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自噬的转录和转录后调控。

Transcriptional and Post-Transcriptional Regulation of Autophagy.

机构信息

Guangdong Provincial Key Laboratory of Agro-animal Genomics and Molecular Breeding, College of Animal Science, South China Agricultural University, Guangzhou 510642, China.

Guangdong Laboratory for Lingnan Modern Agriculture, Guangzhou 510642, China.

出版信息

Cells. 2022 Jan 27;11(3):441. doi: 10.3390/cells11030441.

DOI:10.3390/cells11030441
PMID:35159248
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8833990/
Abstract

Autophagy is a widely conserved process in eukaryotes that is involved in a series of physiological and pathological events, including development, immunity, neurodegenerative disease, and tumorigenesis. It is regulated by nutrient deprivation, energy stress, and other unfavorable conditions through multiple pathways. In general, autophagy is synergistically governed at the RNA and protein levels. The upstream transcription factors trigger or inhibit the expression of autophagy- or lysosome-related genes to facilitate or reduce autophagy. Moreover, a significant number of non-coding RNAs (microRNA, circRNA, and lncRNA) are reported to participate in autophagy regulation. Finally, post-transcriptional modifications, such as RNA methylation, play a key role in controlling autophagy occurrence. In this review, we summarize the progress on autophagy research regarding transcriptional regulation, which will provide the foundations and directions for future studies on this self-eating process.

摘要

自噬是真核生物中广泛保守的过程,涉及一系列生理和病理事件,包括发育、免疫、神经退行性疾病和肿瘤发生。它通过多种途径受到营养剥夺、能量应激和其他不利条件的调节。一般来说,自噬在 RNA 和蛋白质水平上协同调控。上游转录因子触发或抑制自噬或溶酶体相关基因的表达,以促进或减少自噬。此外,大量非编码 RNA(microRNA、circRNA 和 lncRNA)被报道参与自噬调控。最后,转录后修饰,如 RNA 甲基化,在控制自噬发生中起着关键作用。在这篇综述中,我们总结了自噬研究在转录调控方面的进展,为进一步研究自噬这一自我吞噬过程提供了基础和方向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a0a/8833990/2bdbb88b6d11/cells-11-00441-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a0a/8833990/2bdbb88b6d11/cells-11-00441-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a0a/8833990/2bdbb88b6d11/cells-11-00441-g001.jpg

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