J Gen Virol Email Content Delivery
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Gen Virol 84 (2003), 665-676; DOI 10.1099/vir.0.18699-0

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
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 CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hwang, S.
Right arrow Articles by Choe, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hwang, S.
Right arrow Articles by Choe, J.
Agricola
Right arrow Articles by Hwang, S.
Right arrow Articles by Choe, J.
© 2003 Society for General Microbiology

Kaposi's sarcoma-associated herpesvirus K8 protein interacts with hSNF5

Seungmin Hwang1, Daeyoup Lee1, Yousang Gwack1, Hyesun Min2 and Joonho Choe1

1 Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 305-701, Korea
2 Department of Food and Nutrition, Hannam University, Daejeon 306-791, Korea

Correspondence
Joonho Choe
jchoe{at}mail.kaist.ac.kr

Kaposi's sarcoma-associated herpesvirus (KSHV) is a human gammaherpesvirus related to Epstein–Barr virus (EBV) and herpesvirus saimiri. KSHV open reading frame K8 encodes a basic region-leucine zipper protein of 237 aa that homodimerizes. K8 shows significant similarity to the EBV immediate-early protein Zta, a key regulator of EBV reactivation and replication. In this study, a carboxyl-terminal deletion mutant of K8, K8(1–115), that had strong transactivating properties was found. Screening using transcriptionally inactive K8(1–75) showed that K8 interacts and co-localizes with hSNF5, a cellular chromatin-remodelling factor, both in vivo and in vitro. This interaction requires aa 48–183 of hSNF5 and 1–75 of K8. In a yeast expression system, the ability of K8 and K8(1–115) to activate transcription requires the presence of SNF5, the yeast homologue of hSNF5. These data suggest a mechanism by which the SWI–SNF complex is recruited to specific genes. They also suggest that K8 functions as a transcriptional activator under specific conditions and that its transactivation activity requires its interaction with the cellular chromatin remodelling factor hSNF5.

Published ahead of print on 25 November 2002 as DOI 10.1099/vir.0.18699-0.




This article has been cited by other articles:


Home page
J. Virol.Home page
Y. Izumiya, T. J. Ellison, E. T. H. Yeh, J. U. Jung, P. A. Luciw, and H.-J. Kung
Kaposi's Sarcoma-Associated Herpesvirus K-bZIP Represses Gene Transcription via SUMO Modification
J. Virol., August 1, 2005; 79(15): 9912 - 9925.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
INT J SYST EVOL MICROBIOL MICROBIOLOGY J GEN VIROL
J MED MICROBIOL ALL SGM JOURNALS
Copyright © 2003 by the Society for General Microbiology.