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Oncogene. 1998 Apr 23;16(16):2075-86.

Interferon-alpha-induced G1 phase arrest through up-regulated expression of CDK inhibitors, p19Ink4D and p21Cip1 in mouse macrophages.

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Department of Hematology and Oncology, Institute of Medical Science, University of Tokyo, Japan.


The mechanism of cell cycle arrest induced by interferon-alpha (IFN-alpha) was analysed using a mouse macrophage cell line, BAC1.2F5A. IFN-alpha added in media before mid-G1 prohibited cells from entering S phase. The blockage of G1/S transition was associated with diminuition of both cyclin D1/cdk4- and cyclin E/cdk2-associated kinase activities. G1 cyclin-associated kinase activities were down-regulated quickly after the addition of IFN-alpha. Cells treated with IFN-alpha contained excess amounts of cdk inhibitors which down-regulated G1 cyclin/cdk-associated kinase activities in the proliferating cells and this action was counteracted by exogenously-supplied recombinant cyclin D2/cdk4 complexes. In parallel, accumulation of p19Ink4D and p21Cip1, and their attachment to cdks were up-regulated quickly after the addition of IFN-alpha. Expression of p19Ink4D and p21Cip1 was potentiated transcriptionally. We concluded that increased attachment of up-regulated cdk inhibitors including p19Ink4D and p21Cip1 to G1 cyclin/cdk complexes contributed to diminuition of G1 cyclin/cdk-associated kinase activities and resulting G1 phase arrest during the early phase of treatment with IFN-alpha.

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