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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Ras homolog enriched in brain

Rheb, Ras homolog enriched in brain
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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: mTOR, mTORC1, TSC2, Tumor Suppressor, ACID
Papers on Rheb
Antidepressant action of ketamine via mTOR is mediated by inhibition of nitrergic Rheb degradation.
New
Snyder et al., Baltimore, United States. In Mol Psychiatry, Feb 2016
Nitrosylated GAPDH complexes with the ubiquitin-E3-ligase Siah1 and Rheb, a small G protein that activates mTOR.
Mammalian target of rapamycin/eukaryotic initiation factor 4F pathway regulates follicle growth and development of theca cells in mice.
New
Gao et al., In Reprod Fertil Dev, Feb 2016
Then, 3 d.p.p. ovaries were retrieved and used to verify the role of mTOR signalling in follicle and thecal cell development using its activators (Ras homologue enriched in brain (Rheb) and GTP) and inhibitor (rapamycin).
Control of TSC2-Rheb signaling axis by arginine regulates mTORC1 activity.
New
Korolchuk et al., Newcastle upon Tyne, United Kingdom. In Elife, Feb 2016
Instead, arginine specifically suppresses lysosomal localization of the TSC complex and interaction with its target small GTPase protein, Rheb.
Transport to Rhebpress Activity.
New
Djouder et al., Madrid, Spain. In Small Gtpases, Feb 2016
Ras homolog enriched in brain (Rheb) is a member of the Ras GTPase superfamily and a key activator of the mammalian/mechanistic target of rapamycin complex 1 (mTORC1).
RHEB1 expression in embryonic and postnatal mouse.
New
Fedorov et al., Portland, United States. In Histochem Cell Biol, Jan 2016
UNASSIGNED: Ras homolog enriched in brain (RHEB1) is a member within the superfamily of GTP-binding proteins encoded by the RAS oncogenes.
The antioxidant function of sestrins is mediated by promotion of autophagic degradation of Keap1 and Nrf2 activation and by inhibition of mTORC1.
Review
New
Bae et al., Seoul, South Korea. In Free Radic Biol Med, Nov 2015
This inhibition of mTORC1 activity is achieved either via the AMPK-dependent phosphorylation and activation of TSC2 and consequent inhibition of the GTPase Rheb or via inhibition of the GTPase Rag and consequent prevention of the lysosomal localization of mTORC1 triggered by amino acids.
Regulation of mTORC1 by PI3K signaling.
Review
New
Cantley et al., Boston, United States. In Trends Cell Biol, Sep 2015
Activation of mTORC1 [composed of mTOR, regulatory-associated protein of mTOR (Raptor), mammalian lethal with SEC13 protein 8(mLST8), 40-kDa proline-rich Akt substrate (PRAS40), and DEP domain-containing mTOR-interacting protein (DEPTOR)] depends on the Ras-related GTPases (Rags) and Ras homolog enriched in brain (Rheb) GTPase and requires signals from amino acids, glucose, oxygen, energy (ATP), and growth factors (including cytokines and hormones such as insulin).
Rheb signaling and tumorigenesis: mTORC1 and new horizons.
Review
New
Castro et al., Concepción, Chile. In Int J Cancer, Sep 2015
UNASSIGNED: Rheb is a conserved small GTPase that belongs to the Ras superfamily, and is mainly involved in activation of cell growth through stimulation of mTORC1 activity.
Key mediators of intracellular amino acids signaling to mTORC1 activation.
Review
New
Yin et al., Changsha, China. In Amino Acids, May 2015
Ras homolog enriched in brain (Rheb) resides on this surface and directly activates mTORC1.
Metabolism. Lysosomal amino acid transporter SLC38A9 signals arginine sufficiency to mTORC1.
New
Impact
Sabatini et al., Cambridge, United States. In Science, Feb 2015
Amino acids stimulate, in a Rag-, Ragulator-, and vacuolar adenosine triphosphatase-dependent fashion, the translocation of mTORC1 to the lysosomal surface, where it interacts with its activator Rheb.
Rab1A is an mTORC1 activator and a colorectal oncogene.
Impact
Zheng et al., New Brunswick, United States. In Cancer Cell, 2014
AA stimulates Rab1A GTP binding and interaction with mTORC1 and Rheb-mTORC1 interaction in the Golgi.
Regulation of TORC1 in response to amino acid starvation via lysosomal recruitment of TSC2.
Impact
Teleman et al., Heidelberg, Germany. In Cell, 2014
We show here that, upon amino acid removal, the Rag GTPases also recruit TSC2 to the lysosome, where it can act on Rheb.
Spatial control of the TSC complex integrates insulin and nutrient regulation of mTORC1 at the lysosome.
Impact
Manning et al., Boston, United States. In Cell, 2014
Insulin activates mTORC1 through the PI3K-Akt pathway, which inhibits the TSC1-TSC2-TBC1D7 complex (the TSC complex) to turn on Rheb, an essential activator of mTORC1.
Current models of mammalian target of rapamycin complex 1 (mTORC1) activation by growth factors and amino acids.
Review
Wang et al., Hohhot, China. In Int J Mol Sci, 2013
The mTOR-Rheb-TSC-TBC complex co-localizes to the lysosome and the phosphorylation of TSC-TBC effects the dissociation of the complex from the lysosome and activates Rheb.
A tuberous sclerosis complex signalling node at the peroxisome regulates mTORC1 and autophagy in response to ROS.
Impact
Walker et al., Houston, United States. In Nat Cell Biol, 2013
We report that the tuberous sclerosis complex (TSC) signalling node, TSC1, TSC2 and Rheb, localizes to peroxisomes, where it regulates mTORC1 in response to reactive oxygen species (ROS).
Rheb is a critical regulator of autophagy during myocardial ischemia: pathophysiological implications in obesity and metabolic syndrome.
GeneRIF
Sadoshima et al., Newark, United States. In Circulation, 2012
Inactivation of Rheb protects cardiac myocytes during energy deprivation through activation of autophagy.
Raptor and Rheb negatively regulate skeletal myogenesis through suppression of insulin receptor substrate 1 (IRS1).
GeneRIF
Chen et al., Urbana, United States. In J Biol Chem, 2011
Raptor and Rheb negatively regulate skeletal myogenesis through suppression of insulin receptor substrate 1 (IRS1).
Neurofibromatosis-1 regulates mTOR-mediated astrocyte growth and glioma formation in a TSC/Rheb-independent manner.
GeneRIF
Gutmann et al., Saint Louis, United States. In Proc Natl Acad Sci U S A, 2011
Data show that NF-1 regulates mTOR-dependent glial growth and gliomagenesis in a TSC/Rheb-independent mechanism and suggest the design of therapies for individuals with glioma.
Redox regulates mammalian target of rapamycin complex 1 (mTORC1) activity by modulating the TSC1/TSC2-Rheb GTPase pathway.
GeneRIF
Inoki et al., Ann Arbor, United States. In J Biol Chem, 2011
Redox regulates mammalian target of rapamycin complex 1 (mTORC1) activity by modulating the TSC1/TSC2-Rheb GTPase pathway.
Acceleration of autoimmune diabetes in Rheb-congenic NOD mice with β-cell-specific mTORC1 activation.
GeneRIF
Yokono et al., Kōbe, Japan. In Biochem Biophys Res Commun, 2011
in NOD mice, a model of spontaneous autoimmune T1D, Rheb overexpression significantly accelerated diabetes progression.
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