[6] Ras-GRF1 has been shown to mediate long term potentiation (LTP), affecting memory and learning.
Ras-GRF1 knockout mice treated with HFS-LTP have exhibited the inability to induce LTP in direct MSN pathways.
Ras-GRF1 signaling has been thought to be involved with L-DOPA-induced dyskinesia, a condition in which LTP and MSN homeostasis are disrupted.
[7] Alongside its regulation of learning and memory, Ras-GRF1 has exhibited the ability to impact pancreatic β-cell proliferation.
Reduction of β-cell mass and area has correlated to a decrease in circulating insulin levels, exposing a Ras-GRF1 signaling pathway that regulates glucose metabolism.