Document Detail

Constitutive cellular expression of PI 3-kinase is distinct from transient expression.
MedLine Citation:
PMID:  10860837     Owner:  NLM     Status:  MEDLINE    
The discovery that the PTEN tumor suppressor encodes a phosphoinositide 3-phosphatase has raised interest in the effects of constitutive activation of PI 3-kinase. To gain insight into PI 3-kinase function, we have stably expressed a myristoylated form of the catalytic subunit p110alpha (myr-p110) in cells. The myr-p110 associated with the endogenous p85 regulatory subunit and retained lipid and protein kinase activity. Stable lines expressing myr-p110 had 2- to 4-fold more PI 3-kinase activity than controls. Expression of myr-p110 altered cellular morphology and increased the saturation density in culture. These clones were morphologically transformed but Akt and pp70(s6k) were not constitutively activated in contrast to transient assays and from tumor cell lines deficient in PTEN. In addition, the ability of PDGF to induce activation of Akt and pp70(s6k) was diminished. Therefore, expression of a myristoylated PI 3-kinase in murine fibroblasts induces a morphological transformation of the cells.
K R Auger; J Wang; R P Narsimhan; T Holcombe; T M Roberts
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Biochemical and biophysical research communications     Volume:  272     ISSN:  0006-291X     ISO Abbreviation:  Biochem. Biophys. Res. Commun.     Publication Date:  2000 Jun 
Date Detail:
Created Date:  2000-07-26     Completed Date:  2000-07-26     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0372516     Medline TA:  Biochem Biophys Res Commun     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  822-9     Citation Subset:  IM    
Copyright Information:
Copyright 2000 Academic Press.
Cellular and Molecular Biology, Dana-Farber Cancer Institute, Boston, MA, USA.
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MeSH Terms
1-Phosphatidylinositol 3-Kinase / chemistry,  genetics*,  metabolism*
3T3 Cells
Actins / metabolism
Catalytic Domain / genetics,  physiology
Cell Adhesion
Cell Count
Cell Line, Transformed
Cell Size
Cell Transformation, Neoplastic*
Contact Inhibition
Enzyme Activation / drug effects
Gene Expression*
Molecular Weight
Myristic Acid / metabolism
PTEN Phosphohydrolase
Phosphoric Monoester Hydrolases / deficiency,  genetics,  metabolism
Platelet-Derived Growth Factor / pharmacology
Precipitin Tests
Protein-Serine-Threonine Kinases*
Proto-Oncogene Proteins / metabolism
Proto-Oncogene Proteins c-akt
Ribosomal Protein S6 Kinases / metabolism
Signal Transduction / drug effects
Tumor Suppressor Proteins*
Reg. No./Substance:
0/Actins; 0/Platelet-Derived Growth Factor; 0/Proto-Oncogene Proteins; 0/Tumor Suppressor Proteins; 544-63-8/Myristic Acid; EC 3-Kinase; EC Kinases; EC Proteins c-akt; EC Protein S6 Kinases; EC 3.1.3.-/Phosphoric Monoester Hydrolases; EC Phosphohydrolase

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

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