![]() |
|
|
Vol. 15, Issue 6, 2771-2781, June 2004
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||





* Departments of Surgery and Cell and Developmental Biology, Vanderbilt University School of Medicine, Vanderbilt-Ingram Cancer Center, and the Nashville VA Medical Center, Nashville, Tennessee 37232;
Institute of Molecular Medicine and Genetics, Medical College of Georgia, Augusta, Georgia 30912; and
Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892
Submitted October 22, 2003;
Revised March 12, 2004;
Accepted March 15, 2004
Monitoring Editor: Keith Mostov
The A kinase anchoring protein 350 (AKAP350) is a multiply spliced type II protein kinase A anchoring protein that localizes to the centrosomes in most cells and to the Golgi apparatus in epithelial cells. In the present study, we sought to identify AKAP350 interacting proteins that could yield insights into AKAP350 function at the Golgi apparatus. Using yeast two-hybrid and pull-down assays, we found that AKAP350 interacts with a family of structurally related proteins, including FBP17, FBP17b, and cdc42 interacting protein 4 (CIP4). CIP4 interacts with the GTP-bound form of cdc42, with the Wiscott Aldrich Syndrome group of proteins, and with microtubules, and exerts regulatory effects on cytoskeleton and membrane trafficking. CIP4 is phosphorylated by protein kinase A in vitro, and elevation of intracellular cyclic AMP with forskolin stimulates in situ phosphorylation of CIP4. Our results indicate that CIP4 interacts with AKAP350 at the Golgi apparatus and that either disruption of this interaction by expressing the CIP4 binding domain in AKAP350, or reduction of AKAP350 expression by RNA interference leads to changes in Golgi structure. The results suggest that AKAP350 and CIP4 influence the maintenance of normal Golgi apparatus structure.
Corresponding author. E-mail address: jim.goldenring{at}vanderbilt.edu.
This article has been cited by other articles:
![]() |
M. Stone, S. Jia, W. D. Heo, T. Meyer, and K. V. Konan Participation of Rab5, an Early Endosome Protein, in Hepatitis C Virus RNA Replication Machinery J. Virol., May 1, 2007; 81(9): 4551 - 4563. [Abstract] [Full Text] [PDF] |
||||
![]() |
H.-S. Kim, M. Takahashi, K. Matsuo, and Y. Ono Recruitment of CG-NAP to the Golgi apparatus through interaction with dynein-dynactin complex Genes Cells, March 1, 2007; 12(3): 421 - 434. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. Nishimura, M. Takahashi, H.-S. Kim, H. Mukai, and Y. Ono Centrosome-targeting region of CG-NAP causes centrosome amplification by recruiting cyclin E-cdk2 complex Genes Cells, January 1, 2005; 10(1): 75 - 86. [Abstract] [Full Text] [PDF] |
||||