RASD Family, Member 2 Proteine (RASD2)

Human RASD Family, Member 2 (RASD2) Interaktionspartner

1. 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

2. Rhes influences striatal cAMP/PKA-dependent signaling and synaptic plasticity in a gender-sensitive fashion

3. 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 (zeige DRD2 Proteine) modulation of striatal cholinergic excitability.

4. Rhes is reduced in the brains of Huntington's disease patients.

5. The findings of this study suggested that Rhes may play a crucial role in striatal iron homeostasis.

6. Rhes robustly binds the autophagy regulator Beclin-1 (zeige BECN1 Proteine), decreasing its inhibitory interaction with Bcl-2 (zeige BCL2 Proteine) independent of JNK-1 (zeige MAPK8 Proteine) signaling.

7. The sequestering of Rhes through its binding to mutant huntingtin (zeige HTT Proteine) may decrease the ability of Rhes to perform vital physiological functions in the striatum neurons of Huntington disease (zeige HTT Proteine) patients. (Review)

8. Rhes is an imidazoline-regulated transcript in pancreatic beta-cells

9. Rhes can interfere with the functional activity of wt and mutated TSHr (zeige TSHR Proteine) and with the respective hormone-stimulated cAMP production of FSHr (zeige FSHR Proteine) and LHr (zeige LHCGR Proteine).

10. The genes RASD2 might be vulnerability genes for neuropsychologically defined subgroups of schizophrenic patients.

Mouse (Murine) RASD Family, Member 2 (RASD2) Interaktionspartner

1. guanine nucleotide exchange factor (zeige ARHGEF12 Proteine) RasGRP1 (zeige RASGRP1 Proteine) inhibited Rhes-mediated control of striatal motor activity in mice. RasGRP1 (zeige RASGRP1 Proteine) stabilized Rhes, increasing its synaptic accumulation in the striatum.

2. that Rasd2 mutants display deficits in basal prepulse inhibition that, in turn, exacerbate gating disruption under psychotomimetic drug challenge

3. 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

4. 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

5. Rhes influences striatal cAMP/PKA-dependent signaling and synaptic plasticity in a gender-sensitive fashion

6. Brain Rhes expression is decreased in a mouse model of Huntington's disease.

7. Rhes robustly binds the autophagy regulator Beclin-1 (zeige BECN1 Proteine), decreasing its inhibitory interaction with Bcl-2 (zeige BCL2 Proteine) independent of JNK-1 (zeige MAPK8 Proteine) signaling.

8. Rhes is necessary for Akt (zeige AKT1 Proteine) dephosphorylation by the striatal multi-protein complex

9. behavioral symptoms of HD are regulated by Rhes

10. 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.