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RGS encodes a member of the RGS family of GTPase activating proteins that function in various signaling pathways by accelerating the deactivation of G proteins. Additionally we are shipping Regulator of G-Protein Signaling 9 Antibodies (42) and Regulator of G-Protein Signaling 9 Proteins (4) and many more products for this protein.
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Association with the plasma membrane is sufficient for potentiating catalytic activity of RGS7 (show RGS7 ELISA Kits) 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.
gene regulation in the Striatum of RGS9-deficient mice
The complex of G protein regulator RGS9-2 and Gbeta (show SUCLG2 ELISA Kits)(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.
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 (show DRD2 ELISA Kits) over MOR (show OPRM1 ELISA Kits). Finally, RGS7 (show RGS7 ELISA Kits) displayed an four times greater GAP activity relative to RGS9-2.
beta-Arrestin2 (show ARRB2 ELISA Kits) is required for the inhibition of D3R signaling by RGS9-2.
Type 5 G protein beta subunit (show GNB3 ELISA Kits) (Gbeta5 (show GNB5 ELISA Kits)) 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 (show DRD2 ELISA Kits).
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 (show RGS9BP ELISA Kits) who report difficulty adapting to sudden changes in luminance levels mediated by cones
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