| First Author | Goorden SM | Year | 2011 |
| Journal | Mol Cell Biol | Volume | 31 |
| Issue | 8 | Pages | 1672-8 |
| PubMed ID | 21321084 | Mgi Jnum | J:170999 |
| Mgi Id | MGI:4948185 | Doi | 10.1128/MCB.00985-10 |
| Citation | Goorden SM, et al. (2011) Rheb is essential for murine development. Mol Cell Biol 31(8):1672-8 |
| abstractText | Ras homolog enriched in brain (Rheb) couples growth factor signaling to activation of the target of rapamycin complex 1 (TORC1). To study its role in mammals, we generated a Rheb knockout mouse. In contrast to mTOR or regulatory-associated protein of mTOR (Raptor) mutants, the inner cell mass of Rheb(-/-) embryos differentiated normally. Nevertheless, Rheb(-/-) embryos died around midgestation, most likely due to impaired development of the cardiovascular system. Rheb(-/-) embryonic fibroblasts showed decreased TORC1 activity, were smaller, and showed impaired proliferation. Rheb heterozygosity extended the life span of tuberous sclerosis complex 1-deficient (Tsc1(-/-)) embryos, indicating that there is a genetic interaction between the Tsc1 and Rheb genes in mouse. |
