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RASD2 encodes a Ras-related protein that enriched in striatum. Additionally we are shipping RASD Family, Member 2 Antibodies (86) and RASD Family, Member 2 Proteins (7) and many more products for this protein.
Study demonstrated that variation in the gene coding for RASD2 (rs6518956) affects in vivo prefrontal and striatal phenotypes in healthy human subjects that are relevant to schizophrenia
Rhes influences striatal cAMP/PKA-dependent signaling and synaptic plasticity in a gender-sensitive fashion
Findings reveal that ras homolog enriched in striatum is localized also in striatal cholinergic interneurons and, most importantly, lack of this G-protein, significantly alters dopamine D2 receptor (show DRD2 ELISA Kits) modulation of striatal cholinergic excitability.
Rhes is reduced in the brains of Huntington's disease patients.
The findings of this study suggested that Rhes may play a crucial role in striatal iron homeostasis.
Rhes robustly binds the autophagy regulator Beclin-1 (show BECN1 ELISA Kits), decreasing its inhibitory interaction with Bcl-2 (show BCL2 ELISA Kits) independent of JNK-1 (show MAPK8 ELISA Kits) signaling.
The sequestering of Rhes through its binding to mutant huntingtin (show HTT ELISA Kits) may decrease the ability of Rhes to perform vital physiological functions in the striatum neurons of Huntington disease (show HTT ELISA Kits) patients. (Review)
Rhes is an imidazoline-regulated transcript in pancreatic beta-cells
Rhes can interfere with the functional activity of wt and mutated TSHr (show TSHR ELISA Kits) and with the respective hormone-stimulated cAMP production of FSHr (show FSHR ELISA Kits) and LHr (show LHCGR ELISA Kits).
The genes RASD2 might be vulnerability genes for neuropsychologically defined subgroups of schizophrenic patients.
that Rasd2 mutants display deficits in basal prepulse inhibition that, in turn, exacerbate gating disruption under psychotomimetic drug challenge
Study showed that both genetic deletion of Rhes and pharmacological blockade of mTORC1 significantly attenuate dyskinesia development by reducing the sensitization of striato-nigral medium-sized spiny neurons to levodopa
ectopic expression of Rhes in the cerebellum of N171-82Q mice, during the asymptomatic period led to an exacerbation of motor deficits, including loss of balance and motor incoordination with ataxia-like features
Brain Rhes expression is decreased in a mouse model of Huntington's disease.
Rhes is necessary for Akt (show AKT1 ELISA Kits) dephosphorylation by the striatal multi-protein complex
behavioral symptoms of HD are regulated by Rhes
This study demonstrated that Rhes-deleted mice are dramatically protected from neurotoxicity and motor dysfunction in a striatal-specific model of Huntington's disease elicited by 3-nitropropionic acid.
Ths results of this study indicted that Rhes physiologically binds to and activates mTOR (show FRAP1 ELISA Kits) in the striatum and L-DOPA-induced dyskinesia.
This gene encodes a Ras-related protein that enriched in striatum. The product of this gene binds to GTP and possesses intrinsic GTPase activity. The gene belongs to the Ras superfamily of small GTPases. The exact function of this gene is unknown, but most striatum-specific mRNAs characterized to date encode components of signal transduction cascades.
RASD family, member 2
, GTP-binding protein Rhes
, Ras homolog enriched in striatum
, tumor endothelial marker 2
, ras homolog enriched in striatum