Adaptor-Mediated Trafficking of Tank Binding Kinase 1 During Diverse Cellular Processes.

IF 3.6 3区生物学 Q3 CELL BIOLOGY

Traffic Pub Date : 2025-01-01 DOI:10.1111/tra.70000

Swagatika Paul, Sahitya Ranjan Biswas, Julia P Milner, Porter L Tomsick, Alicia M Pickrell

引用次数: 0

Abstract

The serine/threonine kinase, Tank Binding Kinase 1 (TBK1), drives distinct cellular processes like innate immune signaling, selective autophagy, and mitosis. It is suggested that the translocation and activation of TBK1 at different subcellular locations within the cell, downstream of diverse stimuli, are driven by TBK1 adaptor proteins forming a complex directly or indirectly with TBK1. Various TBK1 adaptors and associated proteins like NAP1, TANK, SINTBAD, p62, optineurin (OPTN), TAX1BP1, STING, and NDP52 have been identified in facilitating TBK1 activation and recruitment with varying overlapping redundancy. This review focuses on what is known about these proteins, their interactions with TBK1, and the functional consequences of these associations. We shed light on underexplored areas of research on these TBK1 binding partners while emphasizing how future research is required to understand the function and flexibility of TBK1 signaling and crosstalk or regulation between different biological processes.

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在不同的细胞过程中，受体介导的储罐结合激酶1的运输。

丝氨酸/苏氨酸激酶，坦克结合激酶1 (TBK1)，驱动不同的细胞过程，如先天免疫信号，选择性自噬和有丝分裂。这表明，在不同刺激的下游，TBK1在细胞内不同亚细胞位置的易位和激活是由TBK1接头蛋白直接或间接与TBK1形成复合物驱动的。各种TBK1接头和相关蛋白，如NAP1、TANK、SINTBAD、p62、OPTN、TAX1BP1、STING和NDP52，已被发现在促进TBK1的激活和募集中具有不同的重叠冗余。这篇综述的重点是关于这些蛋白质的已知知识，它们与TBK1的相互作用，以及这些关联的功能后果。我们揭示了这些TBK1结合伙伴的未开发研究领域，同时强调了未来的研究需要如何理解TBK1信号传导的功能和灵活性以及不同生物过程之间的串扰或调节。

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.