Autocrine regulation of Leydig cell differentiated functions by insulin-like growth factor I and transforming growth factor beta

1999 ◽  
Vol 69 (1-6) ◽  
pp. 379-384 ◽  
Author(s):  
Christine Le Roy ◽  
Hervé Lejeune ◽  
Franck Chuzel ◽  
José M Saez ◽  
Dominique Langlois
Keyword(s):  
Growth Factor ◽  
Leydig Cell ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Autocrine Regulation ◽  
Growth Factor Beta ◽  
Growth Factor I

scholarly journals Receptor regulation of phosphoinositide 3-hydroxykinase in the NG115-401L-C3 neuronal cell line: stimulation by insulin-like growth factor-I

1993 ◽  
Vol 290 (3) ◽  
pp. 901-905 ◽  
Author(s):  
D R Poyner ◽  
M R Hanley ◽  
T R Jackson ◽  
P T Hawkins
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Protein Tyrosine Kinase ◽  
Transforming Growth Factor ◽  
Interleukin 1 ◽  
Neuronal Cell ◽  
Insulin Like Growth Factor ◽  
Intact Cells ◽  
Factor I ◽  
Growth Factor I

The activation of phosphoinositide 3-hydroxykinase (P13K) is currently believed to represent the critical regulatory event which leads to the production of a novel intracellular signal. We have examined the control of this pathway by a number of cell-surface receptors in NG115-401L-C3 neuronal cells. Insulin-like growth factor-I stimulated the accumulation of 3-phosphorylated inositol lipids in intact cells and the appearance of P13K in antiphosphotyrosine-antibody-directed immunoprecipitates prepared from lysed cells, suggesting that P13K had been activated by a mechanism involving a protein tyrosine kinase. In contrast, P13K in these cells was not regulated by a variety of G-protein-coupled receptors, nerve growth factor acting via a low affinity receptor, or receptors for transforming growth factor-beta and interleukin-1. The receptor-specificity of P13K activation in these cells places significant constraints on the possible physiological function(s) of this pathway.

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