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The authors show that genetic depletion of RGS9-2 mimics the D2 receptor loss of DYT1 dystonia striatum, whereas RGS9-2 overexpression rescues both receptor levels and electrophysiological responses in Dyt1 striatal neurons.
Association with the plasma membrane is sufficient for potentiating catalytic activity of RGS7 and RGS9-2 proteins.
Data show that the regulator of G-protein signaling 9-2 (RGS9-2) in the nucleus accumbens (NAc) affects the expression of many genes known to be involved in nociception, analgesia, and antidepressant drug actions.
role in sensory and mood related symptoms of neuropathic pain
gene regulation in the Striatum of RGS9-deficient mice
The complex of G protein regulator RGS9-2 and Gbeta(5) controls sensitization and signaling kinetics of type 5 adenylyl cyclase in the striatum.
The expression of RGS9 in two distinct populations of neural precursor cells demonstrates that RGS9 and its accessory proteins may play an important role in neuronal development.
RGS9 knockout causes a short delay in light responses of ON-bipolar cells.
These studies with humans, rats and mice implicate RGS9-2 as a factor in regulating body weight.
RGS9-2 may play a crucial role in opiate-mediated analgesic mechanisms at the level of the spinal cord.
In this study, we report an identification of Hsc70 (Heat shock cognate protein 70) as a critical mediator of RGS9-2 expression that is specifically recruited to the intrinsically disordered C-terminal domain of RGS9-2 following dissociation from R7BP.
The localization of RGS9-2 immunoreactivity at the base or neck of spines along dendritic shafts suggests that they are mainly localized at inhibitory post-synaptic sites or extrasynaptic sites near the excitatory synapses.
identification of protein kinase C isozymes responsible for phosphorylation at Ser475
study demonstrates that the long regulator of G-protein signaling 9 isoform contains a C-terminal domain that provides high-affinity interaction with its target G protein
data demonstrate a functional interaction between RGS9-2 and D2 receptor signaling and the behavioral actions of psychostimulants and suggest that psychostimulant induction of RGS9-2 represents a compensatory adaptation that diminishes drug responsiveness
opiate-induced changes in RGS9 levels contribute to the behavioral and neural plasticity associated with chronic opiate administration
photoreceptors R9AP determines the stability of the RGS9.Gbeta5 complex, and therefore all three proteins, RGS9, Gbeta5 , and R9AP, are obligate members of the regulatory complex that speeds the rate at which transducin hydrolyzes GTP.
In the mouse, R9AP is detectable predominantly in photoreceptors, but it is also weakly expressed in other areas of the central nervous system. It may target GTPase-activating proteins to specific membranous compartments.
Tolerance that develops following an adequate dose of morphine is caused by the stabilization and retention of mu receptor-activated Galpha subunits by RGS9-2 proteins.
Changes in RGS9-2 may be a key factor in the pathway leading from D2 dopamine receptors to the side effects from the treatment of psychoses & Parkinson's disease.
This case series highlights the clinical presentations and features of 5 affected children (3 Arab families) who harbored the same homozygous RGS9 frameshift mutation, which seems to represent a founder effect for the Arabian Peninsula.
To identify single-nucleotide polymorphisms that contribute to the genetic susceptibility to schizophrenia, we examined the potential association between schizophrenia and 9 single nucleotide polymorphisms in the G-protein signaling 9 gene
These findings indicate a role for RGS9 gene polymorphisms in heroin dependence and may be informative for future genetic or biological studies on heroin dependence.
the GAP activity of RGS9-2 showed a strong receptor preference for D2R over MOR. Finally, RGS7 displayed an four times greater GAP activity relative to RGS9-2.
beta-Arrestin2 is required for the inhibition of D3R signaling by RGS9-2.
Type 5 G protein beta subunit (Gbeta5) controls the interaction of regulator of G protein signaling 9 (RGS9) with membrane anchors
The main goal of this review is to illustrate how various functions are fulfilled through the interplay between the intrinsic molecular properties of RGS9 isoforms.
The expression of RGS9-2 inhibits dopamine-mediated cellular internalization of the dopamine 2 (D2) receptor.
no association with schizophrenia in an Israeli Jewish population
This is the first report describing a nonsense mutation in RGS9.
five unrelated patients with recessive mutations in the genes encoding either RGS9 or R9AP who report difficulty adapting to sudden changes in luminance levels mediated by cones
under certain conditions, RGS9 and Gbeta5 may possibly function as betagamma dimer
homozygous mutations in RGS9 gene that encodes the photoreceptor GTPase accelerating protein and its anchor protein, respectively, have been identifird in patients with bradyopsia.
In the haplotype analysis, a significant association of the AGG haplotype (rs8077696-rs8070231-rs2292593) of the RGS9 gene was found (permutation P = 0.007)
This gene encodes a member of the RGS family of GTPase activating proteins that function in various signaling pathways by accelerating the deactivation of G proteins. This protein is anchored to photoreceptor membranes in retinal cells and deactivates G proteins in the rod and cone phototransduction cascades. Mutations in this gene result in bradyopsia. Multiple transcript variants encoding different isoforms have been found for this gene.
regulator of G-protein signalling 9
, regulator of G-protein signaling 9
, ROS GAP