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FAM134B在选择性内质网自噬及疾病中的关键作用。

The pivotal role of FAM134B in selective ER-phagy and diseases.

作者信息

Chen Wei, Mao Hui, Chen Linxi, Li Lanfang

机构信息

Institute of Pharmacy and Pharmacology, Hunan Provincial Key Laboratory of Tumor Microenvironment Responsive Drug Research, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang 421001, Hunan, China.

Institute of Pharmacy and Pharmacology, Hunan Provincial Key Laboratory of Tumor Microenvironment Responsive Drug Research, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang 421001, Hunan, China.

出版信息

Biochim Biophys Acta Mol Cell Res. 2022 Aug;1869(8):119277. doi: 10.1016/j.bbamcr.2022.119277. Epub 2022 Apr 25.

DOI:10.1016/j.bbamcr.2022.119277
PMID:35477002
Abstract

FAM134B is also known as the reticulophagy regulator 1 (RETREG1) or JK-1. FAM134B consists of two long hydrophobic fragments with a reticulon-homology domain, an N-terminal cytoplasmic domain, and a C-terminal cytoplasmic domain. FAM134B plays an important role in regulating selective ER-phagy, and is related to the occurrence and development of many diseases. In the present review, we describe theFAM134B molecular structure, subcellular localization, tissue distribution, and review its mechanisms of action during selective ER-phagy. Furthermore, we summarize the relationship between FAM134B and diseases, including neoplastic diseases, degenerative diseases, central nervous system disease, and infectious diseases. Considering the pleiotropic action of FAM134B, targeting FAM134B may be a potent therapeutic avenue for these diseases.

摘要

FAM134B也被称为网织自噬调节因子1(RETREG1)或JK-1。FAM134B由两个带有网织蛋白同源结构域的长疏水片段、一个N端胞质结构域和一个C端胞质结构域组成。FAM134B在调节选择性内质网自噬中起重要作用,并且与许多疾病的发生和发展有关。在本综述中,我们描述了FAM134B的分子结构、亚细胞定位、组织分布,并综述了其在选择性内质网自噬过程中的作用机制。此外,我们总结了FAM134B与疾病之间的关系,包括肿瘤性疾病、退行性疾病、中枢神经系统疾病和感染性疾病。鉴于FAM134B的多效性作用,靶向FAM134B可能是治疗这些疾病的有效途径。

相似文献

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The pivotal role of FAM134B in selective ER-phagy and diseases.FAM134B在选择性内质网自噬及疾病中的关键作用。
Biochim Biophys Acta Mol Cell Res. 2022 Aug;1869(8):119277. doi: 10.1016/j.bbamcr.2022.119277. Epub 2022 Apr 25.
2
FAM134B oligomerization drives endoplasmic reticulum membrane scission for ER-phagy.FAM134B 寡聚化驱动内质网膜分裂以进行 ER 自噬。
EMBO J. 2020 Mar 2;39(5):e102608. doi: 10.15252/embj.2019102608. Epub 2020 Jan 13.
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Excessive ER-phagy mediated by the autophagy receptor FAM134B results in ER stress, the unfolded protein response, and cell death in HeLa cells.过度的 ER-phagy 通过自噬受体 FAM134B 介导导致 HeLa 细胞内质网应激、未折叠蛋白反应和细胞死亡。
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Molecular dynamics simulations reveal how the reticulon-homology domain of the autophagy receptor RETREG1/FAM134B remodels membranes for efficient selective reticulophagy.分子动力学模拟揭示了自噬受体 RETREG1/FAM134B 的网质蛋白同源结构域如何重塑膜以实现有效的选择性网质溶酶体。
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Curvature induction and membrane remodeling by FAM134B reticulon homology domain assist selective ER-phagy.FAM134B 网质蛋白同源结构域诱导弯曲和重塑,协助选择性内质网自噬。
Nat Commun. 2019 May 30;10(1):2370. doi: 10.1038/s41467-019-10345-3.
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Family with sequence similarity 134 member B-mediated reticulophagy ameliorates hepatocyte apoptosis induced by dithiothreitol.家族性序列相似性 134 成员 B 介导的网质体自噬可改善二硫苏糖醇诱导的肝细胞凋亡。
World J Gastroenterol. 2022 Jun 21;28(23):2569-2581. doi: 10.3748/wjg.v28.i23.2569.
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MiT/TFE factors control ER-phagy via transcriptional regulation of FAM134B.MIT/TFE 因子通过 FAM134B 的转录调控控制 ER 自噬。
EMBO J. 2020 Sep 1;39(17):e105696. doi: 10.15252/embj.2020105696. Epub 2020 Jul 27.
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Degradation of STIM1 through FAM134B-mediated ER-phagy is potentially involved in cell proliferation.通过 FAM134B 介导的内质网自噬降解 STIM1 可能参与细胞增殖。
J Biol Chem. 2024 Sep;300(9):107674. doi: 10.1016/j.jbc.2024.107674. Epub 2024 Aug 14.
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MiR-142-5p/FAM134B Axis Manipulates ER-Phagy to Control PRRSV Replication.miR-142-5p/FAM134B 轴调控 ER 自噬以控制 PRRSV 复制。
Front Immunol. 2022 Jun 20;13:842077. doi: 10.3389/fimmu.2022.842077. eCollection 2022.
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Targeting FAM134B-mediated reticulophagy activates sorafenib-induced ferroptosis in hepatocellular carcinoma.靶向 FAM134B 介导的网质体自噬激活索拉非尼诱导的肝细胞癌铁死亡。
Biochem Biophys Res Commun. 2022 Jan 22;589:247-253. doi: 10.1016/j.bbrc.2021.12.019. Epub 2021 Dec 10.

引用本文的文献

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The intrinsically disordered regions of organellophagy receptors are interchangeable and control organelle fragmentation, ER-phagy and mitophagy flux.细胞器自噬受体的内在无序区域是可互换的,并控制细胞器碎片化、内质网自噬和线粒体自噬通量。
Nat Cell Biol. 2025 Sep;27(9):1431-1447. doi: 10.1038/s41556-025-01728-4. Epub 2025 Aug 4.
2
Membrane Contact Sites in Proteostasis and ER Stress Response.蛋白质稳态和内质网应激反应中的膜接触位点
Contact (Thousand Oaks). 2025 Jul 28;8:25152564251363050. doi: 10.1177/25152564251363050. eCollection 2025 Jan-Dec.
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FAM134B-mediated endoplasmic reticulum autophagy protects against cisplatin-induced spiral ganglion neuron damage.
FAM134B介导的内质网自噬可防止顺铂诱导的螺旋神经节神经元损伤。
Front Pharmacol. 2025 Jan 30;15:1462421. doi: 10.3389/fphar.2024.1462421. eCollection 2024.
4
FAM134B deletion exacerbates apoptosis and epithelial-to-mesenchymal transition in rat lungs exposed to hyperoxia.FAM134B缺失加剧了暴露于高氧环境的大鼠肺部的细胞凋亡和上皮-间质转化。
iScience. 2024 Jun 26;27(7):110385. doi: 10.1016/j.isci.2024.110385. eCollection 2024 Jul 19.
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Molecular characterization of wild-type and HSAN2B-linked FAM134B.野生型和 HSAN2B 连锁 FAM134B 的分子特征。
Mol Biol Rep. 2023 Jul;50(7):6005-6017. doi: 10.1007/s11033-023-08517-y. Epub 2023 Jun 5.