Search results for "Microcephaly"

showing 10 items of 70 documents

CEP63 deficiency promotes p53-dependent microcephaly and reveals a role for the centrosome in meiotic recombination

2015

Artículo escrito por un elevado número de autores, solo se referencian el que aparece en primer lugar, el nombre del grupo de colaboración, si le hubiere, y los autores pertenecientes a la UAM

MaleProgrammed cell deathMicrocephalyGeneral Physics and AstronomyCell Cycle ProteinsDwarfismBiologyReal-Time Polymerase Chain ReactionArticleGeneral Biochemistry Genetics and Molecular BiologyMice03 medical and health sciences0302 clinical medicineChromosome structureSpermatocytesmedicineAnimalscentrioleHomologous Recombination030304 developmental biologyRecombination GeneticfertilityGeneticsCentrosomeMeiotic recombination0303 health sciencesMultidisciplinarySperm CountProtein cep63FaciesGeneral Chemistrymedicine.diseaseBiología y Biomedicina / BiologíaImmunohistochemistryNeural stem cell3. Good healthCEP63MeiosisSeckel syndromeCentrosomeMicrocephalyTumor Suppressor Protein p53Homologous recombinationmicrocephaly ; DNA damage ; centrosome ; meiosis030217 neurology & neurosurgeryDNA Damage
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Perlecan controls neurogenesis in the developing telencephalon.

2006

This article is available from: http://www.biomedcentral.com/1471-213X/7/29

MaleTelencephalonLaminaOrganogenesisApoptosisCell CountNeocortexPerlecanExencephalyBiologyBasement MembraneMiceFetal Organ MaturityInterneuronsPregnancymedicineAnimalsHedgehog Proteinslcsh:QH301-705.5Embryonic Stem CellsCell ProliferationBasement membraneNeuronsCerebrumNeurogenesisAnatomymedicine.diseaseImmunohistochemistryCell biologyNeuroepithelial cellmedicine.anatomical_structurelcsh:Biology (General)embryonic structuresbiology.proteinMicrocephalyBasal laminaFemaleFibroblast Growth Factor 2Heparan Sulfate ProteoglycansDevelopmental BiologyResearch ArticleBMC developmental biology
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Clinical spectrum of eye malformations in four patients with Mowat-Wilson syndrome

2015

Mowat-Wilson syndrome (MWS) is a rare genetic syndrome characterized by a specific facial gestalt, intellectual deficiency, Hirschsprung disease and multiple congenital anomalies. Heterozygous mutations or deletions in the zinc finger E-box-binding homeobox2 gene (ZEB2) cause MWS. ZEB2 encodes for Smad-interacting protein 1, a transcriptional co-repressor involved in TGF-beta and BMP pathways and is strongly expressed in early stages of development in mice. Eye abnormalities have rarely been described in patients with this syndrome. Herein, we describe four patients (two males and two females; mean age 7 years) with MWS and eye malformations. Ocular anomalies included, iris/retinal coloboma…

Malemedicine.medical_specialtyAdolescentgenetic structuresMowat–Wilson syndromeRetinal Pigment EpitheliumBiologyEyeCataractchemistry.chemical_compoundAtrophyIntellectual DisabilityOphthalmologyGeneticsmedicineHumansHirschsprung Disease[SDV.MHEP.OS]Life Sciences [q-bio]/Human health and pathology/Sensory OrgansIris (anatomy)HyphemaGenetics (clinical)Zinc Finger E-box Binding Homeobox 2Homeodomain ProteinsRetinaFaciesOptic NerveRetinalAnatomymedicine.diseaseeye diseasesColobomaRepressor Proteinsmedicine.anatomical_structurechemistryChild PreschoolLens (anatomy)MutationMicrocephalyOptic nerveFemalesense organsAtrophy[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyAmerican Journal of Medical Genetics Part A
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Rubinstein–Taybi syndrome 2 with cerebellar abnormality and neural tube defect

2019

Rubinstein-Taybi syndrome (RSTS) is a rare dominant disorder with intellectual disability, postnatal growth deficiency, and multiple congenital anomalies. Approximately 50-70% of the patients have a mutation in the CREBBP gene (RSTS1) and 5-10% display an EP300 gene mutation (RSTS2). Craniospinal abnormalities such as microcranium, scoliosis, and lordosis are frequent findings in RSTS1, but malformations of the brain or spinal cord are seen only occasionally. Here, we report on a 3-year-old boy with facial abnormalities of RSTS, broad thumbs and halluces, developmental delay, autistic features, cerebellar underdevelopment, and a neural tube defect. Molecular diagnostic of the CREBBP and EP3…

Malespeech delayHeterozygoteCerebellumGenotypecerebellar abnormalityScoliosisGene mutationPathology and Forensic MedicineCerebellummedicinetethered cordHumansmicrocephalyGenetic TestingNeural Tube DefectsFrameshift MutationEP300Genetic Association StudiesGenetics (clinical)Sequence DeletionRubinstein-Taybi Syndromeautistic behaviorRubinstein–Taybi syndromeNeural tube defectGenome Humanbusiness.industryNeural tubeHigh-Throughput Nucleotide Sequencingstereotypic movementsvesicoureteral refluxOriginal Articleslumbosacral myeloceleExonsGeneral MedicineAnatomymedicine.diseaseSpinal cordCREB-Binding Proteinmedicine.anatomical_structuresyringohydromyeliaChild PreschoolMutationPediatrics Perinatology and Child Healthbroad thumbs and hallucesAnatomybusinessE1A-Associated p300 ProteinClinical Dysmorphology
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Characterization of a complex rearrangement involving chromosomes 1, 4 and 8 by fish and array-CGH

2012

Complex chromosomal rearrangements (CCRs) are structural aberrations involving more than two chromosomes with at least three breakpoints. CCRs can be divided into familial and de novo. Balanced CCR are extremely rare in humans and are at high risk of producing unbalanced gametes. Individuals with balanced CCR are usually phenotipically normal but report fertility problems, recurrent miscarriages or congenital anomalies in newborn offsprings as consequence of either meiotic failure or imbalanced chromosomes segregation.We describe the case of an unbalanced CCR involving chromosomes 1, 4 and 8 found in a girl with developmental delay, hexadactilia and microcephaly. The rearrangement, apparent…

MicrocephalyArray-CGHIntellectual disabilityChromosomal rearrangementBiologySettore MED/38 - Pediatria Generale E SpecialisticaFISHMeiosisGeneticsmedicineChromosomes HumanHumansIn Situ Hybridization FluorescenceGene RearrangementGeneticsComparative Genomic HybridizationComplex chromosomal rearrangementBreakpointInfant NewbornInfantChromosomeKaryotypeGeneral Medicinemedicine.diseaseHuman geneticsChromosome BandingSettore MED/03 - Genetica MedicaChromosomes Human Pair 1KaryotypingFish <Actinopterygii>FemaleChromosomes Human Pair 4Chromosomes Human Pair 8Journal of Applied Genetics
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Broadening the phenotypic spectrum and physiological insights related toEIF2S3variants

2021

Mental deficiency, epilepsy, hypogonadism, microcephaly and obesity (MEHMO) syndrome is a severe X-linked syndrome caused by pathogenic variants in EIF2S3. The gene encodes the γ subunit of the eukaryotic translation initiation factor-2, eIF2, essential for protein translation. A recurrent frameshift variant is described in severely affected patients while missense variants usually cause a moderate phenotype. We identified a novel missense variant (c.433A>G, p.(Met145Val)) in EIF2S3 in a mildly affected patient. Studies on zebrafish confirm the pathogenicity of this novel variant and three previously published missense variants. CRISPR/Cas9 knockout of eif2s3 in zebrafish embryos recapitula…

MicrocephalyFrameshift mutation03 medical and health sciencesGeneticsmedicineAnimalsHumansMissense mutationGenitaliaCRISPR/Cas9GeneZebrafishZebrafishGenetics (clinical)030304 developmental biologyGenetics0303 health scienceseIF2EIF2S3biology030305 genetics & heredityapoptosisbiology.organism_classificationmedicine.diseasePhenotypePhenotypeMutationMental Retardation X-LinkedEIF2S3MEHMO syndromeHuman Mutation
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Primary Microcephaly with Novel Variant of MCPH1 Gene in Twins: Both Manifesting in Childhood at the Same Time with Hashimoto's Thyroiditis

2020

AbstractThis study is a clinical report on twin females affected by primary microcephaly who displayed at molecular analysis of heterozygous novel MCPH1 variant. The twins at the age of 10 years developed, in coincidental time, a diagnosis of autoimmune juvenile thyroiditis. The main clinical features presented by the twins consisted of primary microcephaly with occipitofrontal circumference measuring −2 or −3 standard deviation, facial dysmorphism, typical nonsyndromic microcephaly, and mild intellectual disability. Molecular analysis of the major genes involved in primary microcephaly was performed and the following result was found in the twins: MCPH1; chr8.6357416; c.2180 C &gt; T (rs 1…

MicrocephalyPediatricsmedicine.medical_specialtyThyroiditisPathogenesis03 medical and health sciences0302 clinical medicineHashimoto's thyroiditisThyroid peroxidaseIntellectual disabilitymedicineGenetic predispositionMissense mutationGenetics (clinical)0303 health sciencesbiologybusiness.industryprimary microcephaly030305 genetics & hereditytwinsmedicine.diseaseThyroid disorderautoimmune juvenile thyroiditisPediatrics Perinatology and Child Healthbiology.proteinbusinessMCPH1 variants030217 neurology & neurosurgeryJournal of Pediatric Genetics
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Total retinal detachment caused by a KIF11 mutation.

2017

Purpose This is a case report of bilateral retinal detachment associated with KIF11 mutation. Methods In our university hospital, an 8-week-old patient presented with a potential bilateral congenital cataract, iris atrophy, and iridocorneal contact in the left eye. An examination revealed microcephaly and edema of the dorsa of the feet. The eye examination showed a clear lens in both eyes with a dislodged anterior chamber in the left eye with vessels drawn from the iris to the lens. A retrolental white bilateral mass with vessels was also observed. The MRI and the ultrasound revealed a potential peritoneal hyperplastic glass body. Bilateral retinal detachment was diagnosed during surgery. R…

Microcephalymedicine.medical_specialtyDNA Mutational AnalysisKinesinsRetina03 medical and health sciences0302 clinical medicineOphthalmologyDNA Mutational AnalysismedicineTotal retinal detachmentHumans030219 obstetrics & reproductive medicinemedicine.diagnostic_testbusiness.industryInfant NewbornRetinal DetachmentRetinal detachmentMagnetic resonance imagingGeneral Medicinemedicine.diseaseUniversity hospitalMagnetic Resonance ImagingOphthalmologyMutation (genetic algorithm)Mutation030221 ophthalmology & optometryFamilial exudative vitreoretinopathybusinessEuropean journal of ophthalmology
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Mutations in KATNB1 Cause Complex Cerebral Malformations by Disrupting Asymmetrically Dividing Neural Progenitors

2014

SummaryExome sequencing analysis of over 2,000 children with complex malformations of cortical development identified five independent (four homozygous and one compound heterozygous) deleterious mutations in KATNB1, encoding the regulatory subunit of the microtubule-severing enzyme Katanin. Mitotic spindle formation is defective in patient-derived fibroblasts, a consequence of disrupted interactions of mutant KATNB1 with KATNA1, the catalytic subunit of Katanin, and other microtubule-associated proteins. Loss of KATNB1 orthologs in zebrafish (katnb1) and flies (kat80) results in microcephaly, recapitulating the human phenotype. In the developing Drosophila optic lobe, kat80 loss specificall…

Microtubule-associated proteinNeurogenesisNeuroscience(all)Cell CountKataninSpindle ApparatusBiologymedicine.disease_causeArticleMice03 medical and health sciences0302 clinical medicineNeural Stem CellsNeuroblastmedicineAnimalsDrosophila ProteinsHumansProgenitor cellZebrafishMitosisZebrafishAdenosine TriphosphatasesMutationGeneral NeuroscienceOptic Lobe NonmammalianBrainDendritesbiology.organism_classificationSpindle apparatusmedicine.anatomical_structureCentrosome030220 oncology & carcinogenesisCerebral malformationsMutationMicrocephalybiology.proteinDrosophilaNeuronKataninMicrotubule-Associated ProteinsNeuroscienceCell Division030217 neurology & neurosurgery
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Case report: Novel compound heterozygosity for pathogenic variants in MED23 in a syndromic patient with postnatal microcephaly

2023

Biallelic loss-of-function variants in MED23 cause a recessive syndromic intellectual disability condition with or without epilepsy (MRT18). Due to the small number of reported individuals, the clinical phenotype of the disorder has not been fully delineated yet, and the spectrum and frequency of neurologic features have not been fully characterized. Here, we report a 5-year-old girl with compound heterozygous for two additional MED23 variants. Besides global developmental delay, axial hypotonia and peripheral increased muscular tone, absent speech, and generalized tonic seizures, which fit well MRT18, the occurrence of postnatal progressive microcephaly has been here documented. A retrospe…

NeurologyNeurology (clinical)case report epilepsy MED23 post-natal microcephaly whole exome sequencing
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