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Cycling between the inactive GDP- and the active GTP-bound state modulates the backbone dynamics of a C-terminal truncated form, RhebDeltaCT, which is suggested to influence its interactions. We further investigated the interactions between RhebDeltaCT and the proposed Rheb-binding domain of the regulatory protein FKBP38.
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Rheb transcription is regulated by direct Notch1 binding to the Rheb promoter. Rheb expression in the angiomyolipoma and lymphangioleiomyomatosis cells.
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RHEB Y35N expressing cells undergo cancer transformation due to decreased interaction between RHEB and BRAF resulting in overactive RAF/MEK/ERK signaling. Taken together with the previously established function of RHEB to activate mTORC1 signaling, it appears that RHEB performs a dual function; one is to suppress the RAF/MEK/ERK signaling and the other is to activate mTORC1 signaling.
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SNPs of mTORC1-related genes individually or jointly contribute to colorectal cancer susceptibility in Chinese.
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Results identified Rheb as a critical mediator of EP3 expression in cells with mTORC1 hyperactivation.
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RHEB maintained the innate characteristics of chondrocytes by regulating senescence, dedifferentiation and oxidative stress, leading to the upregulation of COL2 expression via SOX9 and the downregulation of p27 expression via MCL1.
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3.0 angstrom cryo-electron microscopy structure of mTORC1 and the 3.4 angstrom Xray structure of activated RHEB-mTORC1
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The mTOR activator gene RHEB is an intellectual disability gene that is associated with megalencephaly when mutated.
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Cellular treatment with AG2037, an inhibitor of the purine biosynthetic enzyme GARFT, profoundly inhibits mTORC1 activity via a reduction in the level of GTP-bound Rheb, an obligate upstream activator of mTORC1, because of a reduction in intracellular guanine nucleotides.
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FADD interference down-regulated Rheb expression and repressed mTORC1 activity in breast cancer cell lines. The autophagy was induced by FADD deficiency in MCF7 or MDA-231 cells but rescued by recovering Rheb expression.
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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.
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activation of mTOR signalling via RHEB over-expression inhibited the starvation-induced autophagy but did not affect trafficking of tf-Amyloid precursor protein (APP). These results show tf-APP can be used to determine how APP is trafficked through the lysosomal system of the cell.
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Data suggest DNM2/RRAGB- (or DNM2/RRAGC-)dependent endocytosis of extracellular amino acids (AAs) plays critical role in mTORC1 transport/activation; recruitment of mTORC1 from cytoplasm to lysosome is suppressed by DNM2 inhibition; AA deprivation appears to be main cause of mTORC1 inactivation via DNM2 inhibition. (RHEB = Ras homolog enriched in brain; DNM2 = dynamin II; RRAG = Ras-related GTP binding protein)
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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.
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Data show that Rheb/p27 axis induces autophagy-dependent cancer cell survival under stress conditions.
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Mutations in the TSC2-RHEB-mTOR signaling axis may lead to a loss of inhibitory inputs thus conferring a survival advantage to a dividing tumor cell.
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Activation of CNTF/CNTFRalpha signaling pathway by hRheb(S16H) transduction of dopaminergic neurons
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RGS10 could serve in a novel, and previously unknown, role by accelerating the hydrolysis of GTP from Rheb in ovarian cancer cells.
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In TSC2-deficient angiomyolipoma patient cells, IRF7 is a pivotal factor in the Rheb/mTOR pathway.
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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)
