Mouse anti-RHEB (Sku# 433210) detects Ras homolog enriched in brain (RHEB), which is the member of small GTPase superfamily, and involved in many cell signaling pathways such as mTor, raf and insulin. Its reactivity is confirmed in human, mouse and rat, with western blot, and based on sequence homology reactivity in chimpanzee, rhesus monkey, bovine and chicken is also expected.
RHEB, Ras homolog enriched in brain, belongs to the small GTPase superfamily. It is ubiquitously expressed with highest levels expressed in skeletal and cardiac muscle. Like other family members, RHEB interacts with Raf-1 kinase and triggers activation of Raf-MEK-MAPK pathway. Mammalian target of rapamycin, mTOR, is a central regulator of cell growth. mTOR is a serine⁄threonine kinase that acts as a sensor for ATP and amino acids. Its activity is regulated by RHEB in response to growth factor stimulation and nutrient availability. This regulation is achieved by preventing the association of mTOR with FKBP38, a member of the FK506-binding protein family. Analysis of RHEB mutants show that switch 2 segment of the molecule is critical for signaling to mTOR. Tuberin and Hamartin, products of TSC2 and TSC1 genes, inhibit mTOR nutrient signaling input. They achieve this by acting as RHEB GTPase activating proteins (GAP). All this data shows that RHEB is one of the major regulators of mTOR signaling, an area of great interest to drug discovery.