内质网应激下诱导 M1 巨噬细胞中的 PERK-eIF2α-ATF4 通路

IF 0.8 4区生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY

Doklady Biochemistry and Biophysics Pub Date : 2024-07-13 DOI:10.1134/S1607672924600301

O. E. Kolodeeva, O. E. Kolodeeva, D. A. Averinskaya, Yu. A. Makarova

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引用次数: 0

摘要

翻译抑制可激活两种细胞死亡途径。第一种途径由翻译畸变激活，第二种途径由内质网（ER）应激激活。本研究调查了核糖体灭活蛋白 II 型（RIP-II）粘蛋白对源自 THP-1 细胞系的 M1 巨噬细胞的影响。实时 PCR 评估了修饰核糖体的数量。转录组分析表明，粘蛋白可诱导由 PERK 传感器激活的 ER 应激。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

Induction of the PERK-eIF2α-ATF4 Pathway in M1 Macrophages under Endoplasmic Reticulum Stress

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Induction of the PERK-eIF2α-ATF4 Pathway in M1 Macrophages under Endoplasmic Reticulum Stress

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.

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来源期刊

Doklady Biochemistry and Biophysics 生物-生化与分子生物学

CiteScore

1.60

自引率

12.50%

发文量

审稿时长

6-12 weeks

期刊介绍： Doklady Biochemistry and Biophysics is a journal consisting of English translations of articles published in Russian in biochemistry and biophysics sections of the Russian-language journal Doklady Akademii Nauk. The journal''s goal is to publish the most significant new research in biochemistry and biophysics carried out in Russia today or in collaboration with Russian authors. The journal accepts only articles in the Russian language that are submitted or recommended by acting Russian or foreign members of the Russian Academy of Sciences. The journal does not accept direct submissions in English.