Binding of Ras to Phosphoinositide 3-Kinase p110α Is Required for Ras- Driven Tumorigenesis in Mice

摘要: Ras proteins signal through direct interaction with a number of effector enzymes, including type I phosphoinositide (PI) 3-kinases. Although the ability to control PI 3-kinase has been well established in manipulated cell culture models, evidence for role endogenous normal and malignant growth vivo lacking. Here we generate mice mutations Pi3kca gene encoding catalytic p110α isoform that block its Ras. Cells from these show proliferative defects selective disruption signaling factors 3-kinase. The display defective development lymphatic vasculature, resulting perinatal appearance chylous ascites. Most importantly, they are highly resistant oncogene-induced tumorigenesis. is thus required certain factor Ras-driven tumor formation.