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By interfering with TSC-Rheb complex, arginine relieves allosteric inhibition of Rheb by TSC. Arginine cooperates with growth factor signaling which further promotes dissociation of TSC2 from lysosomes and activation of mTORC1.
Data show that Rheb/p27 (show PAK2 Proteins) axis induces autophagy-dependent cancer cell survival under stress conditions.
Mutations in the TSC2-RHEB-mTOR (show FRAP1 Proteins) signaling axis may lead to a loss of inhibitory inputs thus conferring a survival advantage to a dividing tumor cell.
Activation of CNTF (show CNTF Proteins)/CNTFRalpha (show CNTFR Proteins) signaling pathway by hRheb(S16H) transduction of dopaminergic neurons
RGS10 (show RGS10 Proteins) could serve in a novel, and previously unknown, role by accelerating the hydrolysis of GTP (show AK3 Proteins) from Rheb in ovarian cancer cells.
In TSC2-deficient angiomyolipoma patient cells, IRF7 (show IRF7 Proteins) is a pivotal factor in the Rheb/mTOR (show FRAP1 Proteins) pathway.
These results establish CAD as a downstream effector of Rheb and suggest a possible role of Rheb in regulating de novo pyrimidine nucleotide synthesis.(Rheb small GTPases, which consist of Rheb1 and Rheb2 (also known as RhebL1 (show RHEBL1 Proteins))
In vitro data indicated that miR (show MLXIP Proteins)-155 suppressed the macrophage-mediated bacterial phagocytosis and intracellular killing of Pseudomonas aeruginosa by targeting Rheb (Ras homolog enriched in brain).
Data indicate that Rheb G63A stimulated phosphorylation of the mTORC1 substrate p70S6 kinase more strongly than wild-type, thus offering a new tool for mammalian target of rapamycin (mTOR (show FRAP1 Proteins)) signaling.
study defines Rheb as a novel physiological regulator of BACE1 (show BACE Proteins) levels and Abeta (show APP Proteins) generation, and the Rheb-BACE1 (show BACE Proteins) circuitry may have a role in brain biology and disease.
Forebrain depletion of Rheb GTPase (show RACGAP1 Proteins) elicits spatial memory deficits.
Rheb is an important negative regulator of beige fat development and thermogenesis. Rheb is able to suppress the beiging effect through an mTORC1-independent mechanism, via PDE4D5-dependent downregulation of the cAMP-PKA signaling pathway.
Rheb and TSC2 have roles in the mechanical activation of mTOR (show FRAP1 Proteins) signaling
EAAT4 (show SLC1A6 Proteins) was downregulated due to the loss of Rheb1 in Purkinje cells; mTORC1 was downregulated and Akt (show AKT1 Proteins) was upregulated in Rheb1 cKO mice, suggesting that mTORC1 and Akt (show AKT1 Proteins) may be related to the downregulation of EAAT4 (show SLC1A6 Proteins); Rheb1 knockout decreased EAAT4 (show SLC1A6 Proteins) currents and slowed down the kinetics of AMPA (show GRIA3 Proteins) currents; Rheb1 deficiency did not affect the morphology of Purkinje cell layer and the development of Purkinje cells
Data suggest that RAS-homolog enriched in brain protein (Rheb1) promotes MLL-AF9 fusion protein initiated acute myeloid leukemia (AML) progression through target of rapamycin complex 1 (mTORC1) signaling pathway.
Rheb activation disrupts neuronal spine synapse formation via syntenin (show SDCBP Proteins) accumulation in tuberous sclerosis complex.
We conclude that in contrast to TORC1 (show CRTC1 Proteins) hyper-activity, cognitive function is not very sensitive to sustained and specific down-regulation of TORC1 (show CRTC1 Proteins) activity.
Rheb protein was mainly detected in apoptotic retinal ganglion cells following light injury.
PDK4 (show PDK4 Proteins) promotes tumorigenesis through activation of the CREB (show CREB1 Proteins)-RHEB-mTORC1 signaling cascade.
The small GTPase (show RACGAP1 Proteins) Rheb is required for spermatogenesis but not oogenesis.
This gene is a member of the small GTPase superfamily and encodes a lipid-anchored, cell membrane protein with five repeats of the RAS-related GTP-binding region. This protein is vital in regulation of growth and cell cycle progression due to its role in the insulin/TOR/S6K signaling pathway. The protein has GTPase activity and shuttles between a GDP-bound form and a GTP-bound form, and farnesylation of the protein is required for this activity. Three pseudogenes have been mapped, two on chromosome 10 and one on chromosome 22.
Ras homolog enriched in brain
, RAS-homolog enriched in brain
, ras homolog enriched in brain
, GTP-binding protein rheb
, GTP-binding protein Rheb
, Ras homolog enriched in brain 2