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Ⅴ型成骨不全症的一项重大突破。

A brilliant breakthrough in OI type V.

作者信息

Lazarus S, Moffatt P, Duncan E L, Thomas G P

机构信息

University of Queensland Diamantina Institute, Level 4, 37 Kent Street, Woolloongabba, QLD, 4102, Australia.

出版信息

Osteoporos Int. 2014 Feb;25(2):399-405. doi: 10.1007/s00198-013-2465-8. Epub 2013 Sep 13.

Abstract

Interferon-induced transmembrane protein 5 or bone-restricted ifitm-like gene (Bril) was first identified as a bone gene in 2008, although no in vivo role was identified at that time. A role in human bone has now been demonstrated with a number of recent studies identifying a single point mutation in Bril as the causative mutation in osteogenesis imperfecta type V (OI type V). Such a discovery suggests a key role for Bril in skeletal regulation, and the completely novel nature of the gene raises the possibility of a new regulatory pathway in bone. Furthermore, the phenotype of OI type V has unique and quite divergent features compared with other forms of OI involving defects in collagen biology. Currently it appears that the underlying genetic defect in OI type V may be unrelated to collagen regulation, which also raises interesting questions about the classification of this form of OI. This review will discuss current knowledge of OI type V, the function of Bril, and the implications of this recent discovery.

摘要

干扰素诱导跨膜蛋白5或骨限制性Ifitm样基因(Bril)于2008年首次被鉴定为骨基因,尽管当时未确定其体内作用。最近的多项研究表明,Bril中的一个单点突变是Ⅴ型成骨不全症(OI Ⅴ型)的致病突变,从而证明了其在人类骨骼中的作用。这一发现表明Bril在骨骼调节中起关键作用,而且该基因的全新性质增加了骨骼中存在新调节途径的可能性。此外,与涉及胶原蛋白生物学缺陷的其他形式的OI相比,OI Ⅴ型的表型具有独特且差异很大的特征。目前看来,OI Ⅴ型潜在的基因缺陷可能与胶原蛋白调节无关,这也引发了关于这种形式的OI分类的有趣问题。本综述将讨论关于OI Ⅴ型的现有知识、Bril的功能以及这一最新发现的意义。

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