遗传 ›› 2015, Vol. 37 ›› Issue (12): 1185-1193.doi: 10.16288/j.yczz.15-192

• 综述 • 上一篇    下一篇

哺乳动物胰岛素样生长因子酸不稳定亚基的结构与功能

李贵林, 牛丽莉, 刘海峰, 郭家中   

  1. 四川农业大学动物科技学院,成都 611130
  • 收稿日期:2015-05-04 出版日期:2015-12-20 发布日期:2015-09-23
  • 通讯作者: 郭家中,博士,讲师,研究方向:动物遗传育种。E-mail: jiazhong.guo@sicau.edu.cn E-mail:lgl403441236@foxmail.com
  • 作者简介:李贵林,硕士研究生,专业方向:动物遗传育种。E-mail: lgl403441236@foxmail.com
  • 基金资助:
    四川省教育厅科技项目(编号:15ZB0005)资助

Structure and function of insulin-like growth factor acid-labile subunits in mammalian homologues

Guilin Li, Lili Niu, Haifeng Liu, Jiazhong Guo   

  1. College of Animal Science and Technology, Sichuan Agricultural University, Chengdu 611130, China
  • Received:2015-05-04 Online:2015-12-20 Published:2015-09-23

摘要: 胰岛素样生长因子(Insulin-like growth factors, IGFs)信号系统是动物体内一条重要的信号通路,广泛作用于机体的生长、发育以及疾病的发生和发展等各种生命活动过程。尽管IGFs系统的各种配体、受体和结合蛋白分子的基因结构、功能及作用机制已被深入地研究,但是有关胰岛素样生长因子酸不稳定亚基(Insulin-like growth factor acid-labile subunit, IGFALS)的功能研究却一直局限于其延长IGFs半衰期方面。近年来,越来越多的研究表明IGFALS基因的突变和蛋白表达量的偏低均可能导致动物体生长发育的延迟甚至缺陷。本文综述了IGFALS基因序列特征、IGFALS蛋白的结构特点及其生物学功能以及表达调控的研究进展,旨在为IGFALS的功能及其作用机制的深入研究提供参考。

关键词: 胰岛素样生长因子酸不稳定亚基, 突变, 功能, 哺乳动物

Abstract: Insulin-like growth factors (IGFs) act as a critical signaling pathway in animals and play significant roles in body growth, development, and occurrence and progression of animal diseases. In the past, structural and functional studies of ligands, receptors and even specific binding proteins in the IGFs system have been extensively investigated. However, the functional study of insulin-like growth factor acid-labile subunit (IGFALS) mainly focused on the prolonging half-life of IGFs. Increasing number of studies indicated that mutations in the IGFALS DNA sequence and low expression level of IGFALS proteins can lead to growth and development retardation in animals. In this review, we summarize recent structural and functional studies of IGFALS in mammals, aiming to further identify detailed genetic mechanism of IGFALS.

Key words: insulin-like growth factor acid-labile subunit, mutations, function, mammals