生长分化因子11:TGF-β超家族的新成员
DOI:
CSTR:
作者:
作者单位:

西安交通大学医学院第一附属医院,西安交通大学医学院第一附属医院

作者简介:

通讯作者:

中图分类号:

基金项目:

国家自然科学基金资助项目(81170383)


GDF11:a New Member of TGF-β Superfamily
Author:
Affiliation:

1st Affiliated Hospital, School of Medicine, Xi’an Jiaotong University,1st Affiliated Hospital, School of Medicine, Xi'an Jiaotong University

Fund Project:

This work was supported by a grant from The National Natural Science Foundation of China(81170383)

  • 摘要
  • |
  • 图/表
  • |
  • 访问统计
  • |
  • 参考文献
  • |
  • 相似文献
  • |
  • 引证文献
  • |
  • 资源附件
  • |
  • 文章评论
    摘要:

    生长分化因子11(growth differentiation factor 11,GDF11),是新近发现的TGF-β超家族成员,属于BMPs亚家族的一种分泌性蛋白.在早期胚胎发育中,GDF11通过负性调节作用,参与包括骨骼、肾脏、胰腺、视网膜、嗅神经等组织器官的形成和分化,是胚胎正常发育不可或缺的分子.近年来研究发现,GDF11有明显的改善大脑认知、逆转心肌肥厚、改善骨骼肌代谢等功能,显示出GDF11广泛的生物学活性和潜在的应用价值.然而,一项最新的研究报道得出与此相反的结果.本文从GDF11的发现、研究历程、结构、表达及表达调控、信号传导通路和功能方面概括GDF11的基本情况及研究现状,为今后的研究提供思路.

    Abstract:

    Secretory protein growth differentiation factor 11 (GDF11) is a newly identified member of the BMPs family and TGF-β superfamily. In early embryo, GDF11 modulates the development and differentiation of a number of vital tissues and organs such as spinal cord, olfactory receptor neurons, bones, kidney, retina, pancreas, etc, showing its essential role in the normal development of the embryo. Recent studies have exhibited that GDF11 significantly improves brain cognition, reverses myocardial hypertrophy and improves the metabolism of skeletal muscle, proposing a wide range of biological effects and its potential in clinical application as a senescence-reversing agent. However, a most recent research obtained opposite results. In this review we will introduce the up-to-date knowledge of GDF11, concerning its discovery and research history, structure, expression regulation, signal transduction pathways and functions in order to provide ideas for future research.

    参考文献
    相似文献
    引证文献
引用本文

李倩,郝志明.生长分化因子11:TGF-β超家族的新成员[J].生物化学与生物物理进展,2015,42(7):616-623

复制
分享
文章指标
  • 点击次数:
  • 下载次数:
  • HTML阅读次数:
  • 引用次数:
历史
  • 收稿日期:2015-01-25
  • 最后修改日期:2015-06-06
  • 接受日期:2015-06-11
  • 在线发布日期: 2015-07-20
  • 出版日期: 2015-07-20
关闭