Document Detail

Overexpression of Akt inhibits NGF-induced growth arrest and neuronal differentiation of PC12 cells.
MedLine Citation:
PMID:  11112692     Owner:  NLM     Status:  MEDLINE    
To investigate the role of Akt in nerve growth factor (NGF)-induced neuronal differentiation, PC12 cells ectopically expressing wild-type or dominant-inhibitory forms of Akt were analyzed. NGF-induced neurite outgrowth was greatly accelerated in cells expressing dominant-inhibitory Akt, compared to parental PC12 cells, but was almost completely blocked in cells expressing wild-type Akt. Since neuronal differentiation requires an arrest of cell growth, several aspects of cell growth of the different cell lines were compared. Cells expressing wild-type Akt were not susceptible to the growth-arresting effect of NGF, whereas parental PC12 cells and notably cells expressing mutant Akt were so affected. Accompanying this, the expressions of CDKs and p21(WAF1) were down- and up-regulated, respectively, in both parental PC12 cells and cells expressing mutant Akt. When treated with some growth arrest-inducing agents such as sodium nitroprusside, forskolin and butyrolactone I, cells expressing wild-type Akt regained their responsiveness to the effects of NGF on differentiation. In summary, our results indicate that Akt overrides the growth-arresting effect of NGF and thereby, negatively regulates neuronal differentiation.
O S Bang; E K Park; S I Yang; S R Lee; T F Franke; S S Kang
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of cell science     Volume:  114     ISSN:  0021-9533     ISO Abbreviation:  J. Cell. Sci.     Publication Date:  2001 Jan 
Date Detail:
Created Date:  2001-01-26     Completed Date:  2001-06-07     Revised Date:  2012-06-22    
Medline Journal Info:
Nlm Unique ID:  0052457     Medline TA:  J Cell Sci     Country:  England    
Other Details:
Languages:  eng     Pagination:  81-88     Citation Subset:  IM    
Department of Biology, College of Natural Sciences, Kyungpook National University, Taegu 702-701, Korea.
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MeSH Terms
4-Butyrolactone / analogs & derivatives*,  pharmacology
CDC2 Protein Kinase / metabolism
Cell Differentiation / physiology*
Cell Division
Cyclin-Dependent Kinase Inhibitor p21
Cyclins / metabolism
Enzyme Inhibitors / pharmacology
Forskolin / pharmacology
Gene Expression
Nerve Growth Factor / physiology
Neurites / drug effects,  physiology*
Neurons / cytology*,  drug effects
Nitroprusside / pharmacology
PC12 Cells
Protein Kinase Inhibitors
Protein-Serine-Threonine Kinases*
Proto-Oncogene Proteins / genetics,  physiology*
Proto-Oncogene Proteins c-akt
Reg. No./Substance:
0/Cdkn1a protein, rat; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/Cyclins; 0/Enzyme Inhibitors; 0/Protein Kinase Inhibitors; 0/Proto-Oncogene Proteins; 15078-28-1/Nitroprusside; 66428-89-5/Forskolin; 87414-49-1/butyrolactone I; 9061-61-4/Nerve Growth Factor; 96-48-0/4-Butyrolactone; EC protein, rat; EC Kinases; EC Proteins c-akt; EC Protein Kinase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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