JBC

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

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
Right arrow Citation Map
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 Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wu, W. J.
Right arrow Articles by Manor, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wu, W. J.
Right arrow Articles by Manor, D.

J Biol Chem, Vol. 273, Issue 27, 16655-16658, July 3, 1998

COMMUNICATION
Transformation Activity of Cdc42 Requires a Region Unique to Rho-related Proteins

Wen Jin Wu, Rui Lin, Richard A. Cerione, and Danny Manor

From the Department of Pharmacology, Veterinary Medical Center, Cornell University, Ithaca, New York 14853

The Rho subfamily GTP-binding protein Cdc42 mediates actin cytoskeletal rearrangements and cell cycle progression and is essential for Ras transformation. Expression of a Cdc42 mutant (Cdc42(F28L)) that undergoes spontaneous activation (guanine nucleotide exchange) results in transformation of NIH3T3 fibroblasts. In this report, we show that deletion of residues 120-139 from Cdc42(F28L), which comprise an insert region unique to Rho subfamily proteins but is missing in other GTP-binding proteins, yields a Cdc42 molecule that still undergoes spontaneous GTP-GDP exchange and stimulates both actin cytoskeletal changes and the activation of the cellular targets p21-activated kinase and the c-Jun kinase (JNK1). However, this Cdc42 mutant is unable to transform cells. These findings indicate that the Rho subfamily insert region is dispensable for many of the known signaling pathways initiated by activated Cdc42 but is essential for its regulation of cell growth.

Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.


This article has been cited by other articles:


Home page
 J. Biol. Chem.Home page
Y. Shen, D. S. Hirsch, C. A. Sasiela, and W. J. Wu
Cdc42 Regulates E-cadherin Ubiquitination and Degradation through an Epidermal Growth Factor Receptor to Src-mediated Pathway
J. Biol. Chem., February 22, 2008; 283(8): 5127 - 5137.
[Abstract] [Full Text] [PDF]

Home page
 Eukaryot CellHome page
B. P. Somesh, G. Vlahou, M. Iijima, R. H. Insall, P. Devreotes, and F. Rivero
RacG Regulates Morphology, Phagocytosis, and Chemotaxis
Eukaryot. Cell, October 1, 2006; 5(10): 1648 - 1663.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
S. Tu, W. J. Wu, J. Wang, and R. A. Cerione
Epidermal Growth Factor-dependent Regulation of Cdc42 Is Mediated by the Src Tyrosine Kinase
J. Biol. Chem., December 5, 2003; 278(49): 49293 - 49300.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Cell. Biol.Home page
J. M. Masuda-Robens, S. N. Kutney, H. Qi, and M. M. Chou
The TRE17 Oncogene Encodes a Component of a Novel Effector Pathway for Rho GTPases Cdc42 and Rac1 and Stimulates Actin Remodeling
Mol. Cell. Biol., March 15, 2003; 23(6): 2151 - 2161.
[Abstract] [Full Text] [PDF]

Home page
 Clin. Cancer Res.Home page
Y.-M. Yang, F. Bost, W. Charbono, N. Dean, R. McKay, J. S. Rhim, C. Depatie, and D. Mercola
C-Jun NH2-terminal Kinase Mediates Proliferation and Tumor Growth of Human Prostate Carcinoma
Clin. Cancer Res., January 1, 2003; 9(1): 391 - 401.
[Abstract] [Full Text] [PDF]

Home page
 Genome Res.Home page
I. G. Serebriiskii, O. Mitina, E. N. Pugacheva, E. Benevolenskaya, E. Kotova, G. G. Toby, V. Khazak, W. G. Kaelin, J. Chernoff, and E. A. Golemis
Detection of Peptides, Proteins, and Drugs That Selectively Interact With Protein Targets
Genome Res., November 1, 2002; 12(11): 1785 - 1791.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
S. J. Walker and H. A. Brown
Specificity of Rho Insert-mediated Activation of Phospholipase D1
J. Biol. Chem., July 12, 2002; 277(29): 26260 - 26267.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Cell. Biol.Home page
H. Zong, K. Kaibuchi, and L. A. Quilliam
The Insert Region of RhoA Is Essential for Rho Kinase Activation and Cellular Transformation
Mol. Cell. Biol., August 15, 2001; 21(16): 5287 - 5298.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Cell. Biol.Home page
A. E. Karnoub, C. J. Der, and S. L. Campbell
The Insert Region of Rac1 Is Essential for Membrane Ruffling but Not Cellular Transformation
Mol. Cell. Biol., April 15, 2001; 21(8): 2847 - 2857.
[Abstract] [Full Text]

Home page
 Cell Growth Differ.Home page
G. A. Murphy, S. A. Jillian, D. Michaelson, M. R. Philips, P. D’Eustachio, and M. G. Rush
Signaling Mediated by the Closely Related Mammalian Rho Family GTPases TC10 and Cdc42 Suggests Distinct Functional Pathways
Cell Growth Differ., March 1, 2001; 12(3): 157 - 167.
[Abstract] [Full Text]

Home page
 J. Biol. Chem.Home page
B. C. Bock, P. O. Vacratsis, E. Qamirani, and K. A. Gallo
Cdc42-induced Activation of the Mixed-Lineage Kinase SPRK in Vivo. REQUIREMENT OF THE Cdc42/Rac INTERACTIVE BINDING MOTIF AND CHANGES IN PHOSPHORYLATION
J. Biol. Chem., May 5, 2000; 275(19): 14231 - 14241.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
J.-P. Mira, V. Benard, J. Groffen, L. C. Sanders, and U. G. Knaus
Endogenous, hyperactive Rac3 controls proliferation of breast cancer cells by a p21-activated kinase-dependent pathway
PNAS, January 4, 2000; 97(1): 185 - 189.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Biol. CellHome page
K. G. Kozminski, A. J. Chen, A. A. Rodal, and D. G. Drubin
Functions and Functional Domains of the GTPase Cdc42p
Mol. Biol. Cell, January 1, 2000; 11(1): 339 - 354.
[Abstract] [Full Text]

Home page
 J. Biol. Chem.Home page
R. Li, B. Debreceni, B. Jia, Y. Gao, G. Tigyi, and Y. Zheng
Localization of the PAK1-, WASP-, and IQGAP1-specifying Regions of Cdc42
J. Biol. Chem., October 15, 1999; 274(42): 29648 - 29654.
[Abstract] [Full Text] [PDF]

Home page
 Microbiol. Mol. Biol. Rev.Home page
D. I. Johnson
Cdc42: An Essential Rho-Type GTPase Controlling Eukaryotic Cell Polarity
Microbiol. Mol. Biol. Rev., March 1, 1999; 63(1): 54 - 105.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
H. Zong, N. Raman, L. A. Mickelson-Young, S. J. Atkinson, and L. A. Quilliam
Loop 6 of RhoA Confers Specificity for Effector Binding, Stress Fiber Formation, and Cellular Transformation
J. Biol. Chem., February 19, 1999; 274(8): 4551 - 4560.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
K. F. Wilson, W. J. Wu, and R. A. Cerione
Cdc42 Stimulates RNA Splicing via the S6 Kinase and a Novel S6 Kinase Target, the Nuclear Cap-binding Complex
J. Biol. Chem., November 22, 2000; 275(48): 37307 - 37310.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
S. J. Walker, W.-J. Wu, R. A. Cerione, and H. A. Brown
Activation of Phospholipase D1 by Cdc42 Requires the Rho Insert Region
J. Biol. Chem., May 19, 2000; 275(21): 15665 - 15668.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
N. Matter, M. Marx, S. Weg-Remers, H. Ponta, P. Herrlich, and H. Konig
Heterogeneous Ribonucleoprotein A1 Is Part of an Exon-specific Splice-silencing Complex Controlled by Oncogenic Signaling Pathways
J. Biol. Chem., November 3, 2000; 275(45): 35353 - 35360.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
S. Tu and R. A. Cerione
Cdc42 Is a Substrate for Caspases and Influences Fas-induced Apoptosis
J. Biol. Chem., May 25, 2001; 276(22): 19656 - 19663.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 All ASBMB Journals   Molecular and Cellular Proteomics 
 Journal of Lipid Research   ASBMB Today 
Copyright © 1998 by the American Society for Biochemistry and Molecular Biology.