homeostasis and the plant response to iron deficiency or cadmium supply. We showed that AtNAS4 is an important source for NA. Whereas atnas4 had normal growth in iron-sufficient medium, it dis…

0106 biological sciences[ SDV.BV ] Life Sciences [q-bio]/Vegetal BiologyMESH : Azetidinecarboxylic AcidFMN ReductaseArabidopsis thalianaMutantArabidopsisGene ExpressionPlant Science01 natural sciencesMESH : Cation Transport ProteinsMESH : IronMESH : Arabidopsis ProteinsNicotianamine synthaseMESH : Plants Genetically Modifiedchemistry.chemical_compoundMESH : ArabidopsisGene Expression Regulation PlantGene expressionMESH: Genes PlantArabidopsis thalianaMESH : DNA BacterialHomeostasisMESH: ArabidopsisNicotianamineMESH: Stress PhysiologicalCation Transport ProteinsMESH : Adaptation PhysiologicalMESH : Cadmium2. Zero hungerchemistry.chemical_classification0303 health sciencesCadmiumMESH: IronbiologyGeneral MedicineIron DeficienciesPlants Genetically ModifiedAdaptation PhysiologicalMESH: Azetidinecarboxylic AcidMESH : PhenotypePhenotypeBiochemistryMESH: HomeostasisMESH : HomeostasisMESH : MutationAzetidinecarboxylic AcidCadmiumDNA BacterialMESH: Gene ExpressionMESH: MutationIronMESH: Cadmiumchemistry.chemical_elementMESH: FerritinsMESH: Arabidopsis ProteinsMESH: Alkyl and Aryl TransferasesGenes PlantMESH: PhenotypeNicotianamine synthase03 medical and health sciencesMESH: Cation Transport ProteinsStress PhysiologicalIron homeostasisGenetics[SDV.BV]Life Sciences [q-bio]/Vegetal BiologyIron deficiency (plant disorder)MESH: Gene Expression Regulation PlantMESH : Genes PlantMESH : Alkyl and Aryl TransferasesMESH : Stress Physiological030304 developmental biologyMESH : FMN ReductaseAlkyl and Aryl TransferasesArabidopsis ProteinsIron deficiencyNitric oxideNicotianaminebiology.organism_classificationMESH: Adaptation PhysiologicalMESH: DNA BacterialMESH : Gene ExpressionEnzymechemistryMESH: FMN ReductaseMESH: Plants Genetically ModifiedFerritinsMutationbiology.proteinMESH : FerritinsAgronomy and Crop ScienceMESH : Gene Expression Regulation Plant010606 plant biology & botany
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Wiedemann-Steiner syndrome as a major cause of syndromic intellectual disability: A study of 33 French cases.

2018

International audience; Wiedemann-Steiner syndrome (WSS) is a rare syndromic condition in which intellectual disability (ID) is associated with hypertrichosis cubiti, short stature, and characteristic facies. Following the identification of the causative gene (KMT2A) in 2012, only 31 cases of WSS have been described precisely in the literature. We report on 33 French individuals with a KMT2A mutation confirmed by targeted gene sequencing, high-throughput sequencing or exome sequencing. Patients' molecular and clinical features were recorded and compared with the literature data. On the molecular level, we found 29 novel mutations. We observed autosomal dominant transmission of WSS in 3 fami…

0301 basic medicineHypertrichosisMalePediatrics[SDV]Life Sciences [q-bio]MESH: Magnetic Resonance ImagingPathognomonicMESH: ChildIntellectual disabilityMESH: SyndromeChildMESH: High-Throughput Nucleotide SequencingGenetics (clinical)Exome sequencingComputingMilieux_MISCELLANEOUSbiologyWiedemann-Steiner syndromeHigh-Throughput Nucleotide SequencingSyndromeKMT2AMESH: Amino Acid SubstitutionMagnetic Resonance Imaginghypertrichosis3. Good healthhairinessKMT2APhenotypeWiedemann-Steiner syndromeChild Preschoolcardiovascular systemFemaleDisease SusceptibilityFrancemedicine.symptomMESH: Tomography X-Ray ComputedMyeloid-Lymphoid Leukemia Proteinmedicine.medical_specialtyMESH: MutationAdolescentMESH: Disease SusceptibilityMESH: PhenotypeShort statureMESH: Intellectual Disability03 medical and health sciencesHypertrichosis cubitiIntellectual DisabilityGeneticsmedicineHumanshistone methylationMESH: Adolescent[SDV.GEN]Life Sciences [q-bio]/GeneticsMESH: Humansbusiness.industryMESH: Child PreschoolMESH: Histone-Lysine N-MethyltransferaseHistone-Lysine N-Methyltransferasemedicine.diseaseMESH: MaleMESH: France030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAmino Acid SubstitutionMESH: Myeloid-Lymphoid Leukemia ProteinMutationbiology.proteinbusinessTomography X-Ray ComputedMESH: FemaleClinical genetics
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Dominant variants in the splicing factor PUF60 cause a recognizable syndrome with intellectual disability, heart defects and short stature

2016

Item does not contain fulltext Verheij syndrome, also called 8q24.3 microdeletion syndrome, is a rare condition characterized by ante- and postnatal growth retardation, microcephaly, vertebral anomalies, joint laxity/dislocation, developmental delay (DD), cardiac and renal defects and dysmorphic features. Recently, PUF60 (Poly-U Binding Splicing Factor 60 kDa), which encodes a component of the spliceosome, has been discussed as the best candidate gene for the Verheij syndrome phenotype, regarding the cardiac and short stature phenotype. To date, only one patient has been reported with a de novo variant in PUF60 that probably affects function (c.505C>T leading to p.(His169Tyr)) associated wi…

0301 basic medicineMaleMESH: Heart Defects Congenital / physiopathologyMicrocephalyPathologyMESH: Heart Defects Congenital / geneticsMESH: Exome / genetics030105 genetics & heredityMESH: RNA Splicing / geneticsMicrophthalmia[SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseasesMESH: ChildExomeMESH: RNA Splicing Factors / geneticsChildFrameshift MutationMESH: High-Throughput Nucleotide SequencingGenetics (clinical)Exome sequencingColobomaMESH: Frameshift MutationHigh-Throughput Nucleotide SequencingMicrodeletion syndromeMicrocephaly Verheij syndrome PUF60ChemistryPhenotypeChild PreschoolDISEASESMicrocephalyMedical geneticsFemaleRNA Splicing Factorsmedicine.symptomChromosome DeletionChromosomes Human Pair 8MESH: Dwarfism / genetics*Heart Defects Congenitalmedicine.medical_specialtyGENESAdolescentRNA SplicingMESH: Chromosome DeletionDwarfismBiologyMESH: PhenotypeShort statureArticlePUF6003 medical and health sciencesInternal medicineIntellectual Disability[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyGeneticsmedicineHumansCraniofacialBiologyMESH: AdolescentNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]MESH: HumansMESH: Child Preschoolmedicine.diseaseMESH: Repressor Proteins / geneticsMESH: MaleRepressor Proteins030104 developmental biologyEndocrinologyMESH: Chromosomes Human Pair 8 / geneticsMESH: Dwarfism / physiopathologyMESH: Intellectual Disability / physiopathologyHuman medicineMESH: Intellectual Disability / geneticsVerheij syndromeMESH: Female[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Human Haemato-Endothelial Precursors: Cord Blood CD34+ Cells Produce Haemogenic Endothelium

2012

Embryologic and genetic evidence suggest a common origin of haematopoietic and endothelial lineages. In the murine embryo, recent studies indicate the presence of haemogenic endothelium and of a common haemato-endothelial precursor, the haemangioblast. Conversely, so far, little evidence supports the presence of haemogenic endothelium and haemangioblasts in later stages of development. Our studies indicate that human cord blood haematopoietic progenitors (CD34+45+144-), triggered by murine hepatocyte conditioned medium, differentiate into adherent proliferating endothelial precursors (CD144+CD105+CD146+CD31+CD45-) capable of functioning as haemogenic endothelium. These cells, proven to give…

CD31MouseCellular differentiationMESH: HematopoiesisAntigens CD34murine hepatocytesMESH: CadherinsMESH: HepatocytesMice0302 clinical medicineMolecular Cell BiologyHematopoiesiHepatocyteMESH: Animalsendothelial lineageMESH: Antigens CDCells Cultured0303 health sciencesMultidisciplinaryMESH: Culture Media ConditionedStem CellsMedicine (all)QMESH: Infant NewbornRMESH: HemangioblastsAntigens CD45Cell DifferentiationAnimal ModelsCadherinsFetal BloodCell biologyAdult Stem CellsHaematopoiesisPhenotypeconditioned mediummedicine.anatomical_structureCord bloodMedicineHemangioblastCD146Cellular TypesAnimals; Antigens CD; Antigens CD34; Antigens CD45; Cadherins; Cell Adhesion; Cell Differentiation; Cell Shape; Cells Cultured; Culture Media Conditioned; Fetal Blood; Hemangioblasts; Hematopoiesis; Hepatocytes; Humans; Immunophenotyping; Infant Newborn; Mice; Phenotype; Agricultural and Biological Sciences (all); Biochemistry Genetics and Molecular Biology (all); Medicine (all)Research ArticleHumanMESH: Cells Culturedendothelial lineage; murine hepatocytes; conditioned mediumMESH: Cell DifferentiationMESH: ImmunophenotypingEndotheliumHemangioblastsScienceMESH: Antigens CD45[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyMESH: PhenotypeImmunophenotypingMESH: Cell Adhesion03 medical and health sciencesModel OrganismsAntigens CDCell AdhesionmedicineAnimalsHumansMESH: Cell ShapeMESH: Fetal BloodProgenitor cellBiologyCell ShapeMESH: Mice030304 developmental biologyBiochemistry Genetics and Molecular Biology (all)MESH: HumansAnimalInfant NewbornMESH: Antigens CD34Hematopoietic Stem CellsHemangioblastHematopoiesisAgricultural and Biological Sciences (all)Culture Media ConditionedImmunologyHepatocytesCadherinLeukocyte Common Antigens030217 neurology & neurosurgeryDevelopmental BiologyPLoS ONE
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The FBN2 gene: new mutations, locus-specific database (Universal Mutation Database FBN2), and genotype-phenotype correlations.

2009

International audience; Congenital contractural arachnodactyly (CCA) is an extremely rare disease, due to mutations in the FBN2 gene encoding fibrillin-2. Another member of the fibrillin family, the FBN1 gene, is involved in a broad phenotypic continuum of connective-tissue disorders including Marfan syndrome. Identifying not only what is in common but also what differentiates these two proteins should enable us to better comprehend their respective functions and better understand the multitude of diseases in which these two genes are involved. In 1995 we created a locus-specific database (LSDB) for FBN1 mutations with the Universal Mutation Database (UMD) tool. To facilitate comparison of …

Fibrillin-2MESH : Polymorphism GeneticFibrillin-1DNA Mutational AnalysisMESH : Genotype[SDV.GEN] Life Sciences [q-bio]/Geneticscomputer.software_genreMESH: Genotype0302 clinical medicineGenotypeDatabases GeneticMissense mutationCongenital contractural arachnodactylyMESH: DNA Mutational AnalysisGenetics (clinical)MESH: Databases GeneticRegulation of gene expressionGenetics0303 health sciencesDatabaseMESH : Gene Expression RegulationMicrofilament ProteinsPhenotypeMESH: Gene Expression RegulationBeals-Hecht syndrome3. Good healthINCMESH : PhenotypePhenotypeMESH : MutationFibrillinmusculoskeletal diseasesMESH: MutationGenotypeMESH : Microfilament Proteinsdatabase OFFICIAL JOURNAL wwwhgvsorg & 2008 WILEY-LISSLocus (genetics)fibrillinMESH : DNA Mutational AnalysisBiologyFibrillinsMESH: PhenotypeMESH: Sequence Homology Nucleic Acidcongenital contractural arachnodactyly03 medical and health sciencesMESH: Microfilament ProteinsSequence Homology Nucleic AcidMESH: Polymorphism GeneticGeneticsmedicineHumansMESH : Sequence Homology Nucleic AcidFBN2CCAMESH : Databases GeneticGene030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsPolymorphism GeneticMESH: HumansMESH : Humansmedicine.diseaseGene Expression RegulationMutation[ SDV.GEN ] Life Sciences [q-bio]/Geneticscomputer030217 neurology & neurosurgery
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Ageing, longevity, exceptional longevity and related genetic and non genetics markers: panel statement

2018

In May 2012, a group of scientists and clinicians met in Athens (Greece) to consider the relevance of ageing, longevity, exceptional longevity and related genetic and non genetic markers. During this meeting, we firstly reviewed recent epidemiological and clinical studies on ageing, longevity and exceptional longevity, briefly analysed the ageing theories and discussed successful and unsuccessful ageing also taking into account the evolutionary perspective. Secondly, we considered the three phenotypes based on the definition of ageing, longevity and exceptional longevity and the associated biomarkers. Third, we discussed proposed treatments suitable to counteract or slow down ageing. Finall…

Genetic MarkersGerontologyAgingStatement (logic)media_common.quotation_subjectLongevityMESH: Genetic MarkersBiologyMESH: Phenotype[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemGenetic MarkerAnimalsHumansMESH: AgingMESH: AnimalsComputingMilieux_MISCELLANEOUSmedia_commonPharmacologyMESH: HumansAnimalLongevityCongresses as TopicPhenotypeAgeing Longevity Age-related diseasesMESH: LongevityAgeingBiological MarkerMESH: BiomarkersCardiology and Cardiovascular MedicineMESH: Congresses as TopicBiomarkersHuman
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Increased Susceptibility to Skin Carcinogenesis Associated with a Spontaneous Mouse Mutation in the Palmitoyl Transferase Zdhhc13 Gene

2015

International audience; Here we describe a spontaneous mutation in the Zdhhc13 (zinc finger, DHHC domain containing 13) gene (also called Hip14l), one of 24 genes encoding palmitoyl acyltransferase (PAT) enzymes in the mouse. This mutation (Zdhhc13luc) was identified as a nonsense base substitution, which results in a premature stop codon that generates a truncated form of the ZDHHC13 protein, representing a potential loss-of-function allele. Homozygous Zdhhc13luc/Zdhhc13luc mice developed generalized hypotrichosis, associated with abnormal hair cycle, epidermal and sebaceous gland hyperplasia, hyperkeratosis, and increased epidermal thickness. Increased keratinocyte proliferation and accel…

KeratinocytesPathologySkin NeoplasmsMutantMESH: Codon TerminatorMESH: Epidermal Cellsmedicine.disease_causeBiochemistryMESH: Acyltransferases / genetics*MESH: Keratinocytes / physiologyMice0302 clinical medicineHair cycleMESH: AnimalsPalmitoyl acyltransferase0303 health sciencesintegumentary systemNF-kappa B3. Good healthPhenotypemedicine.anatomical_structureNeutrophil Infiltration030220 oncology & carcinogenesisCodon TerminatorKeratinocytemedicine.medical_specialtyClinical SciencesOncology and CarcinogenesisDermatologyBiologyMESH: PhenotypeMESH: Skin Neoplasms / etiologyArticleMESH: Skin Neoplasms / genetics*03 medical and health sciencesMESH: Genetic Predisposition to Disease*medicineAnimalsGenetic Predisposition to DiseaseTerminatorMESH: NF-kappa B / physiologyCodonMESH: MiceMolecular Biology030304 developmental biologyEpidermis (botany)Dermatology & Venereal DiseasesMESH: Leukocyte Elastase / metabolismCell BiologyMESH: Bromodeoxyuridine / metabolismNFKB1Molecular biologyMESH: Neutrophil Infiltration[SDV.GEN.GA]Life Sciences [q-bio]/Genetics/Animal geneticsBromodeoxyuridineEpidermal CellsMutationNIH 3T3 CellsMESH: Mutation*Leukocyte ElastaseCarcinogenesisDHHC domainAcyltransferasesMESH: NIH 3T3 CellsJournal of Investigative Dermatology
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Genetics for Pseudoalteromonas provides tools to manipulate marine bacterial virus PM2

2008

ABSTRACT The genetic manipulation of marine double-stranded DNA (dsDNA) bacteriophage PM2 ( Corticoviridae ) has been limited so far. The isolation of an autonomously replicating DNA element of Pseudoalteromonas haloplanktis TAC125 and construction of a shuttle vector replicating in both Escherichia coli and Pseudoalteromonas enabled us to design a set of conjugative shuttle plasmids encoding tRNA suppressors for amber mutations. Using a host strain carrying a suppressor plasmid allows the introduction and analysis of nonsense mutations in PM2. Here, we describe the isolation and characterization of a suppressor-sensitive PM2 sus2 mutant deficient in the structural protein P10. To infect an…

MESH: Corticoviridae[SDV]Life Sciences [q-bio]Bacteriophages Transposons and PlasmidsMutantPlasmidPseudoalteromonasRNA TransferMESH: Genetic VectorsMESH: Models GeneticMESH: Capsid ProteinsGenetics0303 health sciencesbiologyMESH: Escherichia coliPseudoalteromonasMESH: Mutagenesis Site-DirectedPhenotypeMESH: DNA CircularElectrophoresis Polyacrylamide GelDNA CircularMESH: Genome ViralPlasmidsMESH: MutationGenetic VectorsGenome ViralMESH: PhenotypeMicrobiologyPseudoalteromonas haloplanktisViral Proteins03 medical and health sciencesShuttle vectorMESH: PlasmidsHost outer membraneEscherichia coliSeawaterMolecular Biology030304 developmental biologyModels Genetic030306 microbiologyMESH: PseudoalteromonasCorticoviridaeMESH: SeawaterViral membranebiology.organism_classificationMESH: RNA TransferMESH: Viral Proteins[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/BacteriologyMutationMutagenesis Site-DirectedCapsid ProteinsBacterial virusMESH: Electrophoresis Polyacrylamide Gel
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Human OX40 tunes the function of regulatory T cells in tumor and nontumor areas of hepatitis C virus-infected liver tissue.

2014

International audience; Regulatory T cells (Tregs) can be considered as a mixed population of distinct subsets, endowed with a diverse extent and quality of adaptation to microenvironmental signals. Here, we uncovered an opposite distribution of Treg expansion, phenotype, and plasticity in different microenvironments in the same organ (liver) derived from patients with chronic hepatitis C: On the one side, cirrhotic and tumor fragments were moderately and highly infiltrated by Tregs, respectively, expressing OX40 and a T-bet high IFN-c – " T-helper (Th)1-suppressing " phenotype; on the other side, noncirrhotic liver specimens contained low frequencies of Tregs that expressed low levels of O…

MESH: Receptors OX40/metabolism*MESH: Interleukin-12/metabolismLiver CirrhosisMaleMacrophagemedicine.disease_causeMESH: Carcinoma Hepatocellular/immunology*T-Lymphocytes RegulatoryMESH: OX40 Ligand/metabolism0302 clinical medicineMESH: Aged 80 and overMESH: T-Lymphocytes Regulatory/physiology*MESH: Up-RegulationOX40MESH: AgedAged 80 and over0303 health scienceseducation.field_of_studyT REGMESH: Middle AgedMedicine (all)MESH: Liver Cirrhosis/immunology*Liver Neoplasmshemic and immune systemsMiddle AgedMESH: Liver Neoplasms/immunology*PhenotypeHepatitis CInterleukin-123. Good healthUp-RegulationPhenotypeLiver Neoplasm[SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/VirologyInterleukin 12[SDV.IMM]Life Sciences [q-bio]/ImmunologyFemalemedicine.symptomMESH: Hepatitis C/immunology*OX40; T REG; HEPATITIS C VIRUSHumanmedicine.medical_specialtyCarcinoma HepatocellularHepatitis C virusLiver CirrhosiPopulationInflammationchemical and pharmacologic phenomena[SDV.CAN]Life Sciences [q-bio]/CancerOX40 LigandBiologyMESH: PhenotypeMESH: Liver Neoplasms/virology03 medical and health sciencesIkaros Transcription FactorDownregulation and upregulationInternal medicinemedicineHumansMESH: Macrophages/metabolismeducation030304 developmental biologyAgedMESH: HumansHepatologyMacrophagesHEPATITIS C VIRUSMESH: Carcinoma Hepatocellular/virologyHepatologyReceptors OX40MESH: Ikaros Transcription Factor/metabolismMESH: Hepatitis C/complicationsMESH: MaleOX40 ligandImmunologyMESH: Liver Cirrhosis/virologyMESH: Female030215 immunology
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