A novel COL2A1 mutation causing spondyloepiphyseal dysplasia congenita in a Chinese family

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Whole-exome sequencing reveals a novel COL2A1 mutation in a patient with spondylo-epiphyseal dysplasia congenita.

Skeletal dysplasia is a group of disorders with more than 450 entities, many of which cannot be differentiated, especially during infancy, but could lead to different clinical courses and prognoses. In this study, we have described a case of a Thai infant with short stature, flat face, pectus carinatum, indirect inguinal hernia, platyspondyly, and generalized delayed endochondral ossification. ...

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A case report of spondyloepiphyseal dysplasia congenita.

Spondyloepiphyseal dysplasia congenita (SED) is a rare form of skeletal systemic disease, characterized by congenital dwarfism with a short trunk and epiphysial dysplasia in the long bones and vertebral bodies. Patients also frequently suffer from atlanto-axial instability due to os odontoideum. Compression of the spinal cord caused by atlanto-axial instability is a common, serious complication...

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Novel and recurrent COL2A1 mutations in Chinese patients with spondyloepiphyseal dysplasia.

Spondyloepiphyseal dysplasia (SED) is an autosomal dominant skeletal dysplasia characterized by short stature, abnormal epiphyses and flattened vertebral bodies. SED is mainly caused by mutations in the gene encoding the type II procollagen α-1 chain (COL2A1). We looked for mutations in COL2A1 in three unrelated Chinese families with SED. Putative mutations were confirmed by RFLP analysis. We i...

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BACKGROUND Mutations in the COL2A1 gene cause type II collagenopathies characterized by skeletal dysplasia with a wide spectrum of phenotypic severity. Most COL2A1 mutations located in the triple-helical region, and the glycine to bulky amino acid substitutions (e.g., glycine to serine) in the Gly-X-Y repeat were identified frequently. However, the same COL2A1 mutations are associated with diff...

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ژورنال

عنوان ژورنال: Journal of Clinical Laboratory Analysis

سال: 2021

ISSN: 0887-8013,1098-2825

DOI: 10.1002/jcla.23728