在mtor介导的自噬诱导过程中,CSNK2/CK2的功能选择性地影响内质网和高尔基体。

Pablo Sanz-Martinez, Rayene Berkane, Alexandra Stolz
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引用次数: 0

摘要

内质网的选择性大自噬/自噬,即网状自噬/内质网自噬,对于维持内质网的平衡至关重要。我们最近发现,自噬受体家族 RETREG/FAM134 的成员受磷酸化依赖性泛素化的调控。在一次无偏筛选中,我们发现了 MTOR 下游对网状吞噬通量有深远影响的几种激酶,包括 ATR 和 CSNK2/CK2。通过 SGC-CK2-1 抑制 CSNK2 可以阻止自噬激活时 RETREG1/FAM134B 和 RETREG3/FAM134C 的泛素化以及高密度 RETREG1 和 RETREG3 簇的形成。在此,我们报告了分别抑制 CSNK2 和 ATR 后的全局蛋白质组学的额外资源数据。我们的数据表明,CSNK2的功能主要局限于ER/reticulophagy和Golgi/Golgiphagy,而VE-822抑制ATR会影响绝大多数细胞器/选择性自噬途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Function of CSNK2/CK2 selectively affects the endoplasmic reticulum and the Golgi apparatus in mtor-mediated autophagy induction.

Selective macroautophagy/autophagy of the endoplasmic reticulum, known as reticulophagy/ER-phagy, is essential to maintain ER homeostasis. We recently showed that members of the autophagy receptor family RETREG/FAM134 are regulated by phosphorylation-dependent ubiquitination. In an unbiased screen we had identified several kinases downstream of MTOR with profound impact on reticulophagy flux, including ATR and CSNK2/CK2. Inhibition of CSNK2 by SGC-CK2-1 prevented regulatory ubiquitination of RETREG1/FAM134B and RETREG3/FAM134C upon autophagy activation as well as the formation of high-density RETREG1- and RETREG3-clusters. Here we report on additional resource data of global proteomics upon CSNK2 and ATR inhibition, respectively. Our data suggests that the function of CSNK2 is mainly limited to the ER/reticulophagy and Golgi/Golgiphagy, while ATR inhibition by VE-822 affects the vast majority of organelles/selective autophagy pathways.Abbreviation: ATRi: ATR inhibitor VE-822; CSNK2i: CSNK2 inhibitor SGC-CK2-1; ER: endoplasmic reticulum.

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