MGL INDUCES NUCLEAR TRANSLOCATION OF ENDOG AND AIF IN CASPASE-INDEPENDENT T CELL DEATH

MGL INDUCES NUCLEAR TRANSLOCATION OF ENDOG AND AIF IN CASPASE-INDEPENDENT T CELL DEATH
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MGL 在不依赖于 Caspase 的 T 细胞死亡中诱导 ENDOG 和 AIF 的核转位

DOI:
10.1515/cmble-2015-0051
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发表时间:
2015-12-01
影响因子:
8.3
通讯作者:
Wei, Min
Wei, Min
中科院分区:
生物学1区
文献类型:
--
作者:
Bu, Qingpan;Wang, Jianhui;Wei, Min

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巨噬细胞半乳糖型凝集素(MGL)参与调节T细胞凋亡,但其确切的死亡途径尚不清楚。在这里,我们证明了MGL诱导的T细胞死亡发生在一个caspase独立的方式。此外,MGL处理触发核酸内切酶G(EndoG)和凋亡诱导因子(AIF)从线粒体易位到细胞核。由于半乳糖凝集素-1(Gal-1)也可以启动类似的线粒体事件,我们推测这种死亡途径可能被凝集素家族广泛使用。
Macrophage galactose-type lectin (MGL) participates in the regulation of T cell apoptosis, but the exact death pathway remains unclear. Here, we demonstrated that MGL-induced T cell death occurs in a caspaseindependent manner. Furthermore, MGL treatment triggers the translocation of endonuclease G (EndoG) and apoptosis-inducing factor (AIF) from the mitochondria to the nucleus. Because galectin-1 (Gal-1) can also initiate similar mitochondrial events, we speculate that this death pathway may be widely used by the lectin family.