Neurodegeneration: Keeping ATF4 on a Tight Leash.
Neurodegeneration: Keeping ATF4 on a Tight Leash.
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DOI：
10.3389/fncel.2017.00410
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发表时间：
2017
影响因子：
5.3
通讯作者：
Gorbatyuk M
中科院分区：
文献类型：
--
作者：
Pitale PM;Gorbatyuk O;Gorbatyuk M
内质网（ER）应激和ER应激反应（也称为未折叠蛋白反应（UPR））的激活在各种退行性疾病中是常见的。因此，普遍定期审议的信号成分目前正在成为干预和治疗人类疾病的潜在靶点。一个UPR信号成员，激活转录因子4（ATF 4），已被发现在许多病理条件下上调，指出靶向其表达的治疗潜力。在细胞中，ATF4控制多种信号传导途径，包括自噬、氧化应激、炎症和翻译，这表明ATF4在各种病理进展中的多方面作用。然而，ATF 4已被证明可以触发促生存和促死亡途径，这也许可以解释目前文献中关于靶向ATF 4用于临床应用的矛盾观点。在这篇综述中，我们总结了最近发表的研究，从我们的实验室和其他人，重点是治疗潜力的战略控制ATF 4表达在不同的视网膜和神经退行性疾病。
Activation of the endoplasmic reticulum (ER) stress and ER stress response, also known as the unfolded protein response (UPR), is common to various degenerative disorders. Therefore, signaling components of the UPR are currently emerging as potential targets for intervention and treatment of human diseases. One UPR signaling member, activating transcription factor 4 (ATF4), has been found up-regulated in many pathological conditions, pointing to therapeutic potential in targeting its expression. In cells, ATF4 governs multiple signaling pathways, including autophagy, oxidative stress, inflammation, and translation, suggesting a multifaceted role of ATF4 in the progression of various pathologies. However, ATF4 has been shown to trigger both pro-survival and pro-death pathways, and this, perhaps, can explain the contradictory opinions in current literature regarding targeting ATF4 for clinical application. In this review, we summarized recent published studies from our labs and others that focus on the therapeutic potential of the strategy controlling ATF4 expression in different retinal and neurodegenerative disorders.
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影响因子：
21.3
作者：
通讯作者：
--
DOI：
10.1073/pnas.88.9.3720
发表时间：
1991-05-01
影响因子：
11.1
作者：
HAI, T;CURRAN, T
通讯作者：
CURRAN, T
影响因子：
4.8
作者：
Bagheri-Yarmand, Rozita;Sinha, Krishna M.;Gagel, Robert F.
通讯作者：
Gagel, Robert F.
影响因子：
13.8
作者：
KARIN, M;SMEAL, T
通讯作者：
SMEAL, T
影响因子：
8
作者：
Chen D;Fan Z;Rauh M;Buchfelder M;Eyupoglu IY;Savaskan N
通讯作者：
Savaskan N