Peltzer Nieves
Faculty of Medicine, Center for Molecular Medicine Cologne, Department of Translational Genomics and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) Research Center, University of Cologne, Germany.
FEBS J. 2022 Sep;289(17):5176-5179. doi: 10.1111/febs.16427. Epub 2022 Mar 16.
Linear or M1-ubiquitination (Ub) is required for optimal NF-kB activation and for cell death inhibition. Using Drosophila as a model organism, Aalto et al. found that hypoxia, oxidative and mechanical stress induced M1-Ub by the HOIP homolog, LUBEL. Increased M1-Ub had a protective function driven by activation of the NF-κB transcription factor Relish via the Immune deficiency pathway (Imd). This protective M1-Ub was also induced upon cellular stress in colorectal cancer cells. Collectively, they propose that M1-Ub is a conserved, common response to different forms of stresses. These findings may have important implications for the use of HOIP inhibitors for cancer treatment. Comment on: https://doi.org/10.1111/febs.16425.
线性或M1-泛素化（Ub）对于最佳的NF-κB激活和细胞死亡抑制是必需的。以果蝇作为模式生物，阿尔托等人发现缺氧、氧化和机械应激通过HOIP同源物LUBEL诱导M1-Ub。增加的M1-Ub具有由NF-κB转录因子Relish通过免疫缺陷途径（Imd）激活驱动的保护功能。这种保护性M1-Ub在结肠癌细胞受到细胞应激时也会被诱导。他们共同提出M1-Ub是对不同形式应激的一种保守的、常见的反应。这些发现可能对使用HOIP抑制剂进行癌症治疗具有重要意义。评论：https://doi.org/10.1111/febs.16425
