2002
DOI: 10.1038/sj.onc.1205792
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Rheb is in a high activation state and inhibits B-Raf kinase in mammalian cells

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Cited by 124 publications
(119 citation statements)
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“…Yet not all activities of Rheb are mediated by TOR. Rheb interacts with the B-Raf kinase in a rapamycin-resistant manner and inhibits its function, resulting in an interference with H-Ras (G12V)-induced transformation of NIH 3T3 cells (Clark et al, 1997;Yee and Worley, 1997;Im et al, 2002;Karbowniczek et al, 2004Karbowniczek et al, , 2006. The pronounced vacuolization observed in Rheb-expressing cells by Saitc and co-workers and by us appears to reflect another TOR-independent function of Rheb (Saito et al, 2005).…”
Section: Oncogenic Transformations By Rheb Mutants H Jiang and Pk Vogtmentioning
confidence: 68%
See 1 more Smart Citation
“…Yet not all activities of Rheb are mediated by TOR. Rheb interacts with the B-Raf kinase in a rapamycin-resistant manner and inhibits its function, resulting in an interference with H-Ras (G12V)-induced transformation of NIH 3T3 cells (Clark et al, 1997;Yee and Worley, 1997;Im et al, 2002;Karbowniczek et al, 2004Karbowniczek et al, , 2006. The pronounced vacuolization observed in Rheb-expressing cells by Saitc and co-workers and by us appears to reflect another TOR-independent function of Rheb (Saito et al, 2005).…”
Section: Oncogenic Transformations By Rheb Mutants H Jiang and Pk Vogtmentioning
confidence: 68%
“…It contains five G boxes that are involved in the recognition and hydrolysis of GTP (Urano et al, 2000). Biochemical and cell biological evidence suggests that Rheb has a low intrinsic GTPase activity and occurs preferentially in an activated, GTPbound state (Clark et al, 1997;Im et al, 2002). The tuberous sclerosis complex (TSC), a tumor suppressor formed by the TSC1 (hamartin) and TSC2 (tuberin) proteins, functions as a GTPase-activating protein (GAP) and hence as a negative regulator of Rheb (Castro et al, 2003;Garami et al, 2003;Inoki et al, 2003;Tee et al, 2003;Zhang et al, 2003).…”
Section: Introductionmentioning
confidence: 99%
“…Association of LKB1 inactivation clustering with non-V600 BRAF mutations ( Figures 1A and B) was also observed. LKB1 and RAS/RAF/MEK (MAPK) signalling pathways are linked through RHEB, which when active, activates mTOR and inhibits wild-type BRAF, but not the mutated form (Im et al, 2002;Garami et al, 2003;Karbowniczek et al, 2004). It was recently shown that the inhibition of RAF1 (cRAF) activity by RHEB prevents heterodimerisation of BRAF and RAF1 (Karbowniczek et al, 2006).…”
Section: Resultsmentioning
confidence: 99%
“…Overexpression of Rheb leads to its constitutive GTP loading and renders this GTPase insensitive to regulation, 19,63 but when endogenous Rheb, or recombinant Rheb expressed at endogenous levels, was examined, the GTP loading of Rheb was found to be modulated by amino acid concentrations. 64,65 Thus, the potential regulation of Rheb-PLD interaction by amino acids should be investigated with either endogenous Rheb or recombinant Rheb expressed at the endogenous levels.…”
Section: The Pld-mtor Connection: An Asset For Mammalsmentioning
confidence: 99%