Mutations in the SH3 domain of the src oncogene which decrease association of phosphatidylinositol 3'-kinase activity with pp60v-src and alter cellular morphology.

Abstract excerpt

To analyze the signaling pathways utilized in malignant transformation by pp60v-src, we have isolated and characterized src mutants which possess normal levels of protein tyrosine kinase activity but which cause only a partially transformed phenotype. Our hypothesis is that such mutants are partially defective for transformation because they are defective in their ability to activate specific components of the...

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