SEARCH:   Advanced

Blood, 15 May 2005, Vol. 105, No. 10, pp. 3855-3861. Prepublished online as a Blood First Edition Paper on February 1, 2005; DOI 10.1182/blood-2004-08-3342. This Article Full Text (PDF) All Versions of this Article: 2004-08-3342v1 105/10/3855    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Lei, W. Articles by Ness, S. A Search for Related Content PubMed PubMed Citation Articles by Lei, W. Articles by Ness, S. A Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted August 27, 2004 Accepted January 25, 2005 Positive and negative regulation of c-Myb by Cyclin D1, cyclin-dependent kinases and p27 Kip1 Wanli Lei, Fan Liu, and Scott A Ness* Department of Molecular Genetics and Microbiology, University of New Mexico Health Sciences Center, Albuquerque, NM, USA * Corresponding author; email: ness{at}unm.edu. 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 reporter 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 D1 and CDKs and imply that c-Myb activity is regulated during the cell cycle in hematopoietic cells. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: Z. T. Hammoud, S. Badve, Q. Zhao, L. Li, R. Saxena, M. A. Thorat, A. Morimiya, K. M. Rieger, and K. A. Kesler Differential gene expression profiling of esophageal adenocarcinoma J. Thorac. Cardiovasc. Surg., April 1, 2009; 137(4): 829 - 834. [Abstract] [Full Text] [PDF] F. Fang, M. A. Rycyzyn, and C. V. Clevenger Role of c-Myb during Prolactin-Induced Signal Transducer and Activator of Transcription 5a Signaling in Breast Cancer Cells Endocrinology, April 1, 2009; 150(4): 1597 - 1606. [Abstract] [Full Text] [PDF] J. P. O'Rourke and S. A. Ness Alternative RNA Splicing Produces Multiple Forms of c-Myb with Unique Transcriptional Activities Mol. Cell. Biol., March 15, 2008; 28(6): 2091 - 2101. [Abstract] [Full Text] [PDF] W. Lei, R. J. Jaramillo, and K. S. Harrod Transactivation of lung lysozyme expression by Ets family member ESE-1 Am J Physiol Lung Cell Mol Physiol, November 1, 2007; 293(5): L1359 - L1368. [Abstract] [Full Text] [PDF] M. Pilkinton, R. Sandoval, J. Song, S. A. Ness, and O. R. Colamonici Mip/LIN-9 Regulates the Expression of B-Myb and the Induction of Cyclin A, Cyclin B, and CDK1 J. Biol. Chem., January 5, 2007; 282(1): 168 - 175. [Abstract] [Full Text] [PDF]

	Copyright © 2005 by American Society of Hematology         Online ISSN: 1528-0020