Dominant negative effect of the truncated p110 subunit of phosphatidylinositol-3 kinase.
Effects of p110, the catalytic subunit of PI-3 kinase, on induction of TPA response element-driven promoter by EGF was examined. The induction was enhanced by co-expression of the wild type of p110. The truncated p110 mutants containing the binding site for p85 but missing the catalytic activity repressed the induction. A mutant with no binding activity to p85 did not show this effect. These results suggest that PI-3 kinase is involved in signal transduction of EGF and that the truncated p110s capable of binding to p85 serves as a dominant negative reagent for PI-3 kinase.
Takayanagi
J
J
Department of Applied Biological Chemistry, Faculty of Agricultural and Life Science, University of Tokyo, Japan.
Kimura
K
K
Nishioka
N
N
Akimoto
K
K
Moriya
S
S
Ohno
S
S
Fukui
Y
Y
D000818:Animals; D004789:Enzyme Activation; D004815:Epidermal Growth Factor / Q000494:pharmacology; D016297:Mutagenesis, Site-Directed; D019869:Phosphatidylinositol 3-Kinases; D017853:Phosphotransferases (Alcohol Group Acceptor) / Q000737:chemistry* / Q000235:genetics; D011487:Protein Conformation; D051381:Rats
D004815:Epidermal Growth Factor; D019869:Phosphatidylinositol 3-Kinases; D017853:Phosphotransferases (Alcohol Group Acceptor)