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环磷酸腺苷(cAMP)抑制D型细胞周期蛋白和细胞周期蛋白依赖性激酶4(cdk4)的表达,并在粒细胞集落刺激因子(G-CSF)处理的NFS-60细胞中诱导p27Kip1蛋白的产生。

Cyclic AMP inhibits expression of D-type cyclins and cdk4 and induces p27Kip1 in G-CSF-treated NFS-60 cells.

作者信息

Ward A C, Csar X F, Hoffmann B W, Hamilton J A

机构信息

Department of Medicine, Royal Melbourne Hospital, University of Melbourne, Parkville, Victoria, Australia.

出版信息

Biochem Biophys Res Commun. 1996 Jul 5;224(1):10-6. doi: 10.1006/bbrc.1996.0976.

DOI:10.1006/bbrc.1996.0976
PMID:8694794
Abstract

The addition of cAMP inhibits G-CSF-mediated proliferation and suppresses pRB phosphorylation in NFS-60 cells. We show that the latter could be attributed to different effects of cAMP in these cells: (i) down-regulation of the levels of cyclins D2 and D3, and cdk4, and (ii) induction of the p27Kip1 inhibitor of cdk4.

摘要

添加环磷酸腺苷(cAMP)可抑制粒细胞集落刺激因子(G-CSF)介导的增殖,并抑制NFS-60细胞中视网膜母细胞瘤蛋白(pRB)的磷酸化。我们发现,后者可归因于cAMP在这些细胞中的不同作用:(i)细胞周期蛋白D2和D3以及细胞周期蛋白依赖性激酶4(cdk4)水平的下调,以及(ii)细胞周期蛋白依赖性激酶4的p27Kip1抑制剂的诱导。

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Cyclic AMP inhibits expression of D-type cyclins and cdk4 and induces p27Kip1 in G-CSF-treated NFS-60 cells.环磷酸腺苷(cAMP)抑制D型细胞周期蛋白和细胞周期蛋白依赖性激酶4(cdk4)的表达,并在粒细胞集落刺激因子(G-CSF)处理的NFS-60细胞中诱导p27Kip1蛋白的产生。
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