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GD3 ganglioside and apoptosis

机译:GD3神经节苷脂与细胞凋亡

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摘要

Lipid and glycolipid mediators are important messengers of the adaptive responses to stress, including apoptosis. In mammalian cells, the intracellular accumulation of ganglioside GD3, an acidic glycosphingolipid, contributes to mitochondrial damage, a crucial event during the apoptopic program. GD3 is a minor ganglioside in most normal tissues. Its expression increases during development and in pathological conditions such as cancer and neurodegenerative disorders. Intriguingly, GD3 can mediate additional biological events such as cell proliferation and differentiation. These diverse and opposing effects indicate that tightly regulated mechanisms, including 9-O-acetylation, control GD3 function, by affecting intracellular levels, localization and structure of GD3, and eventually dictate biological outcomes and cell fate decisions.
机译:脂质和糖脂介体是对应激(包括细胞凋亡)的适应性反应的重要信使。在哺乳动物细胞中,神经节苷脂GD3(一种酸性糖鞘脂)的细胞内蓄积有助于线粒体损伤,这是在凋亡程序中的关键事件。 GD3在大多数正常组织中是次要的神经节苷脂。它的表达在发育过程中以及在诸如癌症和神经退行性疾病的病理状态下增加。有趣的是,GD3可以介导其他生物学事件,例如细胞增殖和分化。这些不同且相反的作用表明,包括9-O-乙酰化在内的严格调节的机制通过影响GD3的细胞内水平,定位和结构来控制GD3的功能,并最终决定生物学结果和细胞命运的决定。

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