Disease-Associated Factors at the Endoplasmic Reticulum-Golgi Interface.

IF 2.5 3区生物学 Q3 CELL BIOLOGY Traffic Pub Date : 2025-01-01 DOI:10.1111/tra.70001

Miharu Maeda, Masashi Arakawa, Kota Saito

引用次数: 0

Abstract

The endoplasmic reticulum (ER)-Golgi interface is essential for directing the transport of proteins synthesized in the ER to the Golgi apparatus via the ER-Golgi intermediate compartment, as well as for recycling proteins back to the ER. This transport is facilitated by various components, including COPI and COPII coat protein complexes and the transport protein particle complex. Recently, the ER-Golgi transport pathway has gained attention due to emerging evidence of nonvesicular transport mechanisms and the regulation of trafficking through liquid-liquid phase separation. Numerous diseases have been linked to mutations in proteins localized at the ER-Golgi interface, highlighting the need for comprehensive analysis of these conditions. This review examines the disease phenotypes associated with dysfunctional ER-Golgi transport factors and explores their cellular effects, providing insights into potential therapeutic strategies.

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内质网-高尔基界面的疾病相关因素。

内质网(ER)-高尔基界面对于指导内质网合成的蛋白质通过ER-高尔基中间室转运到高尔基体以及将蛋白质再循环回内质网至关重要。这种转运是由多种成分促进的，包括COPI和COPII外壳蛋白复合物以及转运蛋白颗粒复合物。最近，er -高尔基转运途径引起了人们的关注，因为有证据表明非囊泡转运机制和通过液-液相分离调节转运。许多疾病都与内质网-高尔基界面蛋白的突变有关，这凸显了对这些疾病进行全面分析的必要性。本文综述了与er -高尔基转运因子功能失调相关的疾病表型，并探讨了它们的细胞效应，为潜在的治疗策略提供了见解。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Traffic 生物-细胞生物学

CiteScore

8.10

自引率

2.20%

发文量

审稿时长

2 months

期刊介绍： Traffic encourages and facilitates the publication of papers in any field relating to intracellular transport in health and disease. Traffic papers span disciplines such as developmental biology, neuroscience, innate and adaptive immunity, epithelial cell biology, intracellular pathogens and host-pathogen interactions, among others using any eukaryotic model system. Areas of particular interest include protein, nucleic acid and lipid traffic, molecular motors, intracellular pathogens, intracellular proteolysis, nuclear import and export, cytokinesis and the cell cycle, the interface between signaling and trafficking or localization, protein translocation, the cell biology of adaptive an innate immunity, organelle biogenesis, metabolism, cell polarity and organization, and organelle movement. All aspects of the structural, molecular biology, biochemistry, genetics, morphology, intracellular signaling and relationship to hereditary or infectious diseases will be covered. Manuscripts must provide a clear conceptual or mechanistic advance. The editors will reject papers that require major changes, including addition of significant experimental data or other significant revision. Traffic will consider manuscripts of any length, but encourages authors to limit their papers to 16 typeset pages or less.