内质网应激下 M1 巨噬细胞 PERK-eIF2α-ATF4 通路的诱导。
Induction of the PERK-eIF2α-ATF4 Pathway in M1 Macrophages under Endoplasmic Reticulum Stress.
机构信息
Faculty of Biology and Biotechnology, HSE University, Moscow, Russia.
Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, Moscow, Russia.
出版信息
Dokl Biochem Biophys. 2024 Aug;517(1):264-268. doi: 10.1134/S1607672924600301. Epub 2024 Jul 13.
Translation inhibition can activate two cell death pathways. The first pathway is activated by translational aberrations, the second by endoplasmic reticulum (ER) stress. In this work, the effect of ribosome-inactivating protein type II (RIP-II) viscumin on M1 macrophages derived from the THP-1 cell line was investigated. The number of modified ribosomes was evaluated by real-time PCR. Transcriptome analysis revealed that viscumin induces the ER stress activated by the PERK sensor.
翻译抑制可以激活两种细胞死亡途径。第一条途径是由翻译异常激活的，第二条途径是由内质网（ER）应激激活的。在这项工作中，研究了核糖体失活蛋白 II 型（RIP-II）viscumin 对来自 THP-1 细胞系的 M1 巨噬细胞的影响。通过实时 PCR 评估了修饰核糖体的数量。转录组分析表明，viscumin 诱导 PERK 传感器激活的 ER 应激。
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