期刊
INTERNATIONAL JOURNAL OF CANCER
卷 103, 期 1, 页码 21-28出版社
WILEY-LISS
DOI: 10.1002/ijc.10743
关键词
mirk/dyrk1B; cell-cycle regulator; p27(kipl); cyclin D1
类别
资金
- NATIONAL CANCER INSTITUTE [R01CA067405] Funding Source: NIH RePORTER
- NCI NIH HHS [R01 CA67405] Funding Source: Medline
Mirk/dyrkIB is an arginine-directed protein kinase, which functions as a transcriptional activator and mediates serum-free growth of colon carcinoma cells by an unknown mechanism. We now report that turnover of the cdk inhibitor p27(kip1) and the G(1)-phase cyclin cyclin D I is enhanced in each of 4 Mirk stable transfectants compared to vector control transfectants and Mirk kinase-inactive mutant transfectants. This enhanced turnover is proteasome-dependent and leads to lower protein levels of both p(27kip1) and cyclin D1. Lower protein levels of the cdk inhibitor p21(cip1) were also observed in the 4 Mirk stable transfectants. Mirk did not alter the activity of a p27(kip1) promoter construct or p27(kip1) mRNA levels by stable expression, indicating that the decrease in p27(kip1) protein levels was due to a posttranscriptional mechanism. These data are consistent with mirk enhancing the expression of some component common to the proteolysis of both p27(kip1) and cyclin D1. (C) 2002 Wiley-Liss, Inc.
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