| Literature DB >> 15690106 |
Kamini Kalidas1, Adam C Shaw1, Andrew H Crosby1, Ruth Newbury-Ecob2, Lynn Greenhalgh2, Isabel K Temple3, Caroline Law3, Amisha Patel1, Michael A Patton1, Steve Jeffery4.
Abstract
LEOPARD syndrome (lentigines, electrocardiographic conduction abnormalities, ocular hypertelorism, pulmonary stenosis, abnormal genitalia, retardation of growth, and sensorineural deafness) is an autosomal dominant condition. The main clinical features include multiple lentigines, cardiovascular defects, and facial anomalies, some of which are shared with Noonan syndrome (NS). Recent reports have shown that LEOPARD syndrome can be caused by mutations in PTPN11, the gene in which mutations can produce NS. Here we report the findings of mutation screening and linkage analysis of PTPN11 in three families with LEOPARD syndrome. We identified a novel mutation in one family. The mutation (1529A>C) substitutes proline for glutamine at amino acid 510 (Gln510Pro). No variations in sequence were observed in the other two families, and negative LOD scores excluded linkage to the PTPN11 locus, showing that LEOPARD syndrome is genetically heterogeneous.Entities:
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Year: 2004 PMID: 15690106 DOI: 10.1007/s10038-004-0212-x
Source DB: PubMed Journal: J Hum Genet ISSN: 1434-5161 Impact factor: 3.172