Aperçu des produits pour anti-RHEB (RHEB) Anticorps

Human Ras Homolog Enriched in Brain (RHEB) interaction partners

1. results demonstrate that PIM3 is induced upon mTORC1 inhibition, with potential implications for the effects of mTORC1 inhibitors in TSC, cancers, and the many other disease settings influenced by aberrant mTORC1 signaling.

2. 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.

3. Rheb transcription is regulated by direct Notch1 binding to the Rheb promoter. Rheb expression in the angiomyolipoma and lymphangioleiomyomatosis cells.

4. 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.

5. SNPs of mTORC1-related genes individually or jointly contribute to colorectal cancer susceptibility in Chinese.

6. Results identified Rheb as a critical mediator of EP3 expression in cells with mTORC1 hyperactivation.

7. 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.

8. 3.0 angstrom cryo-electron microscopy structure of mTORC1 and the 3.4 angstrom Xray structure of activated RHEB-mTORC1

9. The mTOR activator gene RHEB is an intellectual disability gene that is associated with megalencephaly when mutated.

10. 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.

11. 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.

12. 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.

13. 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.

14. 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)

15. 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.

16. Data show that Rheb/p27 axis induces autophagy-dependent cancer cell survival under stress conditions.

17. 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.

18. Activation of CNTF/CNTFRalpha signaling pathway by hRheb(S16H) transduction of dopaminergic neurons

19. RGS10 could serve in a novel, and previously unknown, role by accelerating the hydrolysis of GTP from Rheb in ovarian cancer cells.

20. In TSC2-deficient angiomyolipoma patient cells, IRF7 is a pivotal factor in the Rheb/mTOR pathway.

Mouse (Murine) Ras Homolog Enriched in Brain (RHEB) interaction partners

1. This study found that cRheb expression promoted regeneration of injured rVRG axons into the lesion site, while we observed no rVRG axon regrowth with AAV2-GFP control.

2. Rheb1 is critical for the polarization of macrophages and inhibition of allergic asthma. Deletion of Rheb1 enhances M2 polarization but decreases M1 polarization in alveolar macrophages, leading to the aggravation of OVA-induced allergic asthma.

3. Ggpps deletion enhanced Rheb farnesylation, which subsequently activated mTORC1 and facilitated spermatogonial differentiation

4. Thus, the various regulatory elements that impinge upstream of mTORC1 activation pathways are differentially required for HSC homeostasis in vivo.

5. Forebrain depletion of Rheb GTPase elicits spatial memory deficits.

6. 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.

7. Rheb and TSC2 have roles in the mechanical activation of mTOR signaling

8. Rheb1 is critical for macrophage production and phagocytosis and executes these activities possibly via mTORC1-dependent pathway.

9. EAAT4 was downregulated due to the loss of Rheb1 in Purkinje cells; mTORC1 was downregulated and Akt was upregulated in Rheb1 cKO mice, suggesting that mTORC1 and Akt may be related to the downregulation of EAAT4; Rheb1 knockout decreased EAAT4 currents and slowed down the kinetics of AMPA currents; Rheb1 deficiency did not affect the morphology of Purkinje cell layer and the development of Purkinje cells

10. The expression pattern of RHEB1 suggests that it likely plays a ubiquitous role in the development of the early embryo with more tissue-specific roles in later development.

11. 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.

12. Rheb activation disrupts neuronal spine synapse formation via syntenin accumulation in tuberous sclerosis complex.

13. We conclude that in contrast to TORC1 hyper-activity, cognitive function is not very sensitive to sustained and specific down-regulation of TORC1 activity.

14. Rheb protein was mainly detected in apoptotic retinal ganglion cells following light injury.

15. PDK4 promotes tumorigenesis through activation of the CREB-RHEB-mTORC1 signaling cascade.

16. We conclude that oligodendrocyte progenitor cells-intrinsic mTORC1 activity mediated by Rheb1 is critical for differentiation of oligodendrocyte progenitor cells

17. The small GTPase Rheb is required for spermatogenesis but not oogenesis.

18. The paper proposed a novel pathway/mechanism involving Rheb/mTORC1/S6K signaling to explain how C2-ceramide impairs insulin signaling via Akt phosphorylation.

19. whereas rapid adaptation in mTORC1 activity requires Rheb, a second Rheb-independent activation mechanism exists that contributes to cell cycle progression.

20. deletion of Rheb1 in the brain causes a reduction in mTORC1 activity and impairs food intake.

Fruit Fly (Drosophila melanogaster) Ras Homolog Enriched in Brain (RHEB) interaction partners

1. Rheb overexpression in the central brain neurons of flies causes not only morphological phenotypes, but behavioral and aging phenotypes that may mirror symptoms of tuberous sclerosis complex

2. Rheb is an essential regulator of S6K in controlling cell growth in Drosophila.

3. Rheb promotes cell growth as a component of the insulin/TOR signaling network.

4. Rheb is a direct target of the tuberous sclerosis suppressor proteins.

5. dRheb is required for both cell growth (increase in mass) and cell cycle progression

6. Results suggest that TSC1/2 and Rheb have different effects on the activity of TORC1 and -2, further supporting the complexity of TOR regulation.

7. Results show that mildly increasing systemic Rheb-TOR-S6K signaling sensitizes the whole organism to oxidative stress and promotes senescence of locomotor activity with age.

8. Our studies identify TCTP as a direct regulator of Rheb and a potential therapeutic target for tuberous sclerosis disease.

9. Rheb-TOR signaling controls S2 cell growth by promoting ribosome production and protein synthesis, not by direct effects on the import of amino acids or glucose.

10. Drosophila TCTP (dTCTP) displays GEF activity to Rheb and is essential for Rheb activation in organ growth