Affinage

RGS9

Regulator of G-protein signaling 9 · UniProt O75916

Length
674 aa
Mass
77.0 kDa
Annotated
2026-06-10
94 papers in source corpus 47 papers cited in narrative 46 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

RGS9 encodes GTPase-accelerating proteins (GAPs) that terminate G-protein signaling, expressed as two splice isoforms with distinct neural roles (PMID:9459445, PMID:10066255). The retinal isoform RGS9-1 accelerates GTP hydrolysis by the visual G protein transducin (Gαt) to deactivate phototransduction, an activity uniquely potentiated by the γ-subunit of cGMP phosphodiesterase (PDEγ), whose C-terminal residues engage structural determinants in the RGS domain (PMID:9459445, PMID:10213594); loss of RGS9-1 severely slows recovery of both rod and cone photoresponses (PMID:10676965, PMID:11262419), and recessive loss-of-function mutations in RGS9 or its anchor cause human bradyopsia (PMID:14702087). Both isoforms obligately dimerize with Gβ5 through the GGL domain, an interaction resolved crystallographically and required for RGS9 folding, stability, and catalytic specificity toward the transducin-PDEγ effector complex (PMID:10840031, PMID:11495924, PMID:12093815, PMID:18204463); Gβ5 also enables association of RGS9 with its membrane anchors (PMID:21511947). In photoreceptors the DEP domain mediates high-affinity binding to the membrane anchor R9AP, which directs RGS9-1 to outer segments, kinetically enhances GAP activity ~70-fold, and is required for proteolytic stability of the RGS9·Gβ5 complex (PMID:12119397, PMID:12006596, PMID:14614075, PMID:14625292). The striatal isoform RGS9-2 acts as a selective GAP for Gi/o-family Gα subunits, negatively modulating dopamine D2 receptor and mu-opioid receptor signaling (PMID:10066255, PMID:12818179, PMID:12531899, PMID:14595021); its abundance and postsynaptic localization are controlled by the anchor R7BP, which shields it from lysosomal cysteine protease degradation (PMID:16574655, PMID:17158100, PMID:18094251). RGS9-2 additionally inhibits agonist-induced D2 receptor internalization via its DEP domain and catalytic activity, suppresses type 5 adenylyl cyclase, and selectively remodels D2 medium spiny neuron synaptic plasticity through NMDAR-dependent retrograde endocannabinoid signaling (PMID:20477943, PMID:22932702, PMID:30006367). Both isoforms are regulated post-translationally by PKA- and PKC-mediated phosphorylation that tunes GAP activity and membrane anchor affinity (PMID:11601986, PMID:12499365).

Mechanistic history

Synthesis pass · year-by-year structured walk · 28 steps
  1. 1998 High

    Established the founding molecular function: identified RGS9-1 as the GAP that terminates the visual transduction cascade by accelerating transducin GTP hydrolysis, and uncovered the unusual PDEγ-dependent potentiation.

    Evidence In vitro GTPase reconstitution and colocalization in rod outer segments

    PMID:9459445

    Open questions at the time
    • Did not resolve obligate partners required in vivo
    • Mechanism of PDEγ potentiation not yet structurally defined
  2. 1998 Low

    Raised the possibility that RGS9-1 links the PDE and guanylyl cyclase arms of phototransduction by directly inhibiting retGC.

    Evidence Co-IP, overlay binding, and in vitro GC activity assays from a single lab

    PMID:9712827

    Open questions at the time
    • Single lab, not independently replicated
    • Physiological significance of retGC inhibition unconfirmed
  3. 1999 High

    Showed that the functional GAP is not RGS9 alone but an obligate RGS9·Gβ5L heterodimer, redefining the active species in photoreceptors.

    Evidence Native purification, co-IP, cell co-expression, in vitro GTPase assay

    PMID:10051575

    Open questions at the time
    • Structural basis of dimerization not yet determined
    • Role of Gβ5 in catalysis vs. stability not separated
  4. 1999 Medium

    Identified the striatum-specific RGS9-2 isoform and assigned it a distinct target class — Gi/o-coupled receptors including the mu-opioid receptor — establishing RGS9 as a two-tissue, two-function gene.

    Evidence Molecular cloning, in vitro functional assay with mu-opioid receptor, immunohistochemistry

    PMID:10066255

    Open questions at the time
    • In vivo role not yet tested
    • Single lab functional characterization
  5. 1999 High

    Mapped the PDEγ effector signal to residues 63–87 and identified RGS domain helices that set whether PDEγ enhances or suppresses GAP activity, defining the effector-coupling interface.

    Evidence In vitro GTPase assays with RGS9/RGS16 chimeras and deletion mutants

    PMID:10213594

    Open questions at the time
    • Structural conformation underlying directionality not resolved
  6. 2000 High

    Knockout confirmed RGS9-1 is required in vivo for timely rod photoresponse recovery and revealed it is necessary for Gβ5L protein stability, coupling the two partners reciprocally.

    Evidence RGS9 knockout mouse, single-cell electrophysiology, GTPase assay, Western blot

    PMID:10676965

    Open questions at the time
    • Mechanism of mutual stabilization not defined
    • Anchoring requirement not yet identified
  7. 2000 High

    Demonstrated that Gβ5L stabilizes RGS9-1 folding and maintains stoichiometry through a non-transcriptional protein-stability mechanism, and is needed for PDEγ-stimulated GAP activity.

    Evidence In vitro reconstitution, transgenic Xenopus, COS-7 co-expression

    PMID:10840031 PMID:10978345

    Open questions at the time
    • Degradation pathway acting on unpaired RGS9 not identified
  8. 2001 High

    Defined substrate selectivity: noncatalytic Gβ5/RGS9 domains, not the catalytic domain alone, direct the GAP toward the transducin-PDEγ effector complex over free transducin.

    Evidence In vitro GTPase assays with deletion/point mutants and affinity measurements

    PMID:11495924 PMID:12093815

    Open questions at the time
    • Structural mechanism of effector discrimination not resolved
  9. 2001 High

    Established cone-specific requirement, showing RGS9-1 deactivates cone as well as rod phototransduction.

    Evidence RGS9-1 knockout mouse, cone ERG, immunohistochemistry

    PMID:11262419

    Open questions at the time
    • Quantitative differences between rod and cone deactivation kinetics not dissected
  10. 2001 Medium

    Opened the question of post-translational control by identifying light- and Ca2+-regulated phosphorylation of RGS9-1, but the responsible kinase and exact sites were initially contested (Ser475 vs Ser427/428).

    Evidence 32P labeling, mass spectrometry, phospho-specific immunoblot, mutagenesis, GAP assay

    PMID:11292825 PMID:11601986

    Open questions at the time
    • Conflicting site assignments (Ser475 vs Ser427/428) between studies
    • Functional impact on photoresponse kinetics not measured in vivo
  11. 2001 Medium

    Localized membrane targeting to the RGS9-1-unique C-terminal domain, distinguishing the determinants of membrane attachment from the Gβ5L dimerization function.

    Evidence Limited proteolysis, recombinant fragment membrane-binding assay, urea extraction

    PMID:11677233

    Open questions at the time
    • Identity of the membrane partner not yet known at this point
  12. 2002 High

    Identified R9AP as the membrane anchor that binds the RGS9-1 N-terminus and assembles a disk-membrane complex with Gβ5 and transducin, explaining how the GAP is positioned at the site of phototransduction.

    Evidence Biochemical purification, co-IP, cDNA cloning, domain binding assay

    PMID:12119397

    Open questions at the time
    • Whether R9AP affects catalysis or only localization not yet separated
  13. 2002 High

    Showed R9AP both enhances GAP activity ~70-fold and that membrane association via the DEP domain is required for the reaction to occur on the physiological timescale.

    Evidence Reconstitution of R9AP into lipid vesicles, single-turnover GTPase, domain deletion

    PMID:12006596 PMID:12560335

    Open questions at the time
    • Affinity vs. catalytic contributions of R9AP not yet disentangled
  14. 2002 Medium

    Identified PKCα/PKCθ as the kinases phosphorylating Ser475 and PP2A as the phosphatase, linking phosphorylation to reduced R9AP affinity, and added light-dependent translocation to membrane rafts as a regulatory layer.

    Evidence Kinase purification, recombinant PKC assays, mutagenesis, phosphatase assay, membrane fractionation

    PMID:11882295 PMID:12499365

    Open questions at the time
    • Physiological role of raft translocation not established
    • Site assignment still in tension with PKA-based study
  15. 2003 High

    In vivo transgenics and R9AP knockout established that the DEP domain delivers RGS9-1 to outer segments and that R9AP is required for proteolytic stability of the RGS9·Gβ5 complex, making R9AP, RGS9, and Gβ5 obligate partners.

    Evidence DEP-deletion transgenic mouse, R9AP knockout mouse, tangential sectioning-Western, electrophysiology

    PMID:14614075 PMID:14625292 PMID:16939221

    Open questions at the time
    • Identity of the protease degrading unanchored complex in retina not defined
  16. 2003 High

    Defined RGS9-2's in vivo neuropharmacological role as a negative modulator of D2 dopamine and mu-opioid receptor signaling, linking it to reward, locomotion, analgesia and dependence.

    Evidence Viral overexpression in rat NAc, RGS9 KO behavior, Xenopus oocyte GIRK electrophysiology, opioid behavioral assays, proteoliposome GTPase

    PMID:12531899 PMID:12818179 PMID:14595021

    Open questions at the time
    • Mechanism of receptor selectivity not yet defined
    • Subcellular targeting in striatum not yet known
  17. 2004 High

    Human genetics closed the loop, showing recessive RGS9 or R9AP loss-of-function causes bradyopsia, confirming the gene's essential deactivation role in human cone vision.

    Evidence Human mutation identification, clinical ERG, psychophysics

    PMID:14702087

    Open questions at the time
    • Genotype-phenotype variation not fully characterized
  18. 2004 Medium

    Extended RGS9-2 function to native striatal neurons, demonstrating selective regulation of D2-receptor modulation of Cav2.2 channels, but a nuclear-localization claim conflicted with later tissue data.

    Evidence Patch-clamp with intracellular RGS9 dialysis; immunocytochemistry and transcriptional reporter (nuclear claim)

    PMID:15110994 PMID:15534226

    Open questions at the time
    • Nuclear localization contradicted by subsequent striatal tissue analysis
    • Transcriptional readout indirect
  19. 2005 High

    Showed RGS9-2 uses its DEP domain to colocalize with and selectively terminate D2 receptor signaling, and that its loss produces dyskinesia-like involuntary movements, defining a motor-control function.

    Evidence Cell co-expression, oocyte electrophysiology, KO mouse behavior and striatal electrophysiology

    PMID:15728856

    Open questions at the time
    • Endogenous DEP-domain partner in striatum not yet identified
  20. 2006 High

    Identified R7BP as the striatal counterpart of R9AP — targeting RGS9-2 to plasma membrane and postsynaptic densities and protecting it from proteolytic degradation — establishing a conserved anchor-stabilization logic across both isoforms.

    Evidence Subcellular fractionation, mutagenesis, RNAi knockdown in striatal neurons, co-expression stability assays

    PMID:16574655 PMID:17158100

    Open questions at the time
    • Protease executing degradation not yet identified at this stage
  21. 2007 High

    Identified lysosomal cysteine proteases as the degradation pathway constitutively turning over RGS9-2 and showed R7BP binding shields the degradation determinants, controlling RGS9-2 abundance through development.

    Evidence Protease inhibitor pharmacology, co-expression stability assays, immunofluorescence, developmental Western blot

    PMID:18094251

    Open questions at the time
    • Adaptor linking RGS9-2 to lysosomal proteolysis not yet identified
  22. 2007 Medium

    Linked RGS9-2 to mu-opioid receptor trafficking by showing it delays MOR internalization, binds MOR and β-arrestin-2 in a morphine-enhanced manner, and blocks opiate-induced ERK signaling.

    Evidence Co-IP, internalization and ERK assays in transfected PC12 cells

    PMID:15632124 PMID:17725581

    Open questions at the time
    • Single-lab cell-based system, native confirmation limited
    • Mechanism of arrestin-RGS9 cooperation not resolved
  23. 2008 High

    The 1.95 Å crystal structure of the Gβ5·RGS9 complex provided the definitive architecture showing the GGL domain mediating obligate Gβ5 dimerization within an integrated regulatory module.

    Evidence X-ray crystallography

    PMID:18204463

    Open questions at the time
    • Structure of the full anchored, transducin-bound complex not determined
  24. 2008 High

    An isoform-swap knockin showed the two isoforms differ functionally in vivo — RGS9-2 inactivates transducin independent of PDEγ while RGS9-1 prefers the effector complex — defining the molecular basis of their tuning to different signaling contexts.

    Evidence Knockin mouse expressing RGS9-2 in rods, single-cell electrophysiology

    PMID:19098104

    Open questions at the time
    • Structural origin of the effector-dependence difference not mapped
  25. 2010 Medium

    Refined the assembly logic by showing Gβ5 is required for RGS9 to bind either anchor and that distinct interface determinants control anchor binding versus proteolytic stabilization, and identified Hsc70 as a degradation mediator recruited to the disordered RGS9-2 C-terminus after R7BP dissociation.

    Evidence Interface mutagenesis with interaction/stability assays; quantitative proteomic interactome with KO controls and co-IP

    PMID:20095651 PMID:21511947

    Open questions at the time
    • How Hsc70 routes RGS9-2 to lysosomal proteases not dissected
    • Single-lab interactome
  26. 2011 Medium

    Resolved a conformational regulatory mechanism in which β-arrestin2 scaffolds the DEP domain, Gβ5, R7BP and D3 receptor, holding RGS9-2 in an open cytosolic state and conferring receptor selectivity; also catalogued agonist-specific RGS9-2·Gα complexes underlying opioid tolerance.

    Evidence Reciprocal co-IP, domain-mutant signaling assays; native-tissue co-IP after in vivo drug treatment

    PMID:20477943 PMID:21490202 PMID:22006018

    Open questions at the time
    • Single-lab co-IP for agonist-specific complexes
    • Physiological role of distinct Gα complexes not causally established
  27. 2012 High

    Uncovered a GAP-independent effector arm: RGS9-2·Gβ5 directly suppresses type 5 adenylyl cyclase, controlling striatal cAMP and opioid-withdrawal-associated AC5 sensitization.

    Evidence Direct interaction assays, cAMP measurements in striatal neurons, RGS9 KO biochemistry

    PMID:22932702

    Open questions at the time
    • Structural basis of direct AC5 interaction not defined
  28. 2018 High

    Connected RGS9-2 to synaptic plasticity, showing its loss selectively alters NMDAR signaling and retrograde endocannabinoid transmission in D2 medium spiny neurons, remodeling presynaptic inputs.

    Evidence Calcium imaging, slice electrophysiology in genetically identified neurons, KO mouse, pharmacology

    PMID:30006367

    Open questions at the time
    • Direct molecular link between RGS9-2 GAP activity and NMDAR regulation not defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the distinct phosphorylation, anchor-dependent stabilization, and effector-coupling layers are integrated to set the precise kinetics of RGS9 GAP activity in vivo — and how RGS9-2 directly engages NMDAR and AC5 signaling structurally — remains open.
  • No structure of the membrane-anchored, substrate-bound complex
  • Conflicting phosphorylation site/kinase assignments unresolved
  • Direct molecular mediators linking RGS9-2 to AC5 and NMDAR pathways not structurally defined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 5 GO:0060089 molecular transducer activity 3 GO:0008092 cytoskeletal protein binding 2
Localization
GO:0005886 plasma membrane 2 GO:0005929 cilium 2 GO:0005829 cytosol 1
Pathway
R-HSA-112316 Neuronal System 3 R-HSA-162582 Signal Transduction 3 R-HSA-9709957 Sensory Perception 3
Partners
ADCY5ARRB2DRD2GNAT1GNB5PDEGR7BPR9AP
Complex memberships
RGS9-1·Gβ5L·R9AP (photoreceptor GAP complex)RGS9-2·Gβ5·R7BP (striatal GAP complex)

Evidence

Reading pass · 46 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 RGS9 (RGS9-1) was identified as the GTPase-accelerating protein (GAP) for the visual G protein transducin (Gαt) in rod outer segments; the RGS domain of RGS9 directly accelerates GTP hydrolysis by Gαt, and this acceleration is uniquely enhanced by the γ-subunit of cGMP phosphodiesterase (PDEγ). In vitro GTPase assay, colocalization with phototransduction components in photoreceptor outer segments Neuron High 9459445
1998 RGS9 directly interacts with retinal guanylyl cyclase (retGC) and inhibits its activity, suggesting RGS9-1 mediates a direct connection between the PDE and guanylyl cyclase systems in phototransduction. 2D gel electrophoresis, co-immunoprecipitation, overlay binding assay, in vitro GC activity assay The Journal of biological chemistry Low 9712827
1999 Functionally active RGS9 in photoreceptors exists as a tight complex with Gβ5L (the long splice variant of G protein β5 subunit); RGS9 and Gβ5L form a complex when co-expressed in cell culture, and this complex is the GTPase-activating factor for transducin. Biochemical purification from native photoreceptors, co-immunoprecipitation, co-expression in cell culture, in vitro GTPase assay Proceedings of the National Academy of Sciences of the United States of America High 10051575
1999 RGS9-2, a striatum-specific alternatively spliced isoform of the RGS9 gene with a unique C-terminal domain, acts as a GAP for Gi/o-coupled receptors (specifically dampens μ-opioid receptor response) in vitro; RGS9-1 does not share this activity. Molecular cloning, in vitro functional assay with μ-opioid receptor, immunohistochemistry The Journal of neuroscience : the official journal of the Society for Neuroscience Medium 10066255
1999 The PDEγ C-terminal domain (residues 63–87) mediates potentiation of RGS9 GAP activity toward Gαt; structural determinants within the RGS9 domain (α3–α5 helices) control the direction (positive vs. negative) of PDEγ effects on RGS-Gαt GTPase activity. In vitro GTPase assay with chimeric RGS9/RGS16 proteins and domain deletion/substitution mutagenesis Biochemistry High 10213594
2000 Mice lacking RGS9-1 show severely slowed rod photoresponse recovery and slower GTP hydrolysis on ROS membranes; Gβ5-L protein was absent from RGS9-/- retinas despite presence of Gβ5-L mRNA, indicating RGS9-1 is required for Gβ5-L protein stability and that the RGS9-1/Gβ5-L complex is essential for GAP activity toward Gαt. RGS9 knockout mouse, electrophysiology (single-cell recordings), GTPase assay on ROS membranes, Western blot Nature High 10676965
2000 Gβ5L promotes folding and stability of RGS9-1, and is required for the effector stimulation of GAP activity by PDEγ; the Gγ-like (GGL)/Gβ5L complex and the C-terminal domain of RGS9-1 together regulate GAP activity; dependence of RGS9-1 on Gβ5 for stability confirmed in transgenic Xenopus. In vitro reconstitution with full-length and truncated proteins, transgenic Xenopus, functional domain analysis The Journal of biological chemistry High 10978345
2000 Native Gβ5 and RGS9 exist exclusively as tightly associated heterodimers in photoreceptors; co-expression in COS-7 cells shows that Gβ5 dramatically increases RGS protein levels via increased protein stability upon dimerization (non-transcriptional mechanism maintaining stoichiometry). Immunoprecipitation from native tissue, conventional chromatography, COS-7 cell co-expression The Journal of biological chemistry High 10840031
2001 RGS9-1 is phosphorylated at Ser475 by an endogenous kinase in rod outer segments; phosphorylation level is regulated by light (decreased in light-adapted retina) and by Ca2+ concentration, suggesting a feedback mechanism regulating photoresponse recovery. 32P-labeling of bovine ROS, mass spectrometry identification of phosphorylation site, site-directed mutagenesis (S475A), immunoblot with phospho-specific antibody on mouse retina The Journal of biological chemistry High 11292825
2001 PKA is the major kinase responsible for RGS9-1 phosphorylation in rod outer segments; phosphorylation sites were mapped to Ser427 and Ser428; phosphomimetic (S→E) substitution at these sites reduces RGS9-1 GAP activity; phosphorylation requires Ca2+ and is inhibited by light. Kinase inhibitor/activator pharmacology in ROS, recombinant PKA phosphorylation of RGS9-1, mutational analysis, GAP activity assay Biochemistry Medium 11601986
2001 RGS9-1 is required for normal inactivation of cone phototransduction (both UV- and M-cone); RGS9-1 knockout mice show ~60-fold slower recovery of cone-driven ERG responses after a conditioning flash. RGS9-1 knockout mouse, ERG measurements of cone responses, immunohistochemistry Molecular vision High 11262419
2001 Gβ5 and other noncatalytic domains of RGS9-Gβ5 play a decisive role in establishing substrate specificity for the transducin-PDEγ effector complex over free transducin; the catalytic domain alone provides some discrimination but noncatalytic domains set the final specificity. In vitro GTPase assay with RGS9 domain deletion/point mutants (L353E/R360P); affinity measurements with free vs. effector-bound transducin The Journal of biological chemistry High 11495924 12093815
2001 The C-terminal domain unique to RGS9-1 (absent in RGS9-2) is critical for tight membrane binding in photoreceptors; removal of this domain greatly reduces membrane binding affinity; Gβ5L is not required for membrane attachment. Limited proteolysis, recombinant fragment membrane-binding assay, urea extraction The Journal of biological chemistry Medium 11677233
2002 R9AP (RGS9-1 Anchor Protein), a 25-kDa retina-specific phosphoprotein with a C-terminal transmembrane helix, binds to the N-terminal domain of RGS9-1 and anchors it to photoreceptor disk membranes; detergent extracts contain a complex of RGS9-1, Gβ5, Gαt, and R9AP. Biochemical purification, co-immunoprecipitation, cDNA cloning, domain binding assay Proceedings of the National Academy of Sciences of the United States of America High 12119397
2002 Membrane-bound R9AP dramatically enhances RGS9-1·Gβ5 GAP activity (~70-fold); specific high-affinity binding of RGS9-1·Gβ5 to R9AP-containing vesicles requires the DEP domain; membrane association is required for the full GAP reaction on the physiological time scale of phototransduction. Reconstitution of recombinant R9AP into lipid vesicles, single-turnover GTPase assay, domain deletion binding assay The Journal of biological chemistry High 12006596
2002 The RGS9-1·Gβ5L complex and transducin undergo signal-dependent translocation to detergent-resistant membrane rafts upon illumination; this translocation requires Gαt activation (blocked by GTPγS or pertussis toxin, triggered in dark by AlF4-); RGS9-1 phosphorylation occurs exclusively in the raft fraction. Detergent-resistant membrane fractionation of photoreceptors, Western blot, pharmacological manipulation of transducin activation state Current biology : CB Medium 11882295
2002 PKCα and PKCθ are the kinases responsible for phosphorylation of RGS9-1 at Ser475 in rod outer segments; protein phosphatase 2A is the endogenous phosphatase that removes this phosphorylation; PKC-mediated phosphorylation at Ser475 reduces RGS9-1 affinity for its membrane anchor R9AP. Purification of kinase activity from ROS, recombinant PKC isoform assays, mutagenesis, phosphatase assays, membrane binding assay with phosphorylated protein The Journal of biological chemistry High 12499365
2003 The DEP domain of RGS9-1 is essential for its delivery to rod outer segments and for interaction with R9AP; transgenic mice expressing DEP-domain-deleted RGS9 show normal expression levels but complete exclusion from rod outer segments and abolished GAP activity in vivo. Transgenic mouse (DEP domain deletion), serial tangential sectioning-Western blot quantification, electrophysiology The Journal of neuroscience : the official journal of the Society for Neuroscience High 14614075
2003 R9AP binding to RGS9-1 increases GAP activity ~4-fold; DEP domain is required for high-affinity R9AP binding (Kd < 10 nM); membrane-delimited GTPase reaction is rate-limiting on the time scale of phototransduction. Reconstitution of R9AP into lipid vesicles with rhodopsin, single-turnover GTPase assay, domain deletion binding analysis The Journal of biological chemistry High 12560335
2003 R9AP knockout mice completely lack RGS9·Gβ5 protein (despite normal RGS9 mRNA), indicating R9AP is required for proteolytic stability of the RGS9·Gβ5 complex in photoreceptors; consequently R9AP, RGS9, and Gβ5 are obligate members of the regulatory complex. R9AP knockout mouse, Western blot, RT-PCR, electrophysiology of rod responses The Journal of biological chemistry High 14625292
2003 RGS9-2 overexpression in rat nucleus accumbens reduces locomotor responses to cocaine and D2 (but not D1) receptor agonists; RGS9 knockout mice show heightened locomotor and rewarding responses to cocaine; in Xenopus oocytes RGS9-2 accelerates off-kinetics of D2 receptor-induced GIRK currents. Viral-mediated overexpression in rat NAc, RGS9 KO mouse behavioral assays, Xenopus oocyte electrophysiology Neuron High 12818179
2003 Gbeta5/RGS9 (R7 subfamily) complexes are selective GAPs for Gi family Gα subunits but not for Gαq/Gα11; Gbeta5/RGS9 and Gbeta5/RGS11 are more potent GAPs for Gαi1/2/3 than Gbeta5/RGS6/7; less efficacious complexes (RGS7, RGS9) can inhibit RGS11-stimulated GTPase activity. Purified Sf9 cell-derived Gbeta5/R7 protein complexes, steady-state GTPase activity assay in proteoliposomes with receptor-coupled G proteins The Journal of biological chemistry High 12531899
2003 RGS9 knockout mice show enhanced behavioral responses to acute and chronic morphine (increased reward, increased analgesia with delayed tolerance, exacerbated physical dependence), establishing RGS9 as a negative modulator of mu-opioid receptor signaling in vivo. RGS9 knockout mouse, morphine behavioral assays (place preference, analgesia, withdrawal) Proceedings of the National Academy of Sciences of the United States of America High 14595021
2004 Humans with recessive loss-of-function mutations in RGS9 or its anchor protein R9AP exhibit bradyopsia (delayed recovery from light responses mediated by cones), confirming RGS9's essential role in cone phototransduction deactivation in vivo. Human genetic analysis (mutation identification), clinical electrophysiology (ERG), visual psychophysics Nature High 14702087
2004 RGS9-2 and Gβ5 are expressed in striatal cholinergic interneurons; dialysis of cholinergic neurons with RGS9 constructs enhanced basal Ca2+ channel currents and reduced D2 dopamine receptor (but not M2 muscarinic receptor) modulation of Cav2.2 channels; the noncatalytic DEP-GGL domain antagonized endogenous RGS9-2 activity. Patch-clamp electrophysiology of identified striatal neurons with intracellular dialysis of RGS9 constructs, in vitro GTPase assay Proceedings of the National Academy of Sciences of the United States of America High 15534226
2004 RGS9-2 brain-specific isoform localizes significantly to the nucleus of forebrain neurons via sequences in its unique proline-rich C-terminus; Gβ5 further enhances nuclear localization of RGS9-2; nuclear RGS9-2 can increase transcriptional activity of a neuronal gene construct. Immunocytochemistry of native brain, transfection of COS-7 cells and cultured striatal neurons with deletion constructs, transcriptional reporter assay Biochimica et biophysica acta Low 15110994
2005 RGS9-2 colocalizes with D2 dopamine receptors via its DEP domain when co-expressed in mammalian cells; RGS9-2 preferentially accelerates termination of D2 receptor (not m2 muscarinic receptor) signals; RGS9 KO mice develop abnormal involuntary movements when D2-like dopamine receptor activation follows dopaminergic inhibition, resembling drug-induced dyskinesia. Co-expression in mammalian cells, Xenopus oocyte electrophysiology, RGS9 KO mouse behavioral recordings, electrophysiology of striatal neurons The Journal of neuroscience : the official journal of the Society for Neuroscience High 15728856
2005 Morphine activates transfer of Gα subunits from mu-opioid receptor to RGS9-2 in PAG; tolerance-inducing morphine doses stabilize Gα subunits in RGS9-2 complexes; this is accompanied by Ser phosphorylation of RGS9-2 and increased co-precipitation with 14-3-3 proteins; RGS9-2 knockdown prevents morphine-induced Gα transfer and tolerance. Co-immunoprecipitation from mouse PAG membranes, in vivo antisense knockdown of RGS9-2, [35S]GTPγS binding and GTPase assays The Journal of biological chemistry Medium 15632124
2006 R7BP (R7 family binding protein) targets RGS9-2 to the plasma membrane and postsynaptic densities in striatal neurons; the C-terminal 21 amino acids of R7BP (containing a polybasic motif and palmitoylated cysteines) are necessary and sufficient for subcellular targeting; depalmitoylation of R7BP enables nuclear import via nuclear localization sequences in R7BP. Subcellular fractionation of native striatal neurons, site-directed mutagenesis of R7BP C-terminus, immunofluorescence in differentiated neurons The Journal of biological chemistry High 16574655
2006 R7BP binding protects RGS9-2·Gβ5 from proteolytic degradation; R7BP co-expression dramatically elevates RGS9-2 protein levels by reducing degradation rate; RNAi knockdown of R7BP in striatal neurons decreases RGS9-2 protein levels; the R7BP binding site in RGS9-2 is formed by the DEP domain paired with the R7H domain. Co-expression protein stability assay, lentiviral RNAi knockdown in striatal neurons, domain mutagenesis The Journal of biological chemistry High 17158100
2006 R9AP potentiates RGS9-1·Gβ5L GAP activity primarily by a direct kinetic enhancement of catalytic activity (not just by enhancing affinity); the N-terminal trihelical domain of R9AP contains the RGS9-1 binding site, but the entire R9AP molecule is required for potentiation of GAP activity. Biochemical kinetic assay (single-turnover GTPase), R9AP domain binding and activity assays with truncation mutants Biochemistry High 16939221
2007 The constitutive degradation of RGS9-2 in striatum is mediated by lysosomal cysteine proteases; R7BP binding shields degradation determinants, protecting RGS9-2 from proteolysis; R7BP binding also targets RGS9-2 to postsynaptic densities; this mechanism controls RGS9-2 abundance in vivo throughout ontogenetic development. Pharmacological inhibition of specific proteases, co-expression stability assays, immunofluorescence in neurons, Western blot developmental analysis The Journal of neuroscience : the official journal of the Society for Neuroscience High 18094251
2007 RGS9-2 overexpression in MPTP-lesioned monkey and 6-OHDA-lesioned rat striatum reduces L-dopa-induced involuntary movement intensity; RGS9-/- mice are more susceptible to L-dopa-induced involuntary movements; RGS9-2 overexpression also reduces anti-parkinsonian effects of the D2/D3 agonist ropinirole but not of L-dopa. Viral vector-mediated RGS9-2 overexpression in primate and rat striatum, RGS9 KO mouse behavioral assay, Western blot of striatal extracts The Journal of neuroscience : the official journal of the Society for Neuroscience High 18160641
2008 Crystal structure of the Gβ5·RGS9 complex at 1.95 Å resolution reveals a canonical RGS domain integrated within a molecular complex; the GGL domain of RGS9 mediates the obligate dimerization with Gβ5, positioning the complex for integration of multiple steps during G-protein activation and deactivation. X-ray crystallography at 1.95 Å resolution Nature structural & molecular biology High 18204463
2008 RGS9-2, when expressed in mouse rods in place of RGS9-1, supports normal photoresponse recovery under moderate light and outperforms RGS9-1 in bright light; this is because RGS9-2 inactivates transducin regardless of effector (PDEγ) interactions, whereas RGS9-1 preferentially inactivates the transducin-effector complex. Knockin transgenic mouse (RGS9-2 replacing RGS9-1 in rods), single-cell electrophysiology of rod responses Proceedings of the National Academy of Sciences of the United States of America High 19098104
2009 RGS9-2 in the striatum is found predominantly at the plasma membrane and postsynaptic densities; the majority is detergent-insoluble (not extracted by non-ionic detergents); RGS9-2 is specifically excluded from the cell nucleus in mouse striatal tissue. Subcellular fractionation, immunofluorescence, detergent extraction of native striatal tissue, Western blot Journal of neurochemistry Medium 19912469
2010 Gβ5 is required for the association of RGS9 with membrane anchors (R7BP or R9AP); distinct molecular determinants in the Gβ5–DEP/DHEY domain interface are differentially involved in R7BP binding vs. proteolytic stabilization. Protein-protein interaction assays, co-localization, protein stability assays, site-directed mutagenesis of Gβ5/RGS9 interface The Journal of biological chemistry Medium 21511947
2010 Hsc70 (Heat shock cognate protein 70) is recruited specifically to the intrinsically disordered C-terminal domain of RGS9-2 following its dissociation from R7BP, and acts as a mediator of RGS9-2 degradation. Quantitative proteomics (interactome analysis in vivo with knockout controls), co-immunoprecipitation Journal of proteome research Medium 20095651
2010 RGS9-2 specifically inhibits agonist-induced internalization of D2 dopamine receptors (but not delta opioid receptors); both the DEP domain and GAP catalytic activity of RGS9-2 are required for this selective inhibition of D2R internalization. Co-expression in cells, D2R internalization assay, mutant RGS9-2 constructs (DEP deletion, catalytic mutant) Journal of neurochemistry Medium 20477943
2011 MOR activation in striatum promotes formation of RGS9-2·Gαi3 complexes (uniquely with morphine) and RGS9-2·Gαq complexes (with multiple MOR agonists except morphine); repeated morphine leads to distinct RGS9-2·Gβ5·Gαq complexes associated with analgesic tolerance. Co-immunoprecipitation from striatal tissue after in vivo drug treatment The Journal of neuroscience : the official journal of the Society for Neuroscience Medium 21490202
2011 β-arrestin2 scaffolds the interaction among the DEP domain of RGS9-2, Gβ5, R7BP, and D3 dopamine receptor; β-arrestin2 competition with R7BP and Gβ5 maintains RGS9-2 in an open cytosolic conformation that enables GPCR signaling inhibition; receptor affinity for β-arrestin2 determines selectivity of RGS9-2 regulation. Co-immunoprecipitation, cell transfection with domain mutants of RGS9-2, GPCR signaling assays Molecular and cellular biology Medium 22006018
2012 RGS9-2·Gβ5 directly interacts with and suppresses basal activity of type 5 adenylyl cyclase (AC5) in the striatum; the complex also attenuates stimulatory Gβγ action on AC5 by facilitating GαoGTP hydrolysis and promotes recovery of AC5 from Gαi inhibition; RGS9 KO mice show increased cAMP production and enhanced AC5 sensitization upon opioid withdrawal. Direct protein-protein interaction assays, cAMP measurements in striatal neurons, RGS9 KO mouse biochemistry Science signaling High 22932702
2013 RGS9-1 and Gβ5L translocate from rod inner segments to outer segments upon dim light exposure during prolonged dark adaptation; in the dark, RGS9-1 is phosphorylated at S475 and Gβ5L dissociates from R9AP; dim light causes rapid RGS9-1 dephosphorylation and translocation. Immunofluorescence of rods during light/dark adaptation, co-immunoprecipitation of Gβ5L with R9AP, Western blot for RGS9-1 phosphorylation PloS one Medium 23555598
2018 RGS9-2 ablation reduces Ca2+ influx through NMDARs and enhances AMPAR/NMDAR ratio selectively in D2-MSNs (not D1-MSNs); this leads to NMDAR-dependent inhibition of retrograde endocannabinoid signaling from D2-MSNs to CB1 receptors on presynaptic terminals, remodeling presynaptic inputs. Calcium imaging in cultured striatal neurons, electrophysiology in striatal slices from genetically identified neuronal populations, RGS9-2 KO mouse, pharmacological dissection The Journal of neuroscience : the official journal of the Society for Neuroscience High 30006367
2001 The N-terminus of RGS9-1 directly inhibits retinal guanylyl cyclase (retGC) activity in vitro; the GGL and RGS domains function as internal suppressors of this inhibitory activity; direct interaction of retGC with RGS9-1 was confirmed by co-immunoprecipitation. In vitro GC activity assay, co-immunoprecipitation, overlay binding assay, domain deletion analysis Biochemical and biophysical research communications Low 11485301
2007 RGS9-2 delays agonist-induced internalization of mu-opioid receptor (MOR) in PC12 cells; RGS9-2 co-immunoprecipitates with HA-tagged MOR, with interaction enhanced by morphine; morphine also promotes association of RGS9-2 with β-arrestin-2; RGS9-2 overexpression prevents opiate-induced ERK phosphorylation. Co-immunoprecipitation, receptor internalization assay in transfected PC12 cells, ERK phosphorylation assay Journal of neurochemistry Medium 17725581

Source papers

Stage 0 corpus · 94 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2000 Slowed recovery of rod photoresponse in mice lacking the GTPase accelerating protein RGS9-1. Nature 375 10676965
1998 RGS9, a GTPase accelerator for phototransduction. Neuron 296 9459445
2003 RGS9 modulates dopamine signaling in the basal ganglia. Neuron 215 12818179
2003 Essential role for RGS9 in opiate action. Proceedings of the National Academy of Sciences of the United States of America 204 14595021
1999 The GTPase activating factor for transducin in rod photoreceptors is the complex between RGS9 and type 5 G protein beta subunit. Proceedings of the National Academy of Sciences of the United States of America 185 10051575
2005 D2 dopamine receptors colocalize regulator of G-protein signaling 9-2 (RGS9-2) via the RGS9 DEP domain, and RGS9 knock-out mice develop dyskinesias associated with dopamine pathways. The Journal of neuroscience : the official journal of the Society for Neuroscience 144 15728856
1999 Cloning and characterization of RGS9-2: a striatal-enriched alternatively spliced product of the RGS9 gene. The Journal of neuroscience : the official journal of the Society for Neuroscience 135 10066255
2004 Defects in RGS9 or its anchor protein R9AP in patients with slow photoreceptor deactivation. Nature 134 14702087
2002 R9AP, a membrane anchor for the photoreceptor GTPase accelerating protein, RGS9-1. Proceedings of the National Academy of Sciences of the United States of America 132 12119397
2000 Complexes of the G protein subunit gbeta 5 with the regulators of G protein signaling RGS7 and RGS9. Characterization in native tissues and in transfected cells. The Journal of biological chemistry 131 10840031
2003 RGS6, RGS7, RGS9, and RGS11 stimulate GTPase activity of Gi family G-proteins with differential selectivity and maximal activity. The Journal of biological chemistry 127 12531899
2003 The DEP domain determines subcellular targeting of the GTPase activating protein RGS9 in vivo. The Journal of neuroscience : the official journal of the Society for Neuroscience 99 14614075
2007 RGS9-2 negatively modulates L-3,4-dihydroxyphenylalanine-induced dyskinesia in experimental Parkinson's disease. The Journal of neuroscience : the official journal of the Society for Neuroscience 94 18160641
2002 Signal-dependent translocation of transducin, RGS9-1-Gbeta5L complex, and arrestin to detergent-resistant membrane rafts in photoreceptors. Current biology : CB 94 11882295
2001 Elevated levels of DeltaFosB and RGS9 in striatum in Parkinson's disease. Biological psychiatry 94 11720701
2008 Crystal structure of the multifunctional Gbeta5-RGS9 complex. Nature structural & molecular biology 90 18204463
2004 RGS9-2 modulates D2 dopamine receptor-mediated Ca2+ channel inhibition in rat striatal cholinergic interneurons. Proceedings of the National Academy of Sciences of the United States of America 83 15534226
2003 Absence of the RGS9.Gbeta5 GTPase-activating complex in photoreceptors of the R9AP knockout mouse. The Journal of biological chemistry 76 14625292
1998 RGS9: a regulator of G-protein signalling with specific expression in rat and mouse striatum. Journal of neuroscience research 75 9556034
2000 Modules in the photoreceptor RGS9-1.Gbeta 5L GTPase-accelerating protein complex control effector coupling, GTPase acceleration, protein folding, and stability. The Journal of biological chemistry 74 10978345
2001 RGS9-1 is required for normal inactivation of mouse cone phototransduction. Molecular vision 72 11262419
2001 RGS9 proteins facilitate acute tolerance to mu-opioid effects. The European journal of neuroscience 71 11207815
2005 Activation of mu-opioid receptors transfers control of Galpha subunits to the regulator of G-protein signaling RGS9-2: role in receptor desensitization. The Journal of biological chemistry 65 15632124
2011 A unique role of RGS9-2 in the striatum as a positive or negative regulator of opiate analgesia. The Journal of neuroscience : the official journal of the Society for Neuroscience 58 21490202
1999 Structure, alternative splicing, and expression of the human RGS9 gene. Gene 58 10564809
2003 Activation of RGS9-1GTPase acceleration by its membrane anchor, R9AP. The Journal of biological chemistry 57 12560335
2007 Consistent with dopamine supersensitivity, RGS9 expression is diminished in the amphetamine-treated animal model of schizophrenia and in postmortem schizophrenia brain. Synapse (New York, N.Y.) 56 17318883
2007 RGS9-2 is a negative modulator of mu-opioid receptor function. Journal of neurochemistry 55 17725581
2007 Expression and localization of RGS9-2/G 5/R7BP complex in vivo is set by dynamic control of its constitutive degradation by cellular cysteine proteases. The Journal of neuroscience : the official journal of the Society for Neuroscience 55 18094251
2002 Specific binding of RGS9-Gbeta 5L to protein anchor in photoreceptor membranes greatly enhances its catalytic activity. The Journal of biological chemistry 55 12006596
2006 Subcellular targeting of RGS9-2 is controlled by multiple molecular determinants on its membrane anchor, R7BP. The Journal of biological chemistry 53 16574655
2006 The membrane anchor R7BP controls the proteolytic stability of the striatal specific RGS protein, RGS9-2. The Journal of biological chemistry 53 17158100
2001 RGS9-G beta 5 substrate selectivity in photoreceptors. Opposing effects of constituent domains yield high affinity of RGS interaction with the G protein-effector complex. The Journal of biological chemistry 53 11495924
2007 Evidence for the involvement of ERbeta and RGS9-2 in 17-beta estradiol enhancement of amphetamine-induced place preference behavior. Hormones and behavior 48 17493623
2019 RGS9-2 rescues dopamine D2 receptor levels and signaling in DYT1 dystonia mouse models. EMBO molecular medicine 44 30552094
2010 RGS9-2 mediates specific inhibition of agonist-induced internalization of D2-dopamine receptors. Journal of neurochemistry 41 20477943
2009 RGS9 concentration matters in rod phototransduction. Biophysical journal 40 19751658
2007 Motor coordination deficits in mice lacking RGS9. Brain research 39 18073128
2009 R7BP complexes with RGS9-2 and RGS7 in the striatum differentially control motor learning and locomotor responses to cocaine. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 38 20043004
2009 RGS9-2: probing an intracellular modulator of behavior as a drug target. Trends in pharmacological sciences 37 19211160
2001 Phosphorylation of the regulator of G protein signaling RGS9-1 by protein kinase A is a potential mechanism of light- and Ca2+-mediated regulation of G protein function in photoreceptors. Biochemistry 37 11601986
2015 RGS9-2--controlled adaptations in the striatum determine the onset of action and efficacy of antidepressants in neuropathic pain states. Proceedings of the National Academy of Sciences of the United States of America 36 26305935
2012 The complex of G protein regulator RGS9-2 and Gβ(5) controls sensitization and signaling kinetics of type 5 adenylyl cyclase in the striatum. Science signaling 36 22932702
2001 RGS proteins: lessons from the RGS9 subfamily. Progress in nucleic acid research and molecular biology 36 11008492
2001 Phosphorylation of RGS9-1 by an endogenous protein kinase in rod outer segments. The Journal of biological chemistry 36 11292825
2014 Nucleus accumbens-specific interventions in RGS9-2 activity modulate responses to morphine. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 34 24561386
2022 Human cone elongation responses can be explained by photoactivated cone opsin and membrane swelling and osmotic response to phosphate produced by RGS9-catalyzed GTPase. Proceedings of the National Academy of Sciences of the United States of America 33 36122241
2009 Novel mutations and electrophysiologic findings in RGS9- and R9AP-associated retinal dysfunction (Bradyopsia). Ophthalmology 30 19818506
2011 β-arrestin2 plays permissive roles in the inhibitory activities of RGS9-2 on G protein-coupled receptors by maintaining RGS9-2 in the open conformation. Molecular and cellular biology 28 22006018
1999 Modulation of transducin GTPase activity by chimeric RGS16 and RGS9 regulators of G protein signaling and the effector molecule. Biochemistry 27 10213594
1998 A possible role of RGS9 in phototransduction. A bridge between the cGMP-phosphodiesterase system and the guanylyl cyclase system. The Journal of biological chemistry 27 9712827
2004 Brain-specific RGS9-2 is localized to the nucleus via its unique proline-rich domain. Biochimica et biophysica acta 26 15110994
2003 Expression patterns of the RGS9-1 anchoring protein R9AP in the chicken and mouse suggest multiple roles in the nervous system. Molecular and cellular neurosciences 26 14664818
2017 RGS9-2 Modulates Responses to Oxycodone in Pain-Free and Chronic Pain States. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 25 28074831
2007 Ontogenetic quinpirole treatment produces long-lasting decreases in the expression of Rgs9, but increases Rgs17 in the striatum, nucleus accumbens and frontal cortex. The European journal of neuroscience 25 17970732
2006 Kinetic mechanism of RGS9-1 potentiation by R9AP. Biochemistry 25 16939221
2014 RGS9-2 modulates sensory and mood related symptoms of neuropathic pain. Neurobiology of learning and memory 23 25150149
2011 Type 5 G protein beta subunit (Gbeta5) controls the interaction of regulator of G protein signaling 9 (RGS9) with membrane anchors. The Journal of biological chemistry 23 21511947
2008 Functional comparison of RGS9 splice isoforms in a living cell. Proceedings of the National Academy of Sciences of the United States of America 23 19098104
2005 RGS-Rz and RGS9-2 proteins control mu-opioid receptor desensitisation in CNS: the role of activated Galphaz subunits. Neuropharmacology 23 15617734
2002 Identification of protein kinase C isozymes responsible for the phosphorylation of photoreceptor-specific RGS9-1 at Ser475. The Journal of biological chemistry 23 12499365
2009 Analysis of genetic variations in the RGS9 gene and antipsychotic-induced tardive dyskinesia in schizophrenia. American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics 20 18548510
2009 Biology and functions of the RGS9 isoforms. Progress in molecular biology and translational science 20 20374717
2002 Noncatalytic domains of RGS9-1.Gbeta 5L play a decisive role in establishing its substrate specificity. The Journal of biological chemistry 20 12093815
2013 Ablation of TrkB expression in RGS9-2 cells leads to hyperphagic obesity. Molecular metabolism 18 24327964
2007 MPTP administration in mice changes the ratio of splice isoforms of fosB and rgs9. Brain research 18 17936734
2004 Opioid peptide receptor studies. 17. Attenuation of chronic morphine effects after antisense oligodeoxynucleotide knock-down of RGS9 protein in cells expressing the cloned Mu opioid receptor. Synapse (New York, N.Y.) 18 15065220
2012 Functional mapping of interacting regions of the photoreceptor phosphodiesterase (PDE6) γ-subunit with PDE6 catalytic dimer, transducin, and regulator of G-protein signaling9-1 (RGS9-1). The Journal of biological chemistry 17 22665478
2008 The loss of the PDE6 deactivating enzyme, RGS9, results in precocious light adaptation at low light levels. Journal of vision 17 18318613
2017 Bright flash response recovery of mammalian rods in vivo is rate limited by RGS9. The Journal of general physiology 16 28302678
2009 Distribution of RGS9-2 in neurons of the mouse striatum. Journal of neurochemistry 15 19912469
2011 RGS9-2 modulates nociceptive behaviour and opioid-mediated synaptic transmission in the spinal dorsal horn. Neuroscience letters 13 21741448
2005 Differential expression of the regulator of G protein signaling RGS9 protein in nociceptive pathways of different age rats. Brain research. Developmental brain research 13 16153714
2004 Kinetic approaches to study the function of RGS9 isoforms. Methods in enzymology 13 15488179
2013 Light-induced translocation of RGS9-1 and Gβ5L in mouse rod photoreceptors. PloS one 12 23555598
2010 Proteomic identification of Hsc70 as a mediator of RGS9-2 degradation by in vivo interactome analysis. Journal of proteome research 12 20095651
2001 Dependence of RGS9-1 membrane attachment on its C-terminal tail. The Journal of biological chemistry 12 11677233
2004 Estrogen modulates RGS9 expression in the nucleus accumbens. Neuroreport 11 15640770
2014 Effects of gender on locomotor sensitivity to amphetamine, body weight, and fat mass in regulator of G protein signaling 9 (RGS9) knockout mice. Physiology & behavior 10 25455864
2001 Inhibition of retinal guanylyl cyclase by the RGS9-1 N-terminus. Biochemical and biophysical research communications 10 11485301
2010 Membrane anchoring subunits specify selective regulation of RGS9·Gbeta5 GAP complex in photoreceptor neurons. The Journal of neuroscience : the official journal of the Society for Neuroscience 9 20943919
2011 RGS9 knockout causes a short delay in light responses of ON-bipolar cells. PloS one 8 22096596
2004 Characterization of R9AP, a membrane anchor for the photoreceptor GTPase-accelerating protein, RGS9-1. Methods in enzymology 8 15488178
2018 Selective Role of RGS9-2 in Regulating Retrograde Synaptic Signaling of Indirect Pathway Medium Spiny Neurons in Dorsal Striatum. The Journal of neuroscience : the official journal of the Society for Neuroscience 6 30006367
2004 Enhancement of pheromone response by RGS9 and Gbeta5 in yeast. Biochemical and biophysical research communications 5 15474482
2002 RGS9-1 phosphorylation and Ca2+. Advances in experimental medicine and biology 5 12596919
2011 Regulator of G protein signaling 9-2 (RGS9-2) mRNA is up regulated during neuronal differentiation of mouse embryonic stem cells. Neuroscience letters 4 21616123
2011 The involvement of RGS9 in l-3,4-dihydroxyphenylalanine-induced dyskinesias in unilateral 6-OHDA lesion rat model. Brain research bulletin 4 21963945
2010 Decreased RGS9 protein level in the striatum of rodents undergoing MPTP or 6-OHDA neurotoxicity. Neuroscience letters 4 20561938
2014 Adaptive gene regulation in the Striatum of RGS9-deficient mice. PloS one 3 24663062
2012 The 5-HT1A-receptor agonist flibanserin reduces drug-induced dyskinesia in RGS9-deficient mice. Journal of neural transmission (Vienna, Austria : 1996) 3 22569849
2002 [Analysis of GUCA1B,GNGT1 and RGS9 genes in patients with retinitis pigmentosa]. Yi chuan = Hereditas 3 15901556
2025 Multimodal imaging and electrophysiological features in bradyopsia associated with homozygous variants (c.895T>C) in Regulator of G-protein Signaling 9 (RGS9). Ophthalmic genetics 0 40955044
2021 Structural information and membrane binding of truncated RGS9-1 Anchor Protein and its C-terminal hydrophobic segment. Biochimica et biophysica acta. Biomembranes 0 33453187

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