Alteration of Golgi structure in senescent cells and its regulation by a G protein γ subunit.

Alteration of Golgi structure in senescent cells and its regulation by a G protein γ subunit.
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DOI:
10.1016/j.cellsig.2011.01.001
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发表时间:
2011-05
影响因子:
4.8
通讯作者:
Gautam N
Gautam N
中科院分区:
生物学2区
文献类型:
--
作者:
Cho JH;Saini DK;Karunarathne WK;Kalyanaraman V;Gautam N

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细胞衰老是一个过程,其中增殖细胞经历永久的细胞周期停滞,同时保持活力。衰老导致促进癌症和炎症的蛋白质分泌增加。我们在这里报告的高尔基复合体的结构,调节分泌改变衰老细胞。在通过复制耗竭实现衰老的细胞中或在其中衰老已经用BrdU处理依赖性应激诱导的细胞中,高尔基复合体分散。G蛋白γ亚基γ11的表达随着衰老而增加,γ11能够在受体活化时从质膜转运到高尔基复合体。敲低γ11或过表达显性负性γ3亚基抑制衰老诱导的高尔基体扩散。总之,这些结果表明,在细胞衰老的上调G蛋白γ亚基介导的高尔基体的结构的改变。
Cellular senescence is a process wherein proliferating cells undergo permanent cell cycle arrest while remaining viable. Senescence results in enhanced secretion of proteins that promote cancer and inflammation. We report here that the structure of the Golgi complex which regulates secretion is altered in senescent cells. In cells where senescence is achieved by replicative exhaustion or in cells wherein senescence has been induced with BrdU treatment dependent stress, the Golgi complex is dispersed. The expression of a G protein γ subunit, γ11, capable of translocation from the plasma membrane to the Golgi complex on receptor activation increases with senescence. Knockdown of γ11 or overexpression of a dominant negative γ3 subunit inhibits Golgi dispersal induced by senescence. Overall these results suggest that in cellular senescence an upregulated G protein gamma subunit mediates alterations in the structure of the Golgi.
二聚体 PKD 调节膜裂变以在 TGN 处形成运输载体。
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