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ATP耗竭会影响核仁磷酸蛋白的易位以及rRNA从细胞核的输出。

ATP depletion affects NPM translocation and exportation of rRNA from nuclei.

作者信息

Finch R A, Chan P K

机构信息

Department of Pharmacology, Baylor College of Medicine, Houston, Texas 77030, USA.

出版信息

Biochem Biophys Res Commun. 1996 May 15;222(2):553-8. doi: 10.1006/bbrc.1996.0782.

DOI:10.1006/bbrc.1996.0782
PMID:8670243
Abstract

Nucleophosmin/B23 (NPM) is a nucleolar phosphoprotein which shifts from nucleoli to the nucleoplasm in cells treated with certain cytotoxic agents (NPM-translocation). NPM requires GTP for localization into nucleoli (J. Biol. Chem. 268, 5823-5827, 1993). To understand more about NPM's dynamic localization, the effects of lowering ATP on NPM-translocation and rRNA synthesis were studied. When the ATP level in HeLa cells was reduced by sodium azide, NPM-translocation was blocked. Similar results were obtained when ATP was depleted by other agents, suggesting that ATP depletion was responsible for the blocking of NPM-translocation. It was found that newly synthesized rRNA accumulated in the nuclei during ATP-depletion. Significantly larger than normal nucleoli were also observed. These results indicate that NPM may be involved in the transportation of newly synthesized ribosomes.

摘要

核磷蛋白/B23(NPM)是一种核仁磷蛋白,在用某些细胞毒性药物处理的细胞中,它会从核仁转移到核质中(NPM易位)。NPM定位于核仁需要GTP(《生物化学杂志》268卷,5823 - 5827页,1993年)。为了更深入了解NPM的动态定位,研究了降低ATP对NPM易位和rRNA合成的影响。当叠氮化钠降低HeLa细胞中的ATP水平时,NPM易位被阻断。当用其他试剂耗尽ATP时也得到了类似结果,表明ATP耗竭是NPM易位受阻的原因。研究发现,在ATP耗竭期间,新合成的rRNA在细胞核中积累。还观察到明显大于正常的核仁。这些结果表明,NPM可能参与新合成核糖体的运输。

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