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TGFBR1 and TGFBR2 mutations in patients with features of Marfan syndrome and Loeys-Dietz syndrome.
- Source :
-
Human mutation [Hum Mutat] 2006 Aug; Vol. 27 (8), pp. 770-7. - Publication Year :
- 2006
-
Abstract
- Marfan syndrome (MFS) is an autosomal dominant connective tissue disorder characterized by manifestations in the cardiovascular, skeletal, ocular, and other organ systems. MFS type1 (MFS1) is caused by mutations in the gene encoding fibrillin (FBN1). Recently, the transforming growth factor-beta receptor-2 gene, TGFBR2, has been shown to be associated with a second type of this disorder with typically mild or absent ocular involvement (MFS type 2; MFS2). Several point mutations were found in the highly conserved serine/threonine kinase domain of TGFBR2. Mutations in both TGFBR1 and TGFBR2 are associated with Loeys-Dietz aortic aneurysm syndrome (LDS). We searched for TGFBR1 and TGFBR2 mutations in 41 unrelated patients fulfilling the diagnostic criteria of Ghent nosology or with the tentative diagnosis of Marfan syndrome, in whom mutations in the FBN1 coding region were not identified. In TGFBR1, two mutations and two polymorphisms were detected. In TGFBR2, five mutations and six polymorphisms were identified. Reexamination of patients with a TGFBR1 or TGFBR2 mutation revealed extensive clinical overlap between patients with MFS1, MFS2, and LDS.
- Subjects :
- Activin Receptors, Type I chemistry
Adolescent
Adult
Alleles
Aortic Aneurysm, Thoracic genetics
Child
Codon, Nonsense
Cohort Studies
DNA Mutational Analysis
Female
Humans
Male
Marfan Syndrome genetics
Middle Aged
Pedigree
Polymorphism, Genetic
Protein Serine-Threonine Kinases
Receptor, Transforming Growth Factor-beta Type I
Receptor, Transforming Growth Factor-beta Type II
Receptors, Transforming Growth Factor beta chemistry
Syndrome
Activin Receptors, Type I genetics
Aortic Aneurysm, Thoracic diagnosis
Marfan Syndrome diagnosis
Mutation, Missense
Receptors, Transforming Growth Factor beta genetics
Subjects
Details
- Language :
- English
- ISSN :
- 1098-1004
- Volume :
- 27
- Issue :
- 8
- Database :
- MEDLINE
- Journal :
- Human mutation
- Publication Type :
- Academic Journal
- Accession number :
- 16799921
- Full Text :
- https://doi.org/10.1002/humu.20354