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在HeLa细胞中敲低ALG-2会导致G2/M细胞周期阶段积累和细胞死亡。

ALG-2 knockdown in HeLa cells results in G2/M cell cycle phase accumulation and cell death.

作者信息

Høj Berit R, la Cour Jonas M, Mollerup Jens, Berchtold Martin W

机构信息

Copenhagen Biocenter, Department of Biology, University of Copenhagen, Ole Maaløes Vej 5, 2200 Copenhagen N, Denmark.

出版信息

Biochem Biophys Res Commun. 2009 Jan 2;378(1):145-8. doi: 10.1016/j.bbrc.2008.11.021. Epub 2008 Nov 14.

Abstract

ALG-2 (apoptosis-linked gene-2 encoded protein) has been shown to be upregulated in a variety of human tumors questioning its previously assumed pro-apoptotic function. The aim of the present study was to obtain insights into the role of ALG-2 in human cancer cells. We show that ALG-2 downregulation induces accumulation of HeLa cells in the G2/M cell cycle phase and increases the amount of early apoptotic and dead cells. Caspase inhibition by the pan-caspase inhibitor zVAD-fmk attenuated the increase in the amount of dead cells following ALG-2 downregulation. Thus, our results indicate that ALG-2 has an anti-apoptotic function in HeLa cells by facilitating the passage through checkpoints in the G2/M cell cycle phase.

摘要

凋亡相关基因2编码蛋白(ALG-2)已被证明在多种人类肿瘤中上调,这对其先前假定的促凋亡功能提出了质疑。本研究的目的是深入了解ALG-2在人类癌细胞中的作用。我们发现,下调ALG-2会导致HeLa细胞在G2/M细胞周期阶段积累,并增加早期凋亡细胞和死亡细胞的数量。泛半胱天冬酶抑制剂zVAD-fmk抑制半胱天冬酶,减弱了下调ALG-2后死亡细胞数量的增加。因此,我们的结果表明,ALG-2通过促进细胞通过G2/M细胞周期阶段的检查点,在HeLa细胞中具有抗凋亡功能。

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