期刊
BLOOD
卷 105, 期 10, 页码 3855-3861出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2004-08-3342
关键词
-
类别
资金
- NCI NIH HHS [R01 CA058443, P30 CA118100, R01 CA58443] Funding Source: Medline
The c-Myb transcription factor controls differentiation and proliferation in hematopoietic and other cell types and has latent transforming activity, but little is known about its regulation during the cell cycle. Here, c-Myb was identified as part of a protein complex from human T cells containing the cyclin-dependent kinase (CDK) CDK6. Assays using model re-porter constructs as well as endogenous target genes showed that the activity of c-Myb was inhibited by cyclin D1 plus CDK4 or CDK6 but stimulated by expression of the CDK inhibitors p16 Ink4a, p21 Cip1, or p27 Kip1. Mapping experiments identified a highly conserved region in c-Myb which, when transferred to the related A-Myb transcription factor, also rendered it responsive to CDKs and p27. The results suggest that c-Myb activity is directly regulated by cyclin 131 and CDKs and imply that c-Myb activity is regulated during the cell cycle in hematopoietic cells. (c) 2005 by The American Society of Hematology.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据