High impact information on HRAS

• In contrast, chick sympathetic neurons derived from the more caudally located lumbosacral chain ganglia (LSCG) do not respond to activated p21ras (G12V-Ha-ras mutant) [1].
• In rat embryonic sympathetic neurons from the superior cervical ganglia (SCG) NGF-mediated survival depends on the activation of the trkA receptor tyrosine kinase and on the activity of the intracellular plasmamembrane-anchored small G-protein p21ras [1].
• We conclude that insulin and IGF-I activate p21ras in fetal chick forebrain neurons by increasing the amount of GTP bound to p21ras [2].
• The aims of this study were to determine if insulin and IGF-I activate p21ras in fetal chick forebrain neurons and if activation of p21ras mediates the neurotrophic actions of these peptides [2].
• Pretreatment of neurons with lovastatin (2 micrograms/ml), an inhibitor of ras isoprenylation, completely blocked the activation of p21ras by insulin and IGF-I [2].

Biological context of HRAS

• The proto-oncogene product p21ras has been shown to play an important role in proliferative and differentiative signalling pathways [3].
• These results suggest an involvement of p21ras in signal transduction pathways leading to motor neurone survival and may be of relevance for the development of therapeutic strategies for motor neurone disease [3].

Anatomical context of HRAS

• Evidence that p21ras mediates the neurotrophic effects of insulin and insulin-like growth factor I in chick forebrain neurons [2].

References