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
Services
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 arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hakata, Y.
Right arrow Articles by Shida, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hakata, Y.
Right arrow Articles by Shida, H.

 Previous Article  |  Next Article 

Journal of Virology, December 2001, p. 11515-11525, Vol. 75, No. 23
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.23.11515-11525.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Rat CRM1 Is Responsible for the Poor Activity of Human T-Cell Leukemia Virus Type 1 Rex Protein in Rat Cells

Yoshiyuki Hakata,1,2 Masami Yamada,2 and Hisatoshi Shida2,*

Institute for Virus Research, Kyoto University, Sakyo-ku, Kyoto 606-8507,1 and Institute for Genetic Medicine, Hokkaido University, Kita-ku, Sapporo 060-0815,2 Japan

Received 20 August 2001/Accepted 25 August 2001

Rat models of human T-cell leukemia virus type 1 (HTLV-1)-related diseases such as adult T-cell leukemia and HTLV-1-associated myelopathy/tropical spastic paraparesis have been reported. However, these models do not completely reproduce human diseases partly because HTLV-1 replicates poorly in rats. We investigated here the possible reason for this. We found that the activity of Rex in rat cells is quite low compared to that in human cells. As Rex function depends largely on the CRM1 protein, whose human type (human CRM1 [hCRM1]) directly binds to Rex and exports it from the nucleus to the cytoplasm, we assessed whether rat CRM1 (rCRM1) could act as well as hCRM1 as a cofactor for Rex activity. We first cloned a cDNA encoding rCRM1 and found that both rCRM1 and hCRM1 could bind to and export Rex protein to the cytoplasm with similar efficiencies. However, unlike hCRM1, rCRM1 could hardly support Rex function because of its poor ability in inducing the Rex-Rex interaction required for RNA export into the cytoplasm. These observations suggest that the poor ability of rCRM1 to act as a cofactor for Rex function may be responsible for the poor replication of HTLV-1 in rats.


* Corresponding author. Mailing address: Institute for Genetic Medicine, Hokkaido University, Kita-15, Nishi-7, Kita-ku, Sapporo 060-0815, Japan. Phone and fax: 81-11-707-6837. E-mail: hshida{at}imm.hokudai.ac.jp


Journal of Virology, December 2001, p. 11515-11525, Vol. 75, No. 23
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.23.11515-11525.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.



This article has been cited by other articles:

  • Takayanagi, R., Ohashi, T., Yamashita, E., Kurosaki, Y., Tanaka, K., Hakata, Y., Komoda, Y., Ikeda, S., Tsunetsugu-Yokota, Y., Tanaka, Y., Shida, H. (2007). Enhanced Replication of Human T-Cell Leukemia Virus Type 1 in T Cells from Transgenic Rats Expressing Human CRM1 That Is Regulated in a Natural Manner. J. Virol. 81: 5908-5918 [Abstract] [Full Text]  
  • Komori, K., Hasegawa, A., Kurihara, K., Honda, T., Yokozeki, H., Masuda, T., Kannagi, M. (2006). Reduction of Human T-Cell Leukemia Virus Type 1 (HTLV-1) Proviral Loads in Rats Orally Infected with HTLV-1 by Reimmunization with HTLV-1-Infected Cells.. J. Virol. 80: 7375-7381 [Abstract] [Full Text]  
  • Hakata, Y., Yamada, M., Shida, H. (2003). A Multifunctional Domain in Human CRM1 (Exportin 1) Mediates RanBP3 Binding and Multimerization of Human T-Cell Leukemia Virus Type 1 Rex Protein. Mol. Cell. Biol. 23: 8751-8761 [Abstract] [Full Text]  
  • Zhang, X., Yamada, M., Mabuchi, N., Shida, H. (2003). Cellular Requirements for CRM1 Import and Export. J Biochem 134: 759-764 [Abstract] [Full Text]  
  • Hasegawa, A., Ohashi, T., Hanabuchi, S., Kato, H., Takemura, F., Masuda, T., Kannagi, M. (2003). Expansion of Human T-Cell Leukemia Virus Type 1 (HTLV-1) Reservoir in Orally Infected Rats: Inverse Correlation with HTLV-1-Specific Cellular Immune Response. J. Virol. 77: 2956-2963 [Abstract] [Full Text]  
  • Hakata, Y., Yamada, M., Mabuchi, N., Shida, H. (2002). The Carboxy-Terminal Region of the Human Immunodeficiency Virus Type 1 Protein Rev Has Multiple Roles in Mediating CRM1-Related Rev Functions. J. Virol. 76: 8079-8089 [Abstract] [Full Text]