Hollemann Thomas
Institute for Physiological Chemistry, Martin-Luther-University Halle-Wittenberg, Germany.
FEBS J. 2025 Jan;292(2):272-274. doi: 10.1111/febs.17342. Epub 2024 Dec 1.
TRIM2 belongs to the TRIM-NHL class of ubiquitin E3-ligases and inhibits apoptosis by a dual function. Liao et al. reported in the recent issue that under glutamine deprivation, TRIM2 transcription is activated by ATF4 to increase the uptake of long fatty acids into mitochondria. Here, TRIM2 acts as a direct activator of CPT1 independent of its E3 ubiquitin ligase activity and prevents apoptosis otherwise triggered by starvation. On the contrary, TRIM E3-ubiquitin ligase has been described to ubiquitinate and thus target proapoptotic BIM for its degradation in the proteasome. Thus, TRIM2 inhibits apoptosis classically via its ligase activity but also independent of this stimulating energy metabolism.
TRIM2属于泛素E3连接酶的TRIM - NHL类别，并通过双重功能抑制细胞凋亡。廖等人在最近一期报道，在谷氨酰胺剥夺条件下，TRIM2转录由ATF4激活，以增加长链脂肪酸进入线粒体的摄取。在这里，TRIM2作为CPT1的直接激活剂，独立于其E3泛素连接酶活性，并防止饥饿引发的细胞凋亡。相反，TRIM E3泛素连接酶已被描述为泛素化促凋亡蛋白BIM，从而使其在蛋白酶体中降解。因此，TRIM2经典地通过其连接酶活性抑制细胞凋亡，但也独立于这种刺激能量代谢的方式。
