ArticleMolecular medicine reports2017
A novel FBN1 mutation causes autosomal dominant Marfan syndrome.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 18 citations in OpenAlex.
- Surgical Outcomes of Lens Removal with or Without Intraocular Lens Implantation in Marfan Syndrome: A Retrospective Cohort Study.Clinical ophthalmology (Auckland, N.Z.) · 2025Article
- Contributions of Germline and Somatic Mosaic Genetics to Thoracic Aortic Aneurysms in Nonsyndromic Individuals.Journal of the American Heart Association · 2024Article
- Visual Outcomes in Ectopia Lentis in Marfan Syndrome: A Study of Four Surgical Techniques in Children and Adults.Medicina (Kaunas, Lithuania) · 2024Article
- Human DNA Mutations and their Impact on Genetic Disorders.Recent patents on biotechnology · 2024Review
- Treatment With Methotrexate Associated With Lipid Core Nanoparticles Prevents Aortic Dilation in a Murine Model of Marfan Syndrome.Frontiers in cardiovascular medicine · 2022Article
- Article
- Two Novel PathogenicGlobal medical genetics · 2020Article
- Mutation screening in the FBN1 gene responsible for Marfan syndrome and related disorder in Chinese families.Molecular genetics & genomic medicine · 2019Article
- A novel mutation inInternational journal of ophthalmology · 2019Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Marfan syndrome (MFS) is an inherited and systemic disorder. It has been reported that mutations in the fibrillin‑1 gene (FBN1) account for ~90% of autosomal dominant cases of MFS. This study was conducted to screen mutations of FBN1 in a Chinese family with autosomal dominant MFS; four individuals including two patients with MFS were recruited. The family members underwent complete physical, cardiovascular and ophthalmologic examinations. Genomic DNA samples were collected from the family along with 383 unrelated healthy subjects. FBN1 coding regions were amplified by polymerase chain reaction and analyzed by direct sequencing. SIFT and PolyPhen‑2 were used to predict the possible structural and functional alterations of the protein. A novel heterozygous mutation c.1708 T>G (p.C570G) in exon 14 was identified, which led to a substitution of cysteine by glycine at codon 570 (p.C570G). The mutation was identified as being associated with the MFS phenotype in the affected members of this family. However, the unaffected family members and the 383 normal controls lacked the mutation. Multiple sequence alignment of the human FBN1 protein revealed that this novel mutation occurred within a highly conserved region of the FBN1 protein across different species and may induce structural alterations in this functional domain. The spectrum of MFS‑associated mutations in the FBN1 gene has been enriched from this study; this may improve understanding of the molecular pathogenesis and clinical diagnosis of MFS.
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