| Literature DB >> 10545614 |
T Sahoo1, E W Johnson, J W Thomas, P M Kuehl, T L Jones, C G Dokken, J W Touchman, C J Gallione, S Q Lee-Lin, B Kosofsky, J H Kurth, D N Louis, G Mettler, L Morrison, A Gil-Nagel, S S Rich, J M Zabramski, M S Boguski, E D Green, D A Marchuk.
Abstract
Cerebral cavernous malformations (CCM) are congenital vascular anomalies of the brain that can cause significant neurological disabilities, including intractable seizures and hemorrhagic stroke. One locus for autosomal dominant CCM ( CCM1 ) maps to chromosome 7q21-q22. Recombination events in linked family members define a critical region of approximately 2 Mb and a shared disease haplotype associated with a presumed founder effect in families of Mexican-American descent points to a potentially smaller region of interest. Using a genomic sequence-based positional cloning strategy, we have identified KRIT1, encoding a protein that interacts with the Krev-1/rap1a tumor suppressor, as the CCM1 gene. Seven different KRIT1 mutations have been identified in 23 distinct CCM1 families. The identical mutation is present in 16 of 21 Mexican-American families analyzed, substantiating a founder effect in this population. Other Mexican-American and non-Hispanic Caucasian CCM1 kindreds harbor other KRIT1 mutations. Identification of a common Mexican-American mutation has potential clinical significance for presymptomatic diagnosis of CCM in this population. In addition, these data point to a key role for the Krev-1/rap1a signaling pathway in angiogenesis and cerebrovascular disease.Entities:
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Year: 1999 PMID: 10545614 DOI: 10.1093/hmg/8.12.2325
Source DB: PubMed Journal: Hum Mol Genet ISSN: 0964-6906 Impact factor: 6.150