Search results for "Homeobox protein Nkx-2.5"

showing 6 items of 6 documents

Sema3a plays a role in the pathogenesis of CHARGE syndrome

2018

CHARGE syndrome is an autosomal dominant malformation disorder caused by heterozygous loss of function mutations in the chromatin remodeler CHD7. Chd7 regulates the expression of Sema3a, which also contributes to the pathogenesis of Kallmann syndrome, a heterogeneous condition with the typical features hypogonadotropic hypogonadism and an impaired sense of smell. Both features are common in CHARGE syndrome suggesting that SEMA3A may provide a genetic link between these syndromes. Indeed, we find evidence that SEMA3A plays a role in the pathogenesis of CHARGE syndrome. First, Chd7 is enriched at the Sema3a promotor in neural crest cells and loss of function of Chd7 inhibits Sema3a expression…

0301 basic medicineEmbryo NonmammalianKallmann syndromePHENOTYPIC SPECTRUMmedicine.disease_causeSeverity of Illness IndexEpigenesis GeneticPathogenesisAXON GUIDANCECHD7CHARGE syndromeXenopus laevis0302 clinical medicineHYPOGONADOTROPIC HYPOGONADISMPromoter Regions GeneticGenetics (clinical)GeneticsMutationGeneral MedicinePhenotypeDNA-Binding ProteinsNEURAL CREST CELLSNeural CrestHomeobox Protein Nkx-2.5MIGRATIONBiology03 medical and health sciencesHypogonadotropic hypogonadismKALLMANN-SYNDROMEGeneticsmedicineAnimalsHumansEpigeneticsSHORT STATUREMolecular BiologyLoss functionMUTATIONSGenetic Complementation TestDNA HelicasesSemaphorin-3AKallmann Syndromemedicine.diseaseDisease Models Animal030104 developmental biologyHEK293 CellsXENOPUS-EMBRYOSMutationCHARGE Syndrome030217 neurology & neurosurgery
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A systematic variant screening in familial cases of congenital heart defects demonstrates the usefulness of molecular genetics in this field

2016

International audience; The etiology of congenital heart defect (CHD) combines environmental and genetic factors. So far, there were studies reporting on the screening of a single gene on unselected CHD or on familial cases selected for specific CHD types. Our goal was to systematically screen a proband of familial cases of CHD on a set of genetic tests to evaluate the prevalence of disease-causing variant identification. A systematic screening of GATA4, NKX2-5, ZIC3 and Multiplex ligation-dependent probe amplification (MLPA) P311 Kit was setup on the proband of 154 families with at least two cases of non-syndromic CHD. Additionally, ELN screening was performed on families with supravalvula…

0301 basic medicineProbandMaleCardiomyopathy22q11.2Disease030204 cardiovascular system & hematologyBioinformatics0302 clinical medicinede-novoEpidemiology3 large registriesGenetics (clinical)zic3 mutationsGeneticsHigh-Throughput Nucleotide Sequencing3. Good healthPedigreeHomeobox Protein Nkx-2.5malformationsFemaleepidemiologyHeart Defects Congenitalmedicine.medical_specialtyGenetic counselingArticle03 medical and health sciences[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyMolecular geneticsGeneticsmedicineHumansMultiplex ligation-dependent probe amplificationGenetic TestingHomeodomain Proteinsdiseasebusiness.industryvariabilityGenetic Variationmedicine.diseaseGATA4 Transcription Factor030104 developmental biologyMutationEtiologycardiovascular defectsbusinessMultiplex Polymerase Chain Reactioncardiomyopathy[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyTranscription Factors
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Arsenic trioxide alters the differentiation of mouse embryonic stem cell into cardiomyocytes

2015

AbstractChronic arsenic exposure is associated with increased morbidity and mortality for cardiovascular diseases. Arsenic increases myocardial infarction mortality in young adulthood, suggesting that exposure during foetal life correlates with cardiac alterations emerging later. Here, we investigated the mechanisms of arsenic trioxide (ATO) cardiomyocytes disruption during their differentiation from mouse embryonic stem cells. Throughout 15 days of differentiation in the presence of ATO (0.1, 0.5, 1.0 μM) we analysed: the expression of i) marker genes of mesoderm (day 4), myofibrillogenic commitment (day 7) and post-natal-like cardiomyocytes (day 15); ii) sarcomeric proteins and their orga…

Fetal ProteinsSarcomeresMesodermTime FactorsCellular differentiationBlotting WesternConnexinFluorescent Antibody TechniqueGene ExpressionAntineoplastic AgentsActininBiologyArticleArsenicalsCell Linechemistry.chemical_compoundMiceArsenic TrioxideTroponin TSpheroids CellularGene expressionmedicineAnimalsActininMyocytes CardiacArsenic trioxideHomeodomain ProteinsSyncytiumMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionCell DifferentiationMouse Embryonic Stem CellsOxidesEmbryonic stem cellCell biologyBiomechanical PhenomenaGATA4 Transcription Factormedicine.anatomical_structurechemistryConnexin 43ImmunologyHomeobox Protein Nkx-2.5T-Box Domain ProteinsTroponin CTranscription FactorsScientific Reports
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In silico characterization of an Iroquois family-related homeodomain protein.

2005

Homeobox genes have been demonstrated to play important roles during cancer differentiation and embryonic development. The subset of Iroquois-related homeobox genes (IRXs) have furthermore been. demonstrated to be involved in several embryonic developmental processes such as patterning of the anterior-posterior and dorso-ventral axis, as well as specific regions of the central nervous system, and differentiation of the otic vesicle, branchial epithelium, and limbs. We have characterized a novel homeodomain protein and corresponding gene by means of computational biology. Since the protein sequence displayed high similarity to the human IRX proteins, the newly identified homeodomain protein …

TBX1EMX2Molecular Sequence DataHomeobox A1BiologyHomeobox protein Nkx-2.5NKX2-3MiceGene OrderGeneticsAnimalsHumansAmino Acid SequenceRNA MessengerPhylogenyZebrafishExpressed Sequence TagsHomeodomain ProteinsBase SequenceGene Expression ProfilingChromosome MappingComputational BiologyGeneral MedicineExonsZebrafish ProteinsMolecular biologyIntronsGenesPAX4HomeoboxOtic vesicleTranscription FactorsInternational journal of molecular medicine
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Tetralogy of Fallot as a Model to Study Cardiac Progenitor Cell Migration and Differentiation During Heart Development

2009

Tetralogy of Fallot (ToF) has long been considered a congenital disorder that occurs due to environmental alterations during gestation. Recently, several mutated genes have been discovered that are thought to be responsible for the malformations observed in ToF. These genetic mutations, which are microdeletions, are sporadic and are frequently also present in trisomy 21 patients. The ToF malformations can be lethal, but for the last 50 years, surgical repairs that place an artificial patch to repair the four features of ToF have improved the survival of patients with ToF. However, 0.5% to 6% of patients who survive after surgical repair of ToF die of sudden cardiac death caused by ventricul…

medicine.medical_specialtyOrganogenesisBiologyVentricular tachycardiaSudden cardiac deathHomeobox protein Nkx-2.5Cell MovementInternal medicinemedicineAnimalsHumansCell LineageCell ProliferationTetralogy of FallotHomeodomain ProteinsSurgical repairHeart developmentMyocardiumStem CellsGene Expression Regulation DevelopmentalCell DifferentiationToF Cardiac Stem Cellsmedicine.diseaseGATA4 Transcription Factormedicine.anatomical_structureVentricleMutationHomeobox Protein Nkx-2.5Tetralogy of FallotCardiologyCardiology and Cardiovascular MedicineTranscription FactorsCongenital disorderTrends in Cardiovascular Medicine
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Mutations in the NKX2.5 Gene and the PAX8 Promoter in a Girl with Thyroid Dysgenesis

2011

Screening of the known candidate genes involved in thyroid organogenesis has revealed mutations in a small subset of patients with congenital hypothyroidism due to thyroid dysgenesis (TD).We studied a girl with TD who had mutations in two transcription factors involved in thyroid development.Sequencing analysis of candidate genes involved in thyroid gland development revealed a new paternally inherited heterozygous mutation in the NKX2.5 gene (S265R) and a new maternally inherited heterozygous mutation in the PAX8 promoter region (-456CT). Both parents and a brother, who was also heterozygous for both mutations, were phenotypically normal. Immunofluorescence microscopy showed a correct nucl…

medicine.medical_specialtyendocrine systemendocrine system diseasesEndocrinology Diabetes and Metabolismmedicine.medical_treatmentClinical BiochemistryBiologyGene mutationDominant-Negative Mutationmedicine.disease_causeBiochemistryThyroid dysgenesisPAX8 Transcription FactorEndocrinologyInternal medicinemedicineCongenital HypothyroidismHumansPaired Box Transcription FactorsPromoter Regions GeneticGeneticsHomeodomain ProteinsMutationBiochemistry (medical)ThyroidJCEM Online: Brief Reportsmedicine.diseaseCongenital hypothyroidismmedicine.anatomical_structureEndocrinologyMutationThyroid DysgenesisCancer researchHomeobox Protein Nkx-2.5ThyroglobulinFemalePAX8Transcription Factors
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