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By interfering with TSC (show SLC12A3 ELISA Kits)-Rheb complex, arginine relieves allosteric inhibition of Rheb by TSC (show SLC12A3 ELISA Kits). Arginine cooperates with growth factor signaling which further promotes dissociation of TSC2 (show TSC2 ELISA Kits) from lysosomes and activation of mTORC1.
Data show that Rheb/p27 (show PAK2 ELISA Kits) axis induces autophagy-dependent cancer cell survival under stress conditions.
Mutations in the TSC2 (show TSC2 ELISA Kits)-RHEB-mTOR (show FRAP1 ELISA Kits) 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 ELISA Kits)/CNTFRalpha (show CNTFR ELISA Kits) signaling pathway by hRheb(S16H) transduction of dopaminergic neurons
RGS10 (show RGS10 ELISA Kits) could serve in a novel, and previously unknown, role by accelerating the hydrolysis of GTP (show AK3 ELISA Kits) from Rheb in ovarian cancer cells.
In TSC2 (show TSC2 ELISA Kits)-deficient angiomyolipoma patient cells, IRF7 (show IRF7 ELISA Kits) is a pivotal factor in the Rheb/mTOR (show FRAP1 ELISA Kits) pathway.
These results establish CAD (show CAD ELISA Kits) 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 ELISA Kits))
In vitro data indicated that miR (show MLXIP ELISA Kits)-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 ELISA Kits)) signaling.
study defines Rheb as a novel physiological regulator of BACE1 (show BACE ELISA Kits) levels and Abeta (show APP ELISA Kits) generation, and the Rheb-BACE1 (show BACE ELISA Kits) circuitry may have a role in brain biology and disease.
EAAT4 (show SLC1A6 ELISA Kits) was downregulated due to the loss of Rheb1 in Purkinje cells; mTORC1 was downregulated and Akt (show AKT1 ELISA Kits) was upregulated in Rheb1 cKO mice, suggesting that mTORC1 and Akt (show AKT1 ELISA Kits) may be related to the downregulation of EAAT4 (show SLC1A6 ELISA Kits); Rheb1 knockout decreased EAAT4 (show SLC1A6 ELISA Kits) currents and slowed down the kinetics of AMPA (show GRIA3 ELISA Kits) 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 ELISA Kits) accumulation in tuberous sclerosis complex.
We conclude that in contrast to TORC1 (show CRTC1 ELISA Kits) hyper-activity, cognitive function is not very sensitive to sustained and specific down-regulation of TORC1 (show CRTC1 ELISA Kits) activity.
Rheb protein was mainly detected in apoptotic retinal ganglion cells following light injury.
PDK4 (show PDK4 ELISA Kits) promotes tumorigenesis through activation of the CREB (show CREB1 ELISA Kits)-RHEB-mTORC1 signaling cascade.
The small GTPase (show RACGAP1 ELISA Kits) Rheb is required for spermatogenesis but not oogenesis.
The paper proposed a novel pathway/mechanism involving Rheb/mTORC1/S6K (show RPS6KB1 ELISA Kits) signaling to explain how C2-ceramide impairs insulin (show INS ELISA Kits) signaling via Akt (show AKT1 ELISA Kits) phosphorylation.
whereas rapid adaptation in mTORC1 activity requires Rheb, a second Rheb-independent activation mechanism exists that contributes to cell cycle progression.
miR (show MLXIP ELISA Kits)-155 bound to the 3'-untranslated region of Ras homologue enriched in brain (Rheb), a negative regulator of autophagy, accelerated the process of autophagy and sequential killing of intracellular mycobacteria by suppressing Rheb expression.
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