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First published online 19 May 2009
doi: 10.1242/jcs.044644

Journal of Cell Science 122, 2024-2033 (2009)
Published by The Company of Biologists 2009
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Research Article

IQGAP1 regulates cell proliferation through a novel CDC42-mTOR pathway

Jian-Bin Wang1, Robert Sonn2, Yemmsrach K. Tekletsadik2, Daniel Samorodnitsky2 and Mahasin A. Osman1,2,*

1 Department of Molecular Medicine, Cornell University, Ithaca, NY 14853, USA
2 Institute for Biotechnology and Life Sciences, Cornell University, Ithaca, NY 14853, USA

* Author for correspondence (e-mail: mo28{at}cornell.edu)

Accepted 11 March 2009

Cell proliferation requires close coordination of cell growth and division to ensure constant cell size through the division cycles. IQGAP1, an effector of CDC42 GTPase has been implicated in the modulation of cell architecture, regulation of exocytosis and in human cancers. The precise mechanism underlying these activities is unclear. Here, we show that IQGAP1 regulates cell proliferation, which requires phosphorylation of IQGAP1 and binding to CDC42. Expression of the C-terminal region of IQGAP1 enhanced cellular transformation and migration, but reduced the cell size, whereas expression of the N-terminus increased the cell size, but inhibited cell transformation and migration. The N-terminus of IQGAP1 interacts with mTOR, which is required for IQGAP1-mediated cell proliferation. These findings are consistent with a model where IQGAP1 serves as a phosphorylation-sensitive conformation switch to regulate the coupling of cell growth and division through a novel CDC42-mTOR pathway, dysregulation of which generates cellular transformation.

Key words: Cell growth, IQGAP1, Protein synthesis


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Growing and dividing with IQGAP1

JCS 2009 122: 1205. [Full Text]  





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