Document Detail

Small GTPase RhoG is a key regulator for neurite outgrowth in PC12 cells.
MedLine Citation:
PMID:  10982854     Owner:  NLM     Status:  MEDLINE    
The Rho family of small GTPases has been implicated in cytoskeletal reorganization and subsequent morphological changes in various cell types. Among them, Rac and Cdc42 have been shown to be involved in neurite outgrowth in neuronal cells. In this study, we examined the role of RhoG, another member of Rho family GTPases, in nerve growth factor (NGF)-induced neurite outgrowth in PC12 cells. Expression of wild-type RhoG in PC12 cells induced neurite outgrowth in the absence of NGF, and the morphology of wild-type RhoG-expressing cells was similar to that of NGF-differentiated cells. Constitutively active RhoG-transfected cells extended short neurites but developed large lamellipodial or filopodial structures at the tips of neurites. RhoG-induced neurite outgrowth was inhibited by coexpression with dominant-negative Rac1 or Cdc42. In addition, expression of constitutively active RhoG elevated endogenous Rac1 and Cdc42 activities. We also found that the NGF-induced neurite outgrowth was enhanced by expression of wild-type RhoG whereas expression of dominant-negative RhoG suppressed the neurite outgrowth. Furthermore, constitutively active Ras-induced neurite outgrowth was also suppressed by dominant-negative RhoG. Taken together, these results suggest that RhoG is a key regulator in NGF-induced neurite outgrowth, acting downstream of Ras and upstream of Rac1 and Cdc42 in PC12 cells.
H Katoh; H Yasui; Y Yamaguchi; J Aoki; H Fujita; K Mori; M Negishi
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Molecular and cellular biology     Volume:  20     ISSN:  0270-7306     ISO Abbreviation:  Mol. Cell. Biol.     Publication Date:  2000 Oct 
Date Detail:
Created Date:  2000-10-19     Completed Date:  2000-10-19     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  8109087     Medline TA:  Mol Cell Biol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  7378-87     Citation Subset:  IM    
Laboratory of Molecular Neurobiology, Graduate School of Biostudies, Kyoto University, Sakyo-ku, Kyoto 606-8502, Japan.
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MeSH Terms
Cell Differentiation / drug effects
GTP Phosphohydrolases / biosynthesis,  genetics,  physiology*
Genes, Dominant
Mutagenesis, Site-Directed
Neoplasm Proteins / physiology*
Nerve Growth Factors / pharmacology
Nerve Tissue Proteins / physiology*
Neurites / metabolism*
PC12 Cells / drug effects,  metabolism*,  ultrastructure
Recombinant Fusion Proteins / physiology
Signal Transduction
cdc42 GTP-Binding Protein / physiology
rac1 GTP-Binding Protein / physiology
Reg. No./Substance:
0/Neoplasm Proteins; 0/Nerve Growth Factors; 0/Nerve Tissue Proteins; 0/Recombinant Fusion Proteins; 0/Rhog protein, rat; EC 3.6.1.-/GTP Phosphohydrolases; EC GTP-Binding Protein; EC GTP-Binding Protein

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