Developmentally upregulated transcriptional elongation factor a like 3 suppresses axon regeneration after optic nerve injury.
Developmentally upregulated transcriptional elongation factor a like 3 suppresses axon regeneration after optic nerve injury.
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DOI：
10.1016/j.neulet.2021.136260
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发表时间：
2021-11-20
影响因子：
2.5
通讯作者：
Trakhtenberg EF
中科院分区：
文献类型：
--
作者：
Lukomska A;Kim J;Rheaume BA;Xing J;Hoyt A;Lecky E;Steidl T;Trakhtenberg EF
哺乳动物中枢神经系统（CNS）的投射神经元不会自发再生因损伤或疾病而受损的轴突，通常会给患者留下影响运动、认知或感觉功能的永久性残疾。虽然已经鉴定了几种在动物模型中促进一定程度的轴突再生的分子靶点，但所得到的恢复非常有限，并且CNS中轴突再生失败的分子机制仍然知之甚少。CNS中轴突再生的研究最多的靶标之一是mTOR途径。许多发育调控基因也被发现在CNS轴突再生中发挥作用。在这里，我们发现，转录延长因子A样3（Tceal 3），属于Bex/Tceal转录调节因子家族，也调节mTOR通路，在视网膜神经节细胞（RGC）投射CNS神经元中发育上调，并抑制它们在损伤后再生轴突的能力。
Projection neurons of the mammalian central nervous system (CNS) do not spontaneously regenerate axons which have been damaged by an injury or disease, often leaving patients with permanent disabilities that affect motor, cognitive, or sensory functions. Although several molecular targets which promote some extent of axon regeneration in animal models have been identified, the resulting recovery is very limited, and the molecular mechanisms underlying the axonal regenerative failure in the CNS are still poorly understood. One of the most studied targets for axon regeneration in the CNS is the mTOR pathway. A number of developmentally regulated genes also have been found to play a role in CNS axon regeneration. Here, we found that Transcriptional Elongation Factor A Like 3 (Tceal3), belonging to the Bex/Tceal transcriptional regulator family, which also modulates the mTOR pathway, is developmentally upregulated in retinal ganglion cell (RGCs) projection CNS neurons, and suppresses their capacity to regenerate axons after injury.
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影响因子：
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作者：
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