Autophagy is a conserved system that adapts to nutrient starvation, after which proteins and organelles are degraded to recycle amino acids in response to starvation. Recently, the ER was added to the list of targets of autophagic degradation. Autophagic degradation pathways of bulk ER and the specific proteins sorted through the ER are considered key mechanisms in maintaining ER homeostasis. Four ER-resident proteins (FAM134B, CCPG1, SEC62, and RTN3) have been identified as ER-resident cargo receptors, which contain LC3-interacting regions. In this study, we identified an N-terminal-truncated isoform of FAM134B (FAM134B-2) that contributes to starvation-induced ER-related autophagy. Hepatic FAM134B-2 but not full-length FAM134B (FAM134B-1) is expressed in a fed state. Starvation drastically induces FAM134B-2 but no other ER-resident cargo receptors through transcriptional activation by C/EBPβ. C/EBPβ overexpression increases FAM134B-2 recruitment into autophagosomes and lysosomal degradation. FAM134B-2 regulates lysosomal degradation of ER-retained secretory proteins such as ApoCIII. This study demonstrates that the C/EBPβ-FAM134B-2 axis regulates starvation-induced selective ER-phagy.

中文翻译：

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FAM134B（FAM134B-2）的N末端截短同工型可调节饥饿诱导的肝脏选择性ER吞噬。

自噬是一种适应营养不足的保守系统，此后蛋白质和细胞器被降解以响应饥饿而回收氨基酸。最近，ER被添加到自噬降解的目标清单。大量内质网和通过内质网分选的特定蛋白的自噬降解途径被认为是维持内质网稳态的关键机制。已经确定了四个内质网驻留蛋白（FAM134B，CCPG1，SEC62和RTN3）是内质网驻留的货物受体，它们包含与LC3相互作用的区域。在这项研究中，我们确定了FAM134B（FAM134B-2）的N末端截短同工型，它有助于饥饿诱导的ER相关自噬。肝FAM134B-2以全长FAM134B（FAM134B-1）表示为进食状态。饥饿通过C /EBPβ的转录激活剧烈诱导FAM134B-2，但不诱导其他ER驻留的货物受体。C /EBPβ的过表达增加FAM134B-2募集进入自噬体和溶酶体降解。FAM134B-2调节ER保留的分泌蛋白（如ApoCIII）的溶酶体降解。这项研究表明，C /EBPβ-FAM134B-2轴调节饥饿诱导的选择性ER吞噬。