The cost of publication in Journal of Biomedical Science is borne by the National Science Council, Taiwan.
Research
ZAK negatively regulates RhoGDIβ-induced Rac1-mediated hypertrophic growth and cell migration
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* Corresponding author: Jaw-Ji Yang jjyang@csmu.edu.tw
- † Equal contributors
1 Graduate Institute of Chinese Medical Science, China Medical University, Taichung 404, Taiwan
2 Graduate Institute of Basic Medical Science, China Medical University, Taichung 404, Taiwan
3 Department of Health and Nutrition Biotechnology, Asia University, Taichung 413, Taiwan
4 School of Dentistry, Chung-Shan Medical University, Taichung 402, Taiwan
5 Institute of Medicine, Chung-Shan Medical University, Taichung 402, Taiwan
6 Chung-Shan Medical University Hospital, Chung-Shan Medical University, Taichung 402, Taiwan
7 Department of Orthopedics Surgery, Chung-Shan Medical University, Taichung 402, Taiwan
8 Midwestern University Chicago College of Osteopathic Medicine, Chicago, USA
9 Cardiovascular Center, Veterans General Hospital, Taichung 407, Taiwan
Journal of Biomedical Science 2009, 16:56 doi:10.1186/1423-0127-16-56
Published: 18 June 2009Abstract
RhoGDIβ, a Rho GDP dissociation inhibitor, induced hypertrophic growth and cell migration in a cultured cardiomyoblast cell line, H9c2. We demonstrated that RhoGDIβ plays a previously undefined role in regulating Rac1 expression through transcription to induce hypertrophic growth and cell migration and that these functions are blocked by the expression of a dominant-negative form of Rac1. We also demonstrated that knockdown of RhoGDIβ expression by RNA interference blocked RhoGDIβ-induced Rac1 expression and cell migration. We demonstrated that the co-expression of ZAK and RhoGDIβ in cells resulted in an inhibition in the activity of ZAK to induce ANF expression. Knockdown of ZAK expression in ZAK-RhoGDIβ-expressing cells by ZAK-specific RNA interference restored the activities of RhoGDIβ.