Skip Navigation


Journal of Biochemistry Advance Access originally published online on September 30, 2008
Journal of Biochemistry 2008 144(6):693-700; doi:10.1093/jb/mvn123
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
144/6/693    most recent
mvn123v2
mvn123v1
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 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 arrow Request Permissions
Google Scholar
Right arrow Articles by Gantulga, D.
Right arrow Articles by Yoshioka, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gantulga, D.
Right arrow Articles by Yoshioka, K.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Authors 2008. Published by Oxford University Press on behalf of the Japanese Biochemical Society. All rights reserved

The Scaffold Protein c-Jun NH2-Terminal Kinase-associated Leucine Zipper Protein Regulates Cell Migration through Interaction with the G Protein G{alpha}13

Davaakhuu Gantulga1, Baljinnyam Tuvshintugs1, Yoshio Endo2, Takahisa Takino2, Hiroshi Sato2, Seishi Murakami1 and Katsuji Yoshioka1,*

1Division of Molecular Cell Signaling, Department of Molecular and Cellular Biology; and 2Division of Molecular Virology and Oncology, Department of Molecular Oncology, Cancer Research Institute, Kanazawa University, Kanazawa, 920-0934, Japan

*To whom correspondence should be addressed. Tel/Fax: +81-76-234-4532, E-mail: katsuji{at}kenroku.kanazawa-u.ac.jp

Received July 11, 2008; Accepted September 9, 2008


  Abstract

Scaffold proteins for MAP kinase (MAPK) signalling modules play an important role in the specific and efficient signal transduction of the relevant MAPK cascades. Here, we investigated the function of the scaffolding protein c-Jun NH2-terminal kinase (JNK)-associated leucine zipper protein (JLP) by depleting it in cultured cells using a short hairpin RNA (shRNA) against human JLP. HeLa and DLD-1 cells stably expressing the shRNA showed a defect in cell migration. The re-expression of full-length shRNA-resistant mouse JLP rescued the impaired cell migration of the JLP-depleted HeLa cells; whereas, a C-terminal deletion mutant of mouse JLP, which failed to bind the G protein G{alpha}13, showed little or no effect on the cell migration defect. Furthermore, although a constitutively active G{alpha}13 enhanced the migration of control HeLa cells, the G{alpha}13-induced cell migration was significantly suppressed in the JLP-depleted HeLa cells. Taken together, these results suggest that JLP regulates cell migration through an interaction with G{alpha}13.

Key Words: cell migration, MAP kinase, p38, RNA interference, scaffold protein

Abbreviations: DMEM, Dulbecco's modified Eagle's medium; EDTA, ethylenediaminetetraacetic acid; GST, glutathione S-transferase; HEK, human embryonic kidney; JLP, JNK-associated leucine zipper protein; JNK, c-Jun NH2-terminal kinase; JSAP1, JNK/stress-activated protein kinase-associated protein 1; KD, knockdown; MAPK, MAP kinase; PCNA, proliferating cell nuclear antigen; PCR, polymerase chain reaction; shRNA, short hairpin RNA


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


This article has been cited by other articles:


Home page
 J. Biol. Chem.Home page
H. Xu, D. N. Dhanasekaran, C. M. Lee, and E. P. Reddy
Regulation of Neurite Outgrowth by Interactions between the Scaffolding Protein, JNK-associated Leucine Zipper Protein, and Neuronal Growth-associated Protein Superior Cervical Ganglia Clone 10
J. Biol. Chem., February 5, 2010; 285(6): 3548 - 3553.
[Abstract] [Full Text] [PDF]


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.