Rhes: A striatal‐specific Ras homolog related to Dexras1

Falk, Jeffrey; Vargiu, Pierfrancesco; Foye, Pamela E.; Usui, H; Pérez, Julio E.; Danielson, Patria E.; Lerner, Danica L.; Bernal, Juan; Sutcliffe, J. Gregor

doi:10.1002/(sici)1097-4547(19990915)57:6<782::aid-jnr3>3.3.co;2-0

Cited by 15 publications

(17 citation statements)

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“…A homologue of Dexras1 called Ras Homolog Enriched in Striatum (Rhes, Dexras2) is induced by thyroid hormone, an interesting contrast to the stimulation of Dexras1 by glucocorticoids (Falk et al, 1999;Vargiu et al, 2001). Rhes is selectively localized to the corpus striatum.…”

Section: Discussionmentioning

confidence: 99%

NMDA Receptor-Nitric Oxide Transmission Mediates Neuronal Iron Homeostasis via the GTPase Dexras1

Cheah

Kim

Hester

et al. 2006

Neuron

260

241

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Dexras1 is a 30 kDa G protein in the Ras subfamily whose discovery was based on its pronounced inducibility by the glucocorticoid dexamethasone. It binds to neuronal nitric oxide synthase (nNOS) via the adaptor protein CAPON, eliciting S-nitrosylation and activation of Dexras1. We report that Dexras1 binds to the peripheral benzodiazepine receptor-associated protein (PAP7), a protein of unknown function that binds to cyclic AMP-dependent protein kinase and the peripheral benzodiazepine receptor. PAP7 in turn binds to the divalent metal transporter (DMT1), an iron import channel. We have identified a signaling cascade in neurons whereby stimulation of NMDA receptors activates nNOS, leading to S-nitrosylation and activation of Dexras1, which, via PAP7 and DMT1, physiologically induces iron uptake. As selective iron chelation prevents NMDA neurotoxicity in cortical cultures, the NMDA-NO-Dexras1-PAP7-DMT1-iron uptake signaling cascade also appears to mediate NMDA neurotoxicity.

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Section: Discussionmentioning

confidence: 99%

NMDA Receptor-Nitric Oxide Transmission Mediates Neuronal Iron Homeostasis via the GTPase Dexras1

Cheah

Kim

Hester

et al. 2006

Neuron

260

241

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“…RasD2/Rhes ( r as h omolog e xpressed in s triatum) is expressed predominately in the striatum [ 62 ] but also in thyroid glands and pancreas β-cells [ 63 ]. It is involved in selected stritial functions, mainly locomotor activity and motor coordination [ 64 ].…”

Section: Discussionmentioning

confidence: 99%

Farnesylation or geranylgeranylation? Efficient assays for testing protein prenylation in vitro and in vivo

et al. 2006

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“…In HD, SUMO modification of mutant huntingtin, which contains polyglutamine repeats, significantly inhibits its aggregation and promotes cell death [121]. This process is facilitated by Rhes (Ras homologue enriched in striatum), a small guanine-binding protein that shows E3 ligase activity and greatly enhances SUMOylation of mutant huntingtin and other proteins [121,122]. Kennedy disease, or spinal and bulbar muscular atrophy, is also characterised by a polyglutamine expansion in the N terminus of the androgen receptor.…”

Section: Sumo In Human Diseasementioning

confidence: 99%

SUMOylation and cell signalling

Andreou

Tavernarakis

2009

Biotechnology Journal

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SUMOylation is a highly transient post-translational protein modification. Attachment of SUMO to target proteins occurs via a number of specific activating and ligating enzymes that form the SUMO-substrate complex, and other SUMO-specific proteases that cleave the covalent bond, thus leaving both SUMO and target protein free for the next round of modification. SUMO modification has major effects on numerous aspects of substrate function, including subcellular localisation, regulation of their target genes, and interactions with other molecules. The modified SUMO-protein complex is a very transient state, and it thus facilitates rapid response and actions by the cell, when needed. Like phosphorylation, acetylation and ubiquitination, SUMOylation has been associated with a number of cellular processes. In addition to its nuclear role, important sides of mitochondrial activity, stress response signalling and the decision of cells to undergo senescence or apoptosis, have now been shown to involve the SUMO pathway. With ever increasing numbers of reports linking SUMO to human disease, like neurodegeneration and cancer metastasis, it is highly likely that novel and equally important functions of components of the SUMOylation process in cell signalling pathways will be elucidated in the near future.

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Rhes: A striatal‐specific Ras homolog related to Dexras1

Cited by 15 publications

References 0 publications

NMDA Receptor-Nitric Oxide Transmission Mediates Neuronal Iron Homeostasis via the GTPase Dexras1

NMDA Receptor-Nitric Oxide Transmission Mediates Neuronal Iron Homeostasis via the GTPase Dexras1

Farnesylation or geranylgeranylation? Efficient assays for testing protein prenylation in vitro and in vivo

SUMOylation and cell signalling

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