| Literature DB >> 17436255 |
Christiane Zweier1, Maarit M Peippo, Juliane Hoyer, Sergio Sousa, Armand Bottani, Jill Clayton-Smith, William Reardon, Jorge Saraiva, Alexandra Cabral, Ina Gohring, Koen Devriendt, Thomy de Ravel, Emilia K Bijlsma, Raoul C M Hennekam, Alfredo Orrico, Monika Cohen, Alexander Dreweke, Andre Reis, Peter Nurnberg, Anita Rauch.
Abstract
Pitt-Hopkins syndrome is a rarely reported syndrome of so-far-unknown etiology characterized by mental retardation, wide mouth, and intermittent hyperventilation. By molecular karyotyping with GeneChip Human Mapping 100K SNP arrays, we detected a 1.2-Mb deletion on 18q21.2 in one patient. Sequencing of the TCF4 transcription factor gene, which is contained in the deletion region, in 30 patients with significant phenotypic overlap revealed heterozygous stop, splice, and missense mutations in five further patients with severe mental retardation and remarkable facial resemblance. Thus, we establish the Pitt-Hopkins syndrome as a distinct but probably heterogeneous entity caused by autosomal dominant de novo mutations in TCF4. Because of its phenotypic overlap, Pitt-Hopkins syndrome evolves as an important differential diagnosis to Angelman and Rett syndromes. Both null and missense mutations impaired the interaction of TCF4 with ASCL1 from the PHOX-RET pathway in transactivating an E box-containing reporter construct; therefore, hyperventilation and Hirschsprung disease in patients with Pitt-Hopkins syndrome might be explained by altered development of noradrenergic derivatives.Entities:
Mesh:
Substances:
Year: 2007 PMID: 17436255 PMCID: PMC1852727 DOI: 10.1086/515583
Source DB: PubMed Journal: Am J Hum Genet ISSN: 0002-9297 Impact factor: 11.025