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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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.