Skip Navigation


International Immunology Advance Access originally published online on October 30, 2009
International Immunology 2009 21(12):1351-1361; doi:10.1093/intimm/dxp106
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
21/12/1351    most recent
dxp106v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Related articles in Int. Immunol.
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 Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Chang, J.-W.
Right arrow Articles by Iwashima, M.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Chang, J.-W.
Right arrow Articles by Iwashima, M.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?


© The Japanese Society for Immunology. 2009. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

hnRNP-K is a nuclear target of TCR-activated ERK and required for T-cell late activation

Jing-Wen Chang1, Toru Koike1,2 and Makio Iwashima1,3

1 Department of Medicine, Immunotherapy Center, Medical College of Georgia, 1120 15th Street, Augusta, GA 30912-2600, USA
2 Department of Biology and Geosciences, Faculty of Science, Shizuoka University, Shizuoka, Japan
3 Department of Microbiology and Immunology, Stritch School of Medicine, Loyola University Chicago, 2160 South First Avenue, Maywood, IL 60513, USA

Correspondence to: M. Iwashima; E-mail: miwashima{at}lumc.edu

Sustained extracellular signal-regulated kinase (ERK)-signaling plays a critical role in T-cell-mediated IL-2 production. Although many downstream targets are known for ERK, details remain unknown about which molecules play functional roles in IL-2 production. Here, we addressed this question using proteomic analysis of nuclear proteins from TCR-activated T cells and identified hnRNP-K as one of the ERK targets essential for IL-2 production. hnRNP-K was previously shown by others to be a direct substrate of ERK and form complexes with multiple signaling proteins as well as DNA and RNA. Our data showed a clear ERK-dependent increase in one form of hnRNP-K after TCR stimulation. Small interfering RNA-mediated gene knockdown of hnRNP-K expression abrogated IL-2 production by T cells. Moreover, reduction of hnRNP-K expression caused a notable increase in proteolysis of Vav1, a binding target of hnRNP-K. Since Vav1 is an essential molecule for T-cell activation, the data suggest that ERK signaling is required for T-cell activation partly by inhibiting activation-induced proteolysis of Vav1.

Keywords: ERK, hnRNP-K, IL-2, signal transduction, T cell, TCR, Vav1

Transmitting editor: S. Koyasu

Received 26 December 2008, accepted 2 October 2009.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?

Related articles in Int. Immunol.:

IN THIS ISSUE

Int. Immunol. 2009 21: NP. [Extract] [Full Text]  





Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.