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FADD (zeige FADD Proteine) interference down-regulated Rheb expression and repressed mTORC1 activity in breast cancer cell lines. The autophagy was induced by FADD (zeige FADD Proteine) deficiency in MCF7 or MDA-231 cells but rescued by recovering Rheb expression.
Describe a novel interaction between Rheb and the tumor suppressor RASSF1A. This interaction may allow coordinate upregulation of Hippo while TOR is suppressed to modulate the balance of apoptosis and autophagy in lung tumor cells.
activation of mTOR (zeige FRAP1 Proteine) signalling via RHEB over-expression inhibited the starvation-induced autophagy but did not affect trafficking of tf-Amyloid precursor protein (APP (zeige APP Proteine)). These results show tf-APP (zeige APP Proteine) can be used to determine how APP (zeige APP Proteine) is trafficked through the lysosomal system of the cell.
Data suggest DNM2 (zeige DNM2 Proteine)/RRAGB (zeige RRAGB Proteine)- (or DNM2 (zeige DNM2 Proteine)/RRAGC (zeige RRAGC Proteine)-)dependent endocytosis of extracellular amino acids (AAs (zeige FGD1 Proteine)) plays critical role in mTORC1 transport/activation; recruitment of mTORC1 from cytoplasm to lysosome is suppressed by DNM2 (zeige DNM2 Proteine) inhibition; AA deprivation appears to be main cause of mTORC1 inactivation via DNM2 (zeige DNM2 Proteine) inhibition. (RHEB = Ras homolog enriched in brain; DNM2 (zeige DNM2 Proteine) = dynamin II (zeige DNM2 Proteine); RRAG = Ras-related GTP binding protein (zeige RAB10 Proteine))
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 (zeige PAK2 Proteine) axis induces autophagy-dependent cancer cell survival under stress conditions.
Mutations in the TSC2-RHEB-mTOR (zeige FRAP1 Proteine) signaling axis may lead to a loss of inhibitory inputs thus conferring a survival advantage to a dividing tumor cell.
Activation of CNTF (zeige CNTF Proteine)/CNTFRalpha (zeige CNTFR Proteine) signaling pathway by hRheb(S16H) transduction of dopaminergic neurons
RGS10 (zeige RGS10 Proteine) could serve in a novel, and previously unknown, role by accelerating the hydrolysis of GTP (zeige AK3 Proteine) from Rheb in ovarian cancer cells.
In TSC2-deficient angiomyolipoma patient cells, IRF7 (zeige IRF7 Proteine) is a pivotal factor in the Rheb/mTOR (zeige FRAP1 Proteine) pathway.
Thus, the various regulatory elements that impinge upstream of mTORC1 activation pathways are differentially required for HSC (zeige FUT1 Proteine) homeostasis in vivo.
Forebrain depletion of Rheb GTPase (zeige RACGAP1 Proteine) 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 (zeige FRAP1 Proteine) signaling
EAAT4 (zeige SLC1A6 Proteine) was downregulated due to the loss of Rheb1 in Purkinje cells; mTORC1 was downregulated and Akt (zeige AKT1 Proteine) was upregulated in Rheb1 cKO mice, suggesting that mTORC1 and Akt (zeige AKT1 Proteine) may be related to the downregulation of EAAT4 (zeige SLC1A6 Proteine); Rheb1 knockout decreased EAAT4 (zeige SLC1A6 Proteine) currents and slowed down the kinetics of AMPA (zeige GRIA3 Proteine) 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 (zeige SDCBP Proteine) accumulation in tuberous sclerosis complex.
We conclude that in contrast to TORC1 (zeige CRTC1 Proteine) hyper-activity, cognitive function is not very sensitive to sustained and specific down-regulation of TORC1 (zeige CRTC1 Proteine) activity.
Rheb protein was mainly detected in apoptotic retinal ganglion cells following light injury.
PDK4 (zeige PDK4 Proteine) promotes tumorigenesis through activation of the CREB (zeige CREB1 Proteine)-RHEB-mTORC1 signaling cascade.
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