The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Effect of IGF-I on phosphatidylinositol 3-kinase in soleus muscle of lean and insulin-resistant obese mice.

Insulin and IGF-I induced a similar stimulation of glucose transport in isolated soleus muscle. These actions require phosphatidylinositol (PI) 3-kinase activation since the PI 3-kinase inhibitor, wortmannin, blocked the stimulation by both peptides. We compared IGF-I with insulin in the ability to activate PI 3-kinase in the isolated soleus muscle from lean and gold thioglucose-induced obese insulin-resistant mice. In muscles from lean mice, IGF-I and insulin were able to activate PI 3-kinase with a similar time course, the effects being maximal within 3-5 min of stimulation. However, the IGF-I concentrations required to obtain similar effects on PI 3-kinase were about 10 times higher than the corresponding insulin doses. To determine through which receptor IGF-I was activating PI 3-kinase, the ability of IGF-I to activate both its own receptor and insulin receptor was simultaneously measured. Whatever the dose used (100 or 500 nmol/l), IGF-I activated to a nearly similar extent both the tyrosine kinase activity of its own receptor and that of the insulin receptor, suggesting that IGF-I was not only activating its receptor but was also able to stimulate the insulin receptor kinase. In muscles of obese insulin-resistant mice, although the defect of PI 3-kinase activation in response to IGF-I was relatively less pronounced (45%) than in response to insulin (70%) when compared with lean mice, PI 3-kinase stimulation was still markedly altered in response to IGF-I.[1]


  1. Effect of IGF-I on phosphatidylinositol 3-kinase in soleus muscle of lean and insulin-resistant obese mice. Jullien, D., Heydrick, S.J., Gautier, N., Van Obberghen, E., Le Marchand-Brustel, Y. Diabetes (1996) [Pubmed]
WikiGenes - Universities