a GTPase activator for normal RAS p21 but not its oncogenic counterpart, converting it to the putatively inactive GDP-bound state. Acting as a suppressor of RAS function, it enhances the weak intrinsic GTPase activity of RAS proteins resulting in the inactive GDP-bound form of RAS, thereby allowing control of cellular proliferation and differentiation. Mutations leading to changes in the binding sites of either protein are associated with basal cell carcinomas. Two alternatively spliced isoforms have been described. Note: This description may include information from UniProtKB.
Protein type: Motility/polarity/chemotaxis; GAPs, Ras; Oncoprotein; GAPs
Biological Process: blood vessel morphogenesis; cytokinesis after mitosis; embryonic development; ephrin receptor signaling pathway; MAPKKK cascade; negative regulation of cell adhesion; negative regulation of cell-matrix adhesion; negative regulation of neuron apoptosis; negative regulation of Ras protein signal transduction; positive regulation of GTPase activity; regulation of actin filament polymerization; regulation of cell shape; regulation of RNA metabolic process; signal transduction; vasculogenesis
LTP: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.