The missing link: TBK1 connects membrane damage sensing with autophagic response upon adenovirus entry.

Autophagy reports Pub Date : 2022-10-25 eCollection Date: 2022-01-01 DOI:10.1080/27694127.2022.2136604
Coralie F Daussy, Noémie Pied, Fabienne Rayne, Harald Wodrich
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Abstract

Most cell entry by invading pathogens involves penetration of either the plasma membrane or the endo-lysosomal compartment to reach the cytosol. This process frequently inflicts membrane damage and provokes a cellular response. This Autophagic Punctum summarizes our recent study investigating how adenovirus endosome penetration is recognized and activates macroautophagy/autophagy. Our key finding is that TBK1 (TANK binding kinase 1) has a dual role in the cell response to membrane damage; it is part of an immediate-acting membrane-damage-sensing complex and is a crucial driver of the resulting autophagic response. Thus, TBK1 is a central factor linking sensors and effectors during the cell response to membrane damage.

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缺失的一环:TBK1连接腺病毒进入时膜损伤感知与自噬反应
大多数入侵的病原体进入细胞都涉及穿透质膜或内溶酶体腔室到达细胞质。这个过程经常造成细胞膜损伤并引起细胞反应。这篇自噬专题综述了我们最近关于腺病毒内体渗透如何被识别和激活巨噬/自噬的研究。我们的主要发现是TBK1 (TANK结合激酶1)在细胞对膜损伤的反应中具有双重作用;它是即时性膜损伤传感复合体的一部分,是导致自噬反应的关键驱动因素。因此,在细胞对膜损伤的反应过程中,TBK1是连接传感器和效应器的中心因子。
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