the insulin-like growth factor i receptor is required for akt activation and suppression of anoikis in cells transformed by the etv6 - ntrk3 chimeric tyrosine kinase .
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Signaling through the insulin-like growth factor I receptor (IGF-IR) axis is essential for transformation by many dominantly acting oncoproteins. However, the mechanism by which IGF-IR contributes to oncogenesis remains unknown. To examine this, we compared transformation properties of the oncogenic ETV6-NTRK3 (EN) chimeric tyrosine kinase in IGF-IR-null R− mouse embryo fibroblasts with R− cells engineered to reexpress IGF-IR (R+ cells). We previously showed that R− cells expressing EN (R−EN cells) are resistant to transformation but that transformation is restored in R+ cells.
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