JBC Focus on PI3-Kinase with Echelon

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Originally published In Press as doi:10.1074/jbc.M206226200 on September 19, 2002

J. Biol. Chem., Vol. 277, Issue 48, 46799-46808, November 29, 2002
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
277/48/46799    most recent
M206226200v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Piluso, D.
Right arrow Articles by Capone, J. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Piluso, D.
Right arrow Articles by Capone, J. P.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Host Cell Factor-1 Interacts with and Antagonizes Transactivation by the Cell Cycle Regulatory Factor Miz-1*

David PilusoDagger , Patricia Bilan, and John P. Capone§

From the Department of Biochemistry, McMaster University, Hamilton, Ontario L8N 3Z5, Canada

Human host cell factor-1 (HCF-1) is essential for cell cycle progression and is required, in conjunction with the herpes simplex virus transactivator VP16, for induction of viral immediate-early gene expression. We show here that HCF-1 directly binds to the Myc-interacting protein Miz-1, a transcription factor that induces cell cycle arrest at G1, in part by directly stimulating expression of the cyclin-dependent kinase inhibitor p15INK4b. A domain encompassing amino acids 750-836, contained within a subregion of HCF-1 required for cell cycle progression, was sufficient to bind Miz-1. Conversely, HCF-1 interacted with two separate regions in Miz-1: the N-terminal POZ domain and a C-terminal domain (residues 637-803) previously shown to harbor determinants for interaction with c-Myc and the coactivator p300. The latter functioned as a potent transactivation domain when tethered to DNA, indicating that HCF-1 targets a transactivation function in Miz-1. HCF-1 or a Miz-1-binding fragment of HCF-1 repressed transactivation by Gal4-Miz-1 in transfection assays. Moreover, HCF-1 repressed Miz-1-mediated transactivation of a reporter gene linked to the p15INK4b promoter. Protein/protein interaction studies and transient transfection assays demonstrated that HCF-1 interferes with recruitment of p300 to Miz-1, similar to what has been reported with c-Myc. Our findings identify Miz-1 as a novel HCF-1-interacting partner and illustrate cross-talk between these two proteins that may be of consequence to their respective functions in gene regulation and their opposing effects on the cell cycle.


* This work was supported in part by the National Cancer Institute of Canada.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Dagger Recipient of Natural Science and Engineering Research Council of Canada graduate studentship.

§ To whom correspondence should be addressed: Dept. of Biochemistry, Faculty of Health Sciences, McMaster University, 1200 Main St. W., Hamilton, Ontario L8N 3Z5, Canada. Tel.: 905-525-9140 (ext. 22184); Fax: 905-546-0800; E-mail: caponej@mcmaster.ca.


Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
J. Virol.Home page
G. Kolb and T. M. Kristie
Association of the Cellular Coactivator HCF-1 with the Golgi Apparatus in Sensory Neurons
J. Virol., October 1, 2008; 82(19): 9555 - 9563.
[Abstract] [Full Text] [PDF]


Home page
Genome ResHome page
A. Rada-Iglesias, S. Enroth, A. Ameur, C. M. Koch, G. K. Clelland, P. Respuela-Alonso, S. Wilcox, O. M. Dovey, P. D. Ellis, C. F. Langford, et al.
Butyrate mediates decrease of histone acetylation centered on transcription start sites and down-regulation of associated genes
Genome Res., June 1, 2007; 17(6): 708 - 719.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
B. Khurana and T. M. Kristie
A Protein Sequestering System Reveals Control of Cellular Programs by the Transcriptional Coactivator HCF-1
J. Biol. Chem., August 6, 2004; 279(32): 33673 - 33683.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
R. L. Luciano and A. C. Wilson
HCF-1 Functions as a Coactivator for the Zinc Finger Protein Krox20
J. Biol. Chem., December 19, 2003; 278(51): 51116 - 51124.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 All ASBMB Journals   Molecular and Cellular Proteomics 
 Journal of Lipid Research   ASBMB Today 
Copyright © 2002 by the American Society for Biochemistry and Molecular Biology.