KLF 转录因子抑制轴突再生的分子机制。
Molecular mechanisms of the suppression of axon regeneration by KLF transcription factors.
机构信息
University of Miami Miller School of Medicine, Miami, FL, USA.
Shiley Eye Center, University of California San Diego, La Jolla, CA, USA.
出版信息
Neural Regen Res. 2014 Aug 1;9(15):1418-21. doi: 10.4103/1673-5374.139454.
Molecular mechanisms of the Krüppel-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.
Krüppel 样转录因子家族（KLFs）的分子机制在增殖细胞中的研究多于在后有丝分裂细胞中，如神经元。我们最近发现，KLFs 调节中枢神经系统（CNS）神经元中的固有轴突生长能力，包括视网膜神经节细胞、海马和皮质神经元。至少有 17 个 KLF 家族成员在神经元中表达，至少有 5 个结构独特的亚家族，因此确定这个复杂家族如何在神经元中发挥作用以调节轴突生长和再生的复杂遗传程序非常重要。通过描述神经系统中 KLF 家族的分子机制，包括结合伙伴和基因靶标，并将其与定义在神经系统之外的机制进行比较，我们可以更好地理解 KLFs 如何调节神经突生长和轴突再生。
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