中国神经再生研究(英文版) ›› 2014, Vol. 9 ›› Issue (15): 1418-1421.doi: 10.4103/1673-5374.139454

• 观点:神经损伤修复保护与再生 • 上一篇    下一篇

KLF转录因子抑制轴突再生的分子机制

  

  • 收稿日期:2014-07-22 出版日期:2014-08-12 发布日期:2014-08-12

Molecular mechanisms of the suppression of axon regeneration by KLF transcription factors

Akintomide Apara 1, Jeffrey L. Goldberg 2   

  1. 1 University of Miami Miller School of Medicine, Miami, FL, USA
    2 Shiley Eye Center, University of California San Diego, La Jolla, CA, USA
  • Received:2014-07-22 Online:2014-08-12 Published:2014-08-12
  • Contact: Jeffrey L. Goldberg, M.D., Ph.D., Shiley Eye Center, University of California San Diego, 9415 Campus Point Dr. #0946, La Jolla, CA 92093, USA, jlgoldberg@ucsd.edu.

摘要:

转录因子(KLFs)的Kruppel-样家族的分子机制在增殖细胞中的研究比在有丝分裂后细胞中的研究更集中,如神经元。KLFs具有调节中枢神经系统神经元,包括视网膜神经节细胞,海马和皮层神经元内在细胞轴突生长的能力。至少有15/17 的KLF家族成员可在神经元中表达,其中至少有5种结构独特的亚科,这对决定了这一复杂的家族因子如何在神经元中调节轴突生长和再生的复杂遗传程序是很重要的。通过细节化神经系统中KLF家族的分子机制,包括结合配体和靶基因,并比较它们在神经系统之外定义的机制,我们可以更好地理解KLFs如何调控神经轴突生长和轴突再生。

Abstract:

Molecular mechanisms of the Kru?ppel-like family of transcription factors (KLFs) have been studied more in proliferating cells than in post-mitotic cells such as neurons. We recently found that KLFs regulate intrinsic axon growth ability in central nervous system (CNS) neurons including retinal ganglion cells, and hippocampal and cortical neurons. With at least 15 of 17 KLF family members expressed in neurons and at least 5 structurally unique subfamilies, it is important to determine how this complex family functions in neurons to regulate the intricate genetic programs of axon growth and regeneration. By characterizing the molecular mechanisms of the KLF family in the nervous system, including binding partners and gene targets, and comparing them to defined mechanisms defined outside the nervous system, we may better understand how KLFs regulate neurite growth and axon regeneration.