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Human Polyclonal RHEB Primary Antibody for ELISA, WB - ABIN1003086
Yamagata, Sanders, Kaufmann, Yee, Barnes, Nathans, Worley: rheb, a growth factor- and synaptic activity-regulated gene, encodes a novel Ras-related protein. in The Journal of biological chemistry 1994
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Human Polyclonal RHEB Primary Antibody for IHC, ELISA - ABIN1003087
Yee, Worley: Rheb interacts with Raf-1 kinase and may function to integrate growth factor- and protein kinase A-dependent signals. in Molecular and cellular biology 1997
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Human Monoclonal RHEB Primary Antibody for ELISA, WB - ABIN519784
Menon, Dibble, Talbott, Hoxhaj, Valvezan, Takahashi, Cantley, Manning: Spatial control of the TSC complex integrates insulin and nutrient regulation of mTORC1 at the lysosome. in Cell 2014
Human Polyclonal RHEB Primary Antibody for WB - ABIN2476356
Kageyama, Takahashi: Pepsinogens and pepsins from gastric mucosa of Japanese Monkey. Purification and characterization. in Journal of biochemistry 1976
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Results identified Rheb as a critical mediator of EP3 (show PTGER3 Antibodies) expression in cells with mTORC1 hyperactivation.
RHEB maintained the innate characteristics of chondrocytes by regulating senescence, dedifferentiation and oxidative stress, leading to the upregulation of COL2 expression via SOX9 (show SOX9 Antibodies) and the downregulation of p27 (show PAK2 Antibodies) expression via MCL1 (show MCL1 Antibodies).
3.0 angstrom cryo-electron microscopy structure of mTORC1 and the 3.4 angstrom Xray structure of activated RHEB-mTORC1
The mTOR (show FRAP1 Antibodies) activator gene RHEB is an intellectual disability gene that is associated with megalencephaly when mutated.
Cellular treatment with AG2037, an inhibitor of the purine biosynthetic enzyme GARFT, profoundly inhibits mTORC1 activity via a reduction in the level of GTP (show AK3 Antibodies)-bound Rheb, an obligate upstream activator of mTORC1, because of a reduction in intracellular guanine nucleotides.
FADD (show FADD Antibodies) interference down-regulated Rheb expression and repressed mTORC1 activity in breast cancer cell lines. The autophagy was induced by FADD (show FADD Antibodies) 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 (show FRAP1 Antibodies) signalling via RHEB over-expression inhibited the starvation-induced autophagy but did not affect trafficking of tf-Amyloid precursor protein (APP (show APP Antibodies)). These results show tf-APP (show APP Antibodies) can be used to determine how APP (show APP Antibodies) is trafficked through the lysosomal system of the cell.
Data suggest DNM2 (show DNM2 Antibodies)/RRAGB (show RRAGB Antibodies)- (or DNM2 (show DNM2 Antibodies)/RRAGC (show RRAGC Antibodies)-)dependent endocytosis of extracellular amino acids (AAs (show FGD1 Antibodies)) plays critical role in mTORC1 transport/activation; recruitment of mTORC1 from cytoplasm to lysosome is suppressed by DNM2 (show DNM2 Antibodies) inhibition; AA deprivation appears to be main cause of mTORC1 inactivation via DNM2 (show DNM2 Antibodies) inhibition. (RHEB = Ras homolog enriched in brain; DNM2 (show DNM2 Antibodies) = dynamin II (show DNM2 Antibodies); RRAG = Ras-related GTP binding protein (show RAB10 Antibodies))
By interfering with TSC (show SLC12A3 Antibodies)-Rheb complex, arginine relieves allosteric inhibition of Rheb by TSC (show SLC12A3 Antibodies). Arginine cooperates with growth factor signaling which further promotes dissociation of TSC2 (show TSC2 Antibodies) from lysosomes and activation of mTORC1.
Ggpps (show GGPS1 Antibodies) deletion enhanced Rheb farnesylation, which subsequently activated mTORC1 and facilitated spermatogonial differentiation
Thus, the various regulatory elements that impinge upstream of mTORC1 activation pathways are differentially required for HSC (show FUT1 Antibodies) homeostasis in vivo.
Forebrain depletion of Rheb GTPase (show RACGAP1 Antibodies) elicits spatial memory deficits.
Rheb is an important negative regulator of beige (show LYST Antibodies) 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 (show TSC2 Antibodies) have roles in the mechanical activation of mTOR (show FRAP1 Antibodies) signaling
EAAT4 (show SLC1A6 Antibodies) was downregulated due to the loss of Rheb1 in Purkinje cells; mTORC1 was downregulated and Akt (show AKT1 Antibodies) was upregulated in Rheb1 cKO mice, suggesting that mTORC1 and Akt (show AKT1 Antibodies) may be related to the downregulation of EAAT4 (show SLC1A6 Antibodies); Rheb1 knockout decreased EAAT4 (show SLC1A6 Antibodies) currents and slowed down the kinetics of AMPA (show GRIA3 Antibodies) 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 Antibodies) accumulation in tuberous sclerosis complex.
We conclude that in contrast to TORC1 (show CRTC1 Antibodies) hyper-activity, cognitive function is not very sensitive to sustained and specific down-regulation of TORC1 (show CRTC1 Antibodies) activity.
Rheb protein was mainly detected in apoptotic retinal ganglion cells following light injury.
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