title: Compensatory modulation of GAP activity in response to oncogenic stimulation.
abstract: GAP is a key negative regulator of the receptor tyrosine kinase (RTK) signal transduction pathway. The purpose of this study was to determine 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 compared to control cells. In addition, a novel GAP isoform appears in all ras-expressing NIH3T3 cell clones. These data indicate that there is compensatory regulation of GAP in response to an increase in RTK pathway activity.
authors.affiliation: Department of Pharmacology, University of Nebraska Medical Center, Omaha 68198-6260, USA.
authors.forename: K J
authors.initials: KJ
authors.lastname: Trouba
authors.forename: L
authors.initials: L
authors.lastname: Liao
authors.forename: R L
authors.initials: RL
authors.lastname: Vorce
mesh_terms: D016475:3T3 Cells; D000818:Animals; D020690:GTPase-Activating Proteins; D051379:Mice; D011506:Proteins / Q000378:metabolism*; D020794:Receptor Protein-Tyrosine Kinases / Q000378:metabolism*; D015398:Signal Transduction; D015854:Up-Regulation; D020703:ras GTPase-Activating Proteins; D018631:ras Proteins / Q000378:metabolism*
chemical_list: D020690:GTPase-Activating Proteins; D011506:Proteins; D020703:ras GTPase-Activating Proteins; D020794:Receptor Protein-Tyrosine Kinases; D018631:ras Proteins