| Literature DB >> 22539340 |
Ramona Haji-Seyed-Javadi1, Sahar Jelodari-Mamaghani, Seyed Hassan Paylakhi, Shahin Yazdani, Naveed Nilforushan, Jian-Bing Fan, Brandy Klotzle, Mohammad Jafar Mahmoudi, Mohammad Jafar Ebrahimian, Noori Chelich, Ehsan Taghiabadi, Kambiz Kamyab, Catherine Boileau, Coro Paisan-Ruiz, Mostafa Ronaghi, Elahe Elahi.
Abstract
Latent transforming growth factor (TGF) beta-binding protein 2 (LTBP2) is an extracellular matrix (ECM) protein that associates with fibrillin-1 containing microfibrils. Various factors prompted considering LTBP2 in the etiology of isolated ectopia lentis and associated conditions such as Weill-Marchesani syndrome (WMS) and Marfan syndrome (MFS). LTBP2 was screened in 30 unrelated Iranian patients. Mutations were found only in one WMS proband and one MFS proband. Homozygous c.3529G>A (p.Val1177Met) was shown to cause autosomal recessive WMS or WM-like syndrome by several approaches, including homozygosity mapping. Light, fluorescent, and electron microscopy evidenced disruptions of the microfibrillar network in the ECM of the proband's skin. In conjunction with recent findings regarding other ECM proteins, the results presented strongly support the contention that anomalies in WMS patients are due to disruptions in the ECM. Heterozygous c.1642C >T (p.Arg548*) possibly contributed to MFS-related phenotypes, including ocular manifestations, mitral valve prolapse, and pectus excavatum, but was not cause of MFS.Entities:
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Year: 2012 PMID: 22539340 DOI: 10.1002/humu.22105
Source DB: PubMed Journal: Hum Mutat ISSN: 1059-7794 Impact factor: 4.878