Journal of medical genetics · 2002
De novo GLI3 mutation in acrocallosal syndrome: broadening the phenotypic spectrum of GLI3 defects and overlap with murine models.
Клинический случайСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Elson E, Perveen R, Donnai D, Wall S, Black G C M
Аннотация
Acrocallosal syndrome (ACS) is characterised by postaxial polydactyly, hallux duplication, macrocephaly, and absence of the corpus callosum, usually with severe developmental delay. The condition overlaps with Greig cephalopolysyndactyly syndrome (GCPS), an autosomal dominant disorder that results from mutations in the GLI3 gene. Here we report a child with agenesis of the corpus callosum and severe retardation, both cardinal features of ACS and rare in GCPS, who has a mutation in GLI3. Since others have excluded GLI3 in ACS, we suggest that ACS may represent a heterogeneous group of disorders that, in some cases, may result from a mutation in GLI3 and represent a severe, allelic form of GCPS. The finding is important for counselling families with suspected ACS.
Предметные рубрики MeSH
Abnormalities, MultipleAgenesis of Corpus CallosumAmino Acid SequenceAnimalsBase SequenceChild, PreschoolDNADNA Mutational AnalysisDNA-Binding ProteinsDisease Models, AnimalHumansIntellectual DisabilityKruppel-Like Transcription FactorsMaleMiceMolecular Sequence DataMutationNerve Tissue ProteinsPhenotypePolydactylyRepressor ProteinsSequence Homology, Amino AcidSequence Homology, Nucleic AcidSyndromeTranscription FactorsXenopus ProteinsZinc Finger Protein Gli3