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自噬的转录调控:机制与疾病

Transcriptional Regulation of Autophagy: Mechanisms and Diseases.

作者信息

Di Malta Chiara, Cinque Laura, Settembre Carmine

机构信息

Telethon Institute of Genetics and Medicine, Pozzuoli, Italy.

Department of Medical and Translational Sciences, University of Naples Federico II, Naples, Italy.

出版信息

Front Cell Dev Biol. 2019 Jul 2;7:114. doi: 10.3389/fcell.2019.00114. eCollection 2019.

DOI:10.3389/fcell.2019.00114
PMID:31312633
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6614182/
Abstract

Macro (Autophagy) is a catabolic process that relies on the cooperative function of two organelles: the lysosome and the autophagosome. The recent discovery of a transcriptional gene network that co-regulates the biogenesis and function of these two organelles, and the identification of transcription factors, miRNAs and epigenetic regulators of autophagy, demonstrated that this catabolic process is controlled by both transcriptional and post-transcriptional mechanisms. In this review article, we discuss the nuclear events that control autophagy, focusing particularly on the role of the MiT/TFE transcription factor family. In addition, we will discuss evidence suggesting that the transcriptional regulation of autophagy could be targeted for the treatment of human genetic diseases, such as lysosomal storage disorders (LSDs) and neurodegeneration.

摘要

巨自噬(自噬)是一种分解代谢过程,它依赖于两种细胞器的协同作用:溶酶体和自噬体。最近发现了一个共同调节这两种细胞器生物发生和功能的转录基因网络,以及自噬转录因子、微小RNA(miRNA)和表观遗传调节因子的鉴定,表明这种分解代谢过程受转录和转录后机制的控制。在这篇综述文章中,我们讨论了控制自噬的核内事件,特别关注MiT/TFE转录因子家族的作用。此外,我们还将讨论有证据表明自噬的转录调节可作为治疗人类遗传疾病的靶点,如溶酶体贮积症(LSDs)和神经退行性变。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd4f/6614182/a550b4f6de25/fcell-07-00114-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd4f/6614182/a550b4f6de25/fcell-07-00114-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd4f/6614182/a550b4f6de25/fcell-07-00114-g001.jpg

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Loss of Sirtuin 1 Alters the Secretome of Breast Cancer Cells by Impairing Lysosomal Integrity.Sirtuin 1 的缺失通过损害溶酶体完整性改变乳腺癌细胞的分泌组。
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Transcriptional regulation of autophagy-lysosomal function in BRAF-driven melanoma progression and chemoresistance.
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