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致死性成骨不全与一个胶原蛋白基因缺失。长度多态性提供了另一种解释。

Lethal osteogenesis imperfecta and a collagen gene deletion. Length polymorphism provides an alternative explanation.

作者信息

Sykes B C, Ogilvie D J, Wordsworth B P

出版信息

Hum Genet. 1985;70(1):35-7. doi: 10.1007/BF00389455.

Abstract

A 300 base pair deletion near the 3'-end of the gene encoding Type II (cartilage) collagen has been implicated in the pathogenesis of perinatal lethal osteogenesis imperfecta. We have found similar deletions occurring at a high frequency in normal Asian Indian and West Indian populations generated by a length polymorphism just beyond the 3'-end of the gene. We suggest that this polymorphism provides an alternative explanation of the original results.

摘要

编码II型(软骨)胶原蛋白的基因3'端附近300个碱基对的缺失与围产期致死性成骨不全的发病机制有关。我们发现在正常的亚洲印度人和西印度人群中,由于该基因3'端外侧的长度多态性,类似的缺失以高频率发生。我们认为这种多态性为原始结果提供了另一种解释。

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