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2
Subcellular distribution and activity of mechanistic target of rapamycin in aged retinal pigment epithelium.雷帕霉素作用机制靶点在老年视网膜色素上皮细胞中的亚细胞分布及活性
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Regulating Set-β's Subcellular Localization Toggles Its Function between Inhibiting and Promoting Axon Growth and Regeneration.调节 Set-β 的亚细胞定位可使其在抑制和促进轴突生长和再生之间转换功能。
J Neurosci. 2014 May 21;34(21):7361-74. doi: 10.1523/JNEUROSCI.3658-13.2014.
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Inducible loss of one Apc allele in Lrig1-expressing progenitor cells results in multiple distal colonic tumors with features of familial adenomatous polyposis.Lrig1 表达祖细胞中一个 Apc 等位基因的诱导缺失导致具有家族性腺瘤性息肉病特征的多个远端结肠肿瘤。
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KLF9与JNK3相互作用以抑制成体中枢神经系统中的轴突再生。

KLF9 and JNK3 Interact to Suppress Axon Regeneration in the Adult CNS.

作者信息

Apara Akintomide, Galvao Joana, Wang Yan, Blackmore Murray, Trillo Allison, Iwao Keiichiro, Brown Dale P, Fernandes Kimberly A, Huang Abigail, Nguyen Tu, Ashouri Masoumeh, Zhang Xiong, Shaw Peter X, Kunzevitzky Noelia J, Moore Darcie L, Libby Richard T, Goldberg Jeffrey L

机构信息

Bascom Palmer Eye Institute.

Interdisciplinary Stem Cell Institute, and.

出版信息

J Neurosci. 2017 Oct 4;37(40):9632-9644. doi: 10.1523/JNEUROSCI.0643-16.2017. Epub 2017 Sep 4.

DOI:10.1523/JNEUROSCI.0643-16.2017
PMID:28871032
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5628408/
Abstract

Neurons in the adult mammalian CNS decrease in intrinsic axon growth capacity during development in concert with changes in Krüppel-like transcription factors (KLFs). KLFs regulate axon growth in CNS neurons including retinal ganglion cells (RGCs). Here, we found that knock-down of KLF9, an axon growth suppressor that is normally upregulated 250-fold in RGC development, promotes long-distance optic nerve regeneration in adult rats of both sexes. We identified a novel binding partner, MAPK10/JNK3 kinase, and found that JNK3 (c-Jun N-terminal kinase 3) is critical for KLF9's axon-growth-suppressive activity. Interfering with a JNK3-binding domain or mutating two newly discovered serine phosphorylation acceptor sites, Ser106 and Ser110, effectively abolished KLF9's neurite growth suppression and promoted axon regeneration These findings demonstrate a novel, physiologic role for the interaction of KLF9 and JNK3 in regenerative failure in the optic nerve and suggest new therapeutic strategies to promote axon regeneration in the adult CNS. Injured CNS nerves fail to regenerate spontaneously. Promoting intrinsic axon growth capacity has been a major challenge in the field. Here, we demonstrate that knocking down Krüppel-like transcription factor 9 (KLF9) via shRNA promotes long-distance axon regeneration after optic nerve injury and uncover a novel and important KLF9-JNK3 interaction that contributes to axon growth suppression and regenerative failure These studies suggest potential therapeutic approaches to promote axon regeneration in injury and other degenerative diseases in the adult CNS.

摘要

在发育过程中,成年哺乳动物中枢神经系统(CNS)中的神经元内在轴突生长能力会下降,这与Krüppel样转录因子(KLFs)的变化同步。KLFs调节包括视网膜神经节细胞(RGCs)在内的中枢神经系统神经元的轴突生长。在这里,我们发现,敲低KLF9(一种轴突生长抑制因子,在RGC发育过程中通常上调250倍)可促进成年雌雄大鼠的视神经长距离再生。我们鉴定出一种新的结合伴侣,即丝裂原活化蛋白激酶10/应激活化蛋白激酶3(MAPK10/JNK3)激酶,并发现JNK3(c-Jun氨基末端激酶3)对于KLF9的轴突生长抑制活性至关重要。干扰JNK3结合域或突变两个新发现的丝氨酸磷酸化受体位点Ser106和Ser110,可有效消除KLF9对神经突生长的抑制作用并促进轴突再生。这些发现证明了KLF9与JNK3相互作用在视神经再生失败中的新生理作用,并提出了促进成年中枢神经系统轴突再生的新治疗策略。受损的中枢神经系统神经无法自发再生。提高内在轴突生长能力一直是该领域的一项重大挑战。在这里,我们证明通过短发夹RNA(shRNA)敲低Krüppel样转录因子9(KLF9)可促进视神经损伤后的长距离轴突再生,并揭示了一种新的重要的KLF9-JNK3相互作用,这种相互作用导致轴突生长抑制和再生失败。这些研究提出了在成年中枢神经系统损伤和其他退行性疾病中促进轴突再生的潜在治疗方法。