Supplementary Figure 4: PTEN and AKT regulate IGF1R expression via feedback mechanism. | Nature Structural & Molecular Biology

Supplementary Figure 4: PTEN and AKT regulate IGF1R expression via feedback mechanism.

From: PTEN is a protein tyrosine phosphatase for IRS1

Supplementary Figure 4

(a) PTEN-/- MEFs express lower level of IGF1R which can be increased by AKT inhibition. WT or PTEN-/- MEFs were treated with 1 μM AKTi for 12 or 24 hrs. γ-tubulin is used as loading control. (b) MEFs harboring long-term PTEN shRNA have a decreased IGF1R expression, which can be reversed by AKT inhibition. β-actin is used as loading control. (c) Expression of wild-type but not CS or GE mutant PTEN increased IGF1R expression in PTEN-/- MEFs. PTEN-/- MEFs were reconstituted with GFP or GFP-S-PTEN (WT/CS/GE), and treated with or without 1 μM AKTi for 24 hrs. (d) Stable PTEN shRNA restored IGF1-induced AKT activation in NEDD4-/- MEFs but had minimal effect on IRS1 phosphorylation. NEDD4-/- MEFs with control knockdown or stable PTEN knockdown were serum-starved, and then stimulated with 50 ng/ml IGF1 for 5 min, with or without 1 μM PI3K inhibitor

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