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EVA1A 在生理和病理过程中通过调控自噬发挥重要作用。

EVA1A Plays an Important Role by Regulating Autophagy in Physiological and Pathological Processes.

机构信息

Henan International Joint Laboratory of Nuclear Protein Regulation, School of Basic Medical Sciences, Henan University, Kaifeng 475000, China.

出版信息

Int J Mol Sci. 2021 Jun 8;22(12):6181. doi: 10.3390/ijms22126181.

DOI:10.3390/ijms22126181
PMID:34201121
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8227468/
Abstract

Eva-1 homolog A (EVA1A) is regarded as TMEM166 (transmembrane protein 166) or FAM176A (family with sequence similarity 176) and a lysosome and endoplasmic reticulum-associated protein involved in regulating autophagy and apoptosis. EVA1A regulates embryonic neurogenesis, cardiac remodeling, islet alpha-cell functions, acute liver failure, and hepatitis B virus replication. However, the related mechanisms are not fully clear. Autophagy is a process in which cells transfer pathogens, abnormal proteins and organelles to lysosomes for degradation. It plays an important role in various physiological and pathological processes, including cancer, aging, neurodegeneration, infection, heart disease, development, cell differentiation and nutritional starvation. Recently, there are many studies on the important role of EVA1A in many physiological and pathological processes by regulating autophagy. However, the related molecular mechanisms need further study. Therefore, we summarize the above-mentioned researches about the role of EVA1A in physiological and pathological processes through regulating autophagy in order to provide theoretical basis for future researches.

摘要

Eva-1 同源物 A(EVA1A)被认为是 TMEM166(跨膜蛋白 166)或 FAM176A(与序列相似家族 176),是一种与溶酶体和内质网相关的蛋白,参与调节自噬和细胞凋亡。EVA1A 调节胚胎神经发生、心脏重塑、胰岛α细胞功能、急性肝衰竭和乙型肝炎病毒复制。然而,相关机制尚不完全清楚。自噬是细胞将病原体、异常蛋白和细胞器转移到溶酶体进行降解的过程。它在多种生理和病理过程中发挥着重要作用,包括癌症、衰老、神经退行性疾病、感染、心脏病、发育、细胞分化和营养饥饿。最近,有许多研究表明 EVA1A 通过调节自噬在许多生理和病理过程中发挥重要作用。然而,相关的分子机制需要进一步研究。因此,我们通过调节自噬总结了上述关于 EVA1A 在生理和病理过程中作用的研究,为未来的研究提供理论基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0fa8/8227468/6ee5b4018af5/ijms-22-06181-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0fa8/8227468/f5e285a82e91/ijms-22-06181-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0fa8/8227468/6ee5b4018af5/ijms-22-06181-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0fa8/8227468/f5e285a82e91/ijms-22-06181-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0fa8/8227468/6ee5b4018af5/ijms-22-06181-g002.jpg

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