FGFR and PTEN signaling interact during lens development to regulate cell survival.

摘要: Lens epithelial cells express many receptor tyrosine kinases (RTKs) that stimulate PI3K-AKT and RAS-RAF-MEK-ERK intracellular signaling pathways. These pathways ultimately activate the phosphorylation of key cellular transcription factors other proteins control proliferation, survival, metabolism, differentiation in virtually all cells. Among RTKs lens, only stimulation fibroblast growth factor receptors (FGFRs) elicits a lens cell to fiber response mammals. Moreover, although expresses three different Fgfr genes, isolated removal Fgfr2 at placode stage inhibits both survival differentiation. Phosphatase tensin homolog (PTEN), commonly known as tumor suppressor, ERK AKT activation initiates apoptotic pathways, cycle arrest. Here, we show combined deletion Pten rescues death phenotype associated with loss alone. Additionally, increased activation, above levels controls, presence or absence Fgfr2. However, failed ectopic differentiation, restore differentiation-specific Aquaporin0 DnaseIIβ expression