ArticleReproductive sciences (Thousand Oaks, Calif.)2021
A Novel Mutation in the Myosin Binding Protein C Gene in a Prader-Willi Syndrome Pedigree.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 2 citations in OpenAlex.
- Proteins and proteases of Prader-Willi syndrome: a comprehensive review and perspectives.Bioscience reports · 2022Review
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4 authors at 1 institution in 1 country.
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Abstract
Prader-Willi syndrome (PWS) is a neurogenetic disorder caused by deficiency expression of paternally imprinted genes of the chromosomal region 15. In this study, we report a novel mutation in the myosin binding protein C (MYBPC3) gene in a Prader-Willi syndrome pedigree. Next-generation sequencing (NGS) and Sanger sequencing were performed to define and confirm the MYBPC3 gene mutation. Bioinformatics analysis was also performed for the mutated MYBPC3 protein using available software tools. The proband was diagnosed as PWS with about 4.727Mb copy number missed in the long arm of chromosome 15 and treated with growth hormone on 0.3 IU/day. Sanger sequencing identified a novel heterozygous mutation in the MYBPC3 gene, c.2002C>G (p.R668G). Bioinformatics analysis suggested the variant disease-causing; the Pro residue at 668 in the MYBPC3 protein was highly conserved. Moreover, interactions among MYBPC3 and other proteins suggested the potential effects on the development of cardiomyopathies. This is the first report of PWS with MYBPC3 gene mutation. Besides general examinations, it is vital for physicians to amply molecular genetics to get an accurate diagnosis in the clinic especially for rare diseases.
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