COMPENSATORY MODULATION OF GAP ACTIVITY IN RESPONSE TO ONCOGENIC STIMULATION

GAP is a key negative regulator of the receptor tyrosine kinase (RTK) signal transduction pathway. The purpose of this study was to determin e if expression or activity of GAP is modulated by hyperstimulation of the RTK pathway. It was found that cells forced to express wild-type Ha-ras, viral Ha-ras, or v-src exhibit increased GAP activity as compa red to control cells. In addition, a novel GAP isoform appears in all ras-expressing NIH3T3 cell clones. These data indicate that there is c ompensatory regulation of GAP in response to an increase in RTK pathwa y activity.