Literature DB >> 14597039

A new mutation (Leu569Arg) within exon 13 of the TGFBI (BIGH3) gene causes lattice corneal dystrophy type I.

John F Warren1, Richard L Abbott, Michael K Yoon, J Brooks Crawford, William H Spencer, Todd P Margolis.   

Abstract

PURPOSE: To describe an American family with lattice corneal dystrophy type I, which associates with a novel mutation, Leu569Arg, of the TGFBI (BIGH3) gene.
DESIGN: Experimental study.
METHODS: Genomic DNA was extracted from buccal epithelial cells of four affected members of an American family with lattice corneal dystrophy type I. All 17 exons of the TGFBI gene were evaluated by PCR amplification and direct sequencing. Clinical and histologic data were also collected.
RESULTS: Three generations of this family have been positively diagnosed with lattice corneal dystrophy, indicating autosomal dominant inheritance. We identified a heterozygous point mutation that associates with the disease phenotype. The single base-pair substitution (T1753G) results in an amino acid substitution (Leu569Arg) in exon 13 of the TGFBI gene.
CONCLUSIONS: Substitution of arginine for leucine at position 569 of the TGFBI gene results in a form of lattice corneal dystrophy that is phenotypically similar to other genetically distinct forms of type I disease. This is the first report of disease correlated with changes in exon 13 of the TGFBI gene.

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Year:  2003        PMID: 14597039     DOI: 10.1016/s0002-9394(03)00541-5

Source DB:  PubMed          Journal:  Am J Ophthalmol        ISSN: 0002-9394            Impact factor:   5.258


  9 in total

1.  A novel H572R mutation in the transforming growth factor-beta-induced gene in a Thai family with lattice corneal dystrophy type I.

Authors:  La-Ongsri Atchaneeyasakul; Binoy Appukuttan; Sarinee Pingsuthiwong; Pa-Thai Yenchitsomanus; Adisak Trinavarat; Chatchawan Srisawat
Journal:  Jpn J Ophthalmol       Date:  2006 Sep-Oct       Impact factor: 2.447

2.  Development of a DNA chip for the diagnosis of the most common corneal dystrophies caused by mutations in the betaigh3 gene.

Authors:  So Young Yoo; Tae-Im Kim; Sang Yup Lee; Eung Kweon Kim; Ki Chang Keum; Nae Choon Yoo; Won Min Yoo
Journal:  Br J Ophthalmol       Date:  2007-01-10       Impact factor: 4.638

3.  Rapid genotyping for most common TGFBI mutations with real-time polymerase chain reaction.

Authors:  Shigeo Yoshida; Yoko Yamaji; Ayako Yoshida; Yoshihiro Noda; Yuji Kumano; Tatsuro Ishibashi
Journal:  Hum Genet       Date:  2005-03-03       Impact factor: 4.132

4.  A novel variant of combined granular-lattice corneal dystrophy associated with the Met619Lys mutation in the TGFBI gene.

Authors:  Anthony J Aldave; Vivek S Yellore; Baris Sonmez; Nirit Bourla; Andrew K Salem; M Ali Khan; Sylvia A Rayner; Ben J Glasgow
Journal:  Arch Ophthalmol       Date:  2008-03

5.  TGFBI (βIG-H3) is a diabetes-risk gene based on mouse and human genetic studies.

Authors:  Bing Han; Hongyu Luo; John Raelson; Jie Huang; Yun Li; Johanne Tremblay; Bing Hu; Shijie Qi; Jiangping Wu
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Authors:  Jayne S Weiss; H U Møller; Walter Lisch; Shigeru Kinoshita; Anthony J Aldave; Michael W Belin; Tero Kivelä; Massimo Busin; Francis L Munier; Berthold Seitz; John Sutphin; Cecilie Bredrup; Mark J Mannis; Christopher J Rapuano; Gabriel Van Rij; Eung Kweon Kim; Gordon K Klintworth
Journal:  Cornea       Date:  2008-12       Impact factor: 2.651

8.  A pathogenic variant in the transforming growth factor beta I (TGFBI) in four Iranian extended families segregating granular corneal dystrophy type II: A literature review.

Authors:  Aliasgar Mohammadi; Azam Ahmadi Shadmehri; Mahnaz Taghavi; Gholamhossein Yaghoobi; Mohammad Reza Pourreza; Mohammad Amin Tabatabaiefar
Journal:  Iran J Basic Med Sci       Date:  2020-08       Impact factor: 2.699

9.  TGF-β1 enhanced myocardial differentiation through inhibition of the Wnt/β-catenin pathway with rat BMSCs.

Authors:  Yang Lv; Xiu-Juan Li; Hai-Ping Wang; Bo Liu; Wei Chen; Lei Zhang
Journal:  Iran J Basic Med Sci       Date:  2020-08       Impact factor: 2.699

  9 in total

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