Affinage

RGS2

Regulator of G-protein signaling 2 · UniProt P41220

Length
211 aa
Mass
24.4 kDa
Annotated
2026-06-10
100 papers in source corpus 34 papers cited in narrative 34 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

RGS2 is a GTPase-accelerating protein (GAP) that selectively and potently terminates Gq-coupled GPCR signaling, functioning as a critical brake on calcium-mobilizing pathways across vascular, cardiac, airway, and neuronal tissues (PMID:9405622, PMID:12588882). It binds Gqalpha but not other Galpha families and is markedly more potent than RGS4 at inhibiting Gq-directed PLCbeta activation, with quantitative potency differences toward Gi versus Gq mapping to defined residues in the switch I binding pocket and alpha8-alpha9 loop; crystallography of a triple-mutant RGS2-Galphai complex established that three conserved residues specialized RGS2 as a dedicated Gq GAP (PMID:9405622, PMID:10567399, PMID:19478087). Beyond catalytic GAP activity, RGS2 acts as a receptor-proximal effector antagonist: its N-terminal amphipathic helix binds acidic phospholipids to target the plasma membrane and directly engages the third intracellular loops of specific receptors including M1 mAChR, alpha1A-AR, beta2-AR, and PAR1, frequently organized by the scaffold spinophilin and in some cases stabilized by activated Gq or adenylyl cyclase (PMID:11278586, PMID:14976183, PMID:15917235, PMID:15793568, PMID:24743392). The same N-terminal region independently inhibits type V adenylyl cyclase by binding its C1 domain, decoupling cAMP suppression from GAP function (PMID:12604604). RGS2 activity and abundance are tightly regulated by PKC and cGMP-dependent protein kinase (cGKI/PKG) phosphorylation, which modulate GAP activity and membrane association, and by proteasomal turnover through a CUL4B/DDB1/FBXO44 E3 ligase complex and K71 polyubiquitination opposed by the deubiquitinase MCPIP1 (PMID:11063746, PMID:17681944, PMID:24777815, PMID:25970626, PMID:25187114). RGS2 also carries G-protein-independent functions: a 37-residue segment within its RGS domain binds eIF2Bepsilon to inhibit mRNA translation and reprogram stress responses through ATF4/CHOP and persistent eIF2alpha phosphorylation, driving translational arrest in dormant cancer cells; it binds tubulin to promote microtubule polymerization and neurite outgrowth, binds STAT3 in the nucleus to repress Nox1 transcription, and modulates LRRK2 kinase activity (PMID:19736320, PMID:30826455, PMID:33393490, PMID:16820281, PMID:22120521, PMID:24794857). Physiologically, RGS2 controls blood pressure principally through renal Gq signaling, mediates ANP/cGMP/PKG antagonism of angiotensin signaling in cardiomyocytes, governs LABA-induced airway smooth muscle bronchoprotection, and shapes short-term synaptic plasticity and GABA(B)-GIRK coupling in neurons (PMID:12588882, PMID:20847141, PMID:22080612, PMID:24794857, PMID:16950156, PMID:17965710). A human hypertension-associated R44H mutation in the N-terminal helix impairs membrane association and Gq inhibition, directly linking RGS2 to blood pressure regulation (PMID:18230714).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 1997 High

    Established RGS2 as a selective, potent inhibitor of Gqalpha, defining its founding biochemical identity distinct from other RGS proteins.

    Evidence Pulldown binding, in vitro GTPase assay, and phospholipid vesicle reconstitution with PLCbeta1 activation

    PMID:9405622

    Open questions at the time
    • Did not resolve structural basis of Gq selectivity
    • Receptor-coupled specificity in cells not yet defined
  2. 1998 High

    Showed RGS2 can also accelerate Gi1alpha GTPase activity under receptor-reconstituted conditions, defining context-dependent G protein selectivity.

    Evidence In vitro GTPase assay with M2 muscarinic receptor reconstitution and transfection-based signaling

    PMID:9736641

    Open questions at the time
    • Physiological relevance of Gi activity versus dominant Gq role unclear
  3. 1999 High

    Quantified the Gq-versus-Gi potency differences distinguishing RGS2 from RGS4 and mapped selectivity-determining residues, framing RGS2 as a Gq-specialized GAP and demonstrating GIRK current modulation via Gi/o.

    Evidence Cell-based phosphoinositide hydrolysis, RGS2 mutagenesis, and Xenopus oocyte GIRK electrophysiology with pertussis toxin controls

    PMID:10332086 PMID:10567399

    Open questions at the time
    • High-resolution structure of selectivity determinants not yet available
  4. 2001 High

    Identified the N-terminal amphipathic helix as necessary and sufficient for plasma membrane targeting via acidic phospholipid binding, explaining how RGS2 reaches its receptor/G protein substrates.

    Evidence GFP live-cell microscopy, liposome binding, and biophysical (CD/fluorescence) analysis of the helix

    PMID:11278586

    Open questions at the time
    • Nuclear function of RGS2 not resolved at this stage
  5. 2003 High

    Revealed a GAP-independent function: the N-terminus directly inhibits type V adenylyl cyclase via its C1 domain, and showed selective G-protein/receptor-driven membrane recruitment.

    Evidence Co-IP, deletion and alanine-scanning mutagenesis, cAMP assays, and GFP recruitment by Galphas/Galphaq and receptors; in vivo blood pressure phenotyping of RGS2 knockouts

    PMID:12588882 PMID:12604604 PMID:12920194

    Open questions at the time
    • Whether AC inhibition contributes to in vivo phenotypes untested
    • Mechanism of recruitment specificity incompletely defined
  6. 2004 High

    Demonstrated direct, selective binding of the RGS2 N-terminus to the M1 mAChR i3 loop, establishing RGS2 as a receptor-targeted effector antagonist separable from its GAP activity.

    Evidence GST pulldown, co-localization, ternary complex co-IP, and N-terminal deletion with phosphoinositide assays across receptor subtypes

    PMID:14976183

    Open questions at the time
    • Scaffolding that organizes the receptor-RGS2 complex not yet identified
  7. 2005 High

    Identified spinophilin as a scaffold bridging RGS2 to GPCR i3 loops and extended direct receptor binding to alpha1A-AR and adenylyl cyclase isoforms, defining the architecture of receptor-proximal RGS2 recruitment.

    Evidence Reciprocal co-IP, GST pulldown, BRET, Xenopus oocyte Ca2+ assays, and single/double knockout cell assays

    PMID:15793568 PMID:15917235 PMID:16095880

    Open questions at the time
    • Stoichiometry and dynamics of the full receptor-RGS2-spinophilin complex unresolved
  8. 2006 Medium

    Uncovered GPCR-independent roles: direct binding to TRPV6 channels, tubulin-driven microtubule polymerization and neurite outgrowth, and nuclear STAT3 binding repressing Nox1, broadening RGS2's functional repertoire.

    Evidence Yeast two-hybrid, GST pulldown, patch clamp, in vitro polymerization, PC12 outgrowth assays, and Nox1 reporter assays

    PMID:16820281 PMID:16895908 PMID:22120521

    Open questions at the time
    • In vivo significance of TRPV6, tubulin, and STAT3 interactions not established
    • Several rely on overexpression in single labs
  9. 2007 High

    Established cGKIalpha/PKG phosphorylation as a positive regulator of RGS2 membrane association and GAP activity and defined RGS2's role in synaptic plasticity and GABA(B)-GIRK coupling, linking second-messenger control to function.

    Evidence Phosphorylation-site mutagenesis, confocal microscopy, VSMC Ca2+ assays, and hippocampal/VTA electrophysiology in knockout mice

    PMID:16950156 PMID:17681944 PMID:17965710

    Open questions at the time
    • Mechanism by which cGK regulates RGS2 degradation distinct from phosphorylation sites unresolved
  10. 2008 High

    Linked RGS2 to human hypertension by showing the R44H N-terminal mutation impairs membrane entrenchment and Gq inhibition, providing direct genetic-mechanistic evidence for the blood pressure role.

    Evidence Confocal microscopy, tryptophan fluorescence, circular dichroism, and Gq functional assays of the mutant

    PMID:18230714

    Open questions at the time
    • Causality in human hypertension cohorts not addressed here
  11. 2009 High

    Defined a GAP-independent translational-control function: RGS2 binds eIF2Bepsilon via a 37-residue RGS-domain segment to inhibit mRNA translation, and crystallography resolved the structural basis of Gq selectivity.

    Evidence Co-IP, in vitro translation and domain mapping; x-ray crystallography of triple-mutant RGS2-Galphai with GAP assays

    PMID:19478087 PMID:19736320

    Open questions at the time
    • Physiological contexts where translational versus GAP function dominates unclear at this stage
  12. 2010 High

    Localized blood pressure control to renal RGS2 and established RGS2 as the required downstream effector of cardiac ANP/GC-A/PKG antagonism of angiotensin Gq signaling.

    Evidence Kidney cross-transplantation in RGS2-deficient mice and voltage-clamp/Ca2+ imaging in GC-A, PKG I, and RGS2 knockout cardiomyocytes

    PMID:20352235 PMID:20847141

    Open questions at the time
    • Renal cell type and signaling pathway mediating the effect not fully defined
  13. 2011 High

    Demonstrated RGS2 is required for glucocorticoid/LABA-induced airway smooth muscle bronchoprotection against multiple spasmogens, extending its Gq-braking role to respiratory physiology.

    Evidence Ca2+ flux in human ASM cells with siRNA and Rgs2-/- mouse bronchoconstriction assays

    PMID:21779398 PMID:22080612

    Open questions at the time
    • Transcriptional induction mechanism by glucocorticoid/LABA only partially defined
  14. 2014 Medium

    Expanded the interactome to LRRK2 (regulating its kinase activity and neuroprotection), PAR1 (Gq/11-dependent receptor binding), and defined PKG phosphorylation at Ser46/Ser64 promoting Gi3 GAP activity.

    Evidence Co-IP, kinase/GTPase assays, BRET, GST pulldown, PI hydrolysis assays, and phosphorylation-site mutagenesis

    PMID:24743392 PMID:24777815 PMID:24794857

    Open questions at the time
    • LRRK2 and PAR1 interactions from single labs without reciprocal in vivo validation
  15. 2015 Medium

    Defined the proteostatic control of RGS2 abundance through a non-canonical CUL4B/DDB1/FBXO44 E3 ligase and K71 polyubiquitination opposed by the deubiquitinase MCPIP1.

    Evidence Genome-wide siRNA screen, co-IP, K71 mutagenesis, and proteasome inhibitor assays

    PMID:25187114 PMID:25970626

    Open questions at the time
    • Signals triggering CUL4B complex assembly on RGS2 unknown
    • Interplay between the two degradation routes unresolved
  16. 2019 Medium

    Connected RGS2's eIF2B-binding domain to selective promotion of ATF4 and CHOP translation, defining its role in the integrated stress response independent of eIF2alpha phosphorylation.

    Evidence Full-length and RGS2eb domain overexpression with ATF4/CHOP immunoblotting and translation assays

    PMID:30826455

    Open questions at the time
    • Mechanism reconciling translation inhibition with selective ATF4/CHOP enhancement incompletely defined
  17. 2021 Medium

    Established RGS2 as a driver of cancer cell dormancy through persistent eIF2alpha phosphorylation and proteasomal ATF4 degradation, identifying it as a therapeutic vulnerability.

    Evidence Dye-labeled slow-cycling cell selection, lentiviral perturbation, eIF2alpha/ATF4 assays, and in vivo apoptosis assays

    PMID:33393490

    Open questions at the time
    • Generalizability across tumor types not established
    • Single-lab mechanistic model
  18. 2023 Medium

    Revealed a reproductive role in which RGS2 enhances trophoblast estradiol biosynthesis by promoting HAND1 degradation via USP14 suppression, with reciprocal repression of RGS2 GAP activity by aromatase.

    Evidence JEG-3 overexpression/knockdown, co-IP, ubiquitination/stability assays, E2 ELISA, and reporter assays

    PMID:36653442

    Open questions at the time
    • In vivo placental relevance not tested
    • Single-lab finding

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the multiple GAP-independent activities (translation control, tubulin binding, STAT3/Nox1, LRRK2, channel and aromatase interactions) are integrated and prioritized in specific cell types, and what governs the choice between them, remains unresolved.
  • No unifying framework linking GAP and non-GAP functions
  • Tissue-specific dominance of each function undetermined
  • Structural basis of most non-G-protein interactions unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 5 GO:0045182 translation regulator activity 3 GO:0060089 molecular transducer activity 2 GO:0008092 cytoskeletal protein binding 1 GO:0008289 lipid binding 1 GO:0140096 catalytic activity, acting on a protein 1
Localization
GO:0005886 plasma membrane 5 GO:0005634 nucleus 3 GO:0005856 cytoskeleton 1
Pathway
R-HSA-162582 Signal Transduction 5 R-HSA-392499 Metabolism of proteins 3 R-HSA-112316 Neuronal System 2 R-HSA-8953897 Cellular responses to stimuli 2
Partners
ADRA1AADRB2EIF2B5F2RGNAQLRRK2SPINOPHILINSTAT3

Evidence

Reading pass · 34 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1997 RGS2 is a selective and potent inhibitor of Gqα function. RGS2 selectively binds Gqα but not Giα, Goα, Gsα, or G12/13α in brain membranes and in pulldown assays with purified recombinant proteins. RGS2 does not stimulate the GTPase activities of Gsα or Giα family members even at concentrations 3000-fold higher than those sufficient for RGS4 effects on Giα. When reconstituted with phospholipid vesicles, RGS2 is 10-fold more potent than RGS4 in blocking Gqα-directed activation of PLCβ1. Pulldown binding assays (brain membranes and purified recombinant proteins), in vitro GTPase assay, phospholipid vesicle reconstitution with PLCβ1 activation assay Proceedings of the National Academy of Sciences of the United States of America High 9405622
1998 RGS2 stimulates the GTPase activity of Gqα and Gi1α in biochemical assays. The effect on Gi1 was observed only after reconstitution in phospholipid vesicles containing M2 muscarinic acetylcholine receptors. RGS2 also inhibits both Gq- and Gi-dependent responses in transfected cells. In vitro GTPase assay, phospholipid vesicle reconstitution with M2 muscarinic receptor, transfection-based functional signaling assays The Journal of neuroscience High 9736641
1999 RGS2 function is governed by quantitative differences in potency toward Gq vs Gi family members: RGS2 is 5-fold more potent than RGS4 as an inhibitor of Gq-stimulated phosphoinositide hydrolysis in vivo, whereas RGS4 is 8-fold more potent than RGS2 as an inhibitor of Gi-mediated signaling. RGS2 mutants were identified that display increased potency toward Gi family members without affecting potency toward Gq, mapping to the switch I binding pocket geometry and the α8–α9 loop interacting with αA of Gi class α subunits. Cell-based phosphoinositide hydrolysis assay, RGS2 mutational analysis, structural inference from RGS4–Giα1 crystal structure The Journal of biological chemistry High 10567399
2000 PKC phosphorylates RGS2 in vitro to near-stoichiometric levels using both a mixture of PKC isozymes and individual calcium/phospholipid-dependent PKC isoforms. RGS2 is also phosphorylated in intact COS7 cells in response to PKC activation by PMA and, to a lesser extent, by the P2Y2 receptor agonist UTP. In vitro phosphorylation of RGS2 by PKC decreased its capacity to attenuate GTP- and GTPγS-stimulated PLCβ activation, and the extent of inhibition correlated with RGS2 phosphorylation level. A phosphorylation-dependent inhibition of RGS2 GAP activity was also observed in proteoliposomes reconstituted with purified P2Y1 receptor and Gqαβγ. In vitro kinase assay with purified PKC, 32P labeling in intact COS7 cells, proteoliposome reconstitution assay, PLCβ activation assay The Journal of biological chemistry High 11063746
2001 RGS2 contains a conserved N-terminal amphipathic α-helix domain that is necessary and sufficient for plasma membrane localization. This domain binds vesicles containing acidic phospholipids. Activated Gq increases RGS2 association with the plasma membrane and decreases its nuclear accumulation. The RGS2 N terminus directs nuclear accumulation of GFP and enters the nucleus by passive diffusion despite possessing a nuclear targeting motif but lacking a nuclear import signal. Excluding RGS2 from the nucleus did not affect its ability to attenuate Gq signaling. GFP-fusion live-cell confocal microscopy, liposome binding assay, mutational analysis, truncation constructs, fluorescence/CD biophysical analysis of the amphipathic helix The Journal of biological chemistry High 11278586
2003 RGS2 directly inhibits the activity of type V adenylyl cyclase (AC) by binding to its C1 domain (not C2 domain). The interaction requires the N-terminal 19 amino acids of RGS2; the C terminus, RGS GAP activity, and RGS box domain are not required. Alanine scanning of the N terminus identified three residues essential for AC inhibition. This inhibition of cAMP accumulation is independent of Giα inhibition. Co-immunoprecipitation, deletion mutagenesis, alanine scanning mutagenesis, cAMP accumulation assay in HEK293 cells expressing type V AC The Journal of biological chemistry High 12604604
2003 GFP-RGS2 localizes to the nucleus in HEK293 cells and is selectively recruited to the plasma membrane when co-expressed with Gαs, β2-adrenergic receptor, Gαq, or AT1A angiotensin II receptor, but not by Gi-coupled receptors or G protein mutants with reduced RGS affinity. This recruitment involves direct binding to G proteins and is independent of downstream signaling events. RGS2 inhibited Gs-dependent increases in intracellular cAMP, consistent with its selective recruitment by Gs. GFP-tagged RGS2 confocal microscopy, co-expression with wild-type and mutant Gα subunits and GPCRs, steady-state Gi GTPase activity assay, cAMP accumulation assay Molecular pharmacology Medium 12920194
2004 RGS2 binds directly and selectively to the third intracellular (i3) loop of the M1 muscarinic acetylcholine receptor (M1 mAChR). The N-terminal region of RGS2 is both necessary and sufficient for binding to M1i3. RGS2 forms a stable heterotrimeric complex with activated Gqα and M1i3. Deletion of the N terminus abolishes RGS2 effector antagonist activity but not its GAP activity toward G11α. RGS2 and M1 mAChR co-localize at the plasma membrane. Closely related RGS16 does not bind M1i3, and neither protein binds M2i3. GST pulldown (in vitro binding), co-localization by fluorescence microscopy, phosphoinositide hydrolysis assay in cell membranes, N-terminal deletion constructs, co-immunoprecipitation of ternary complex The Journal of biological chemistry High 14976183
2005 The scaffold protein spinophilin (SPL) binds the N-terminal domain of RGS2 and also binds the third intracellular loop (3iL) of several GPCRs including the α-adrenergic receptor (αAR). When expressed in Xenopus oocytes, SPL markedly increased RGS2 inhibition of αAR Ca2+ signaling. A constitutively active αAR mutant (A293E) in the 3iL did not bind SPL and was relatively resistant to RGS2 inhibition. In rgs2−/− cells, αAR-evoked Ca2+ signaling is less sensitive to SPL inhibition, and in spl−/− cells less sensitive to RGS2 inhibition. Co-immunoprecipitation, GST pulldown, Xenopus oocyte electrophysiology/Ca2+ assay, αAR–βAR chimeras, knockout cell assays Nature cell biology High 15793568
2005 RGS2 binds directly and selectively to the third intracellular loop of the α1A-adrenergic receptor (α1A-AR) in vitro and is recruited by the unstimulated α1A-AR to the plasma membrane in cells to inhibit Gq/11 signaling. The N terminus of RGS2 is required for this interaction. Residues Lys219, Ser220, and Arg238 within the α1A-AR i3 loop are essential. RGS2 does not interact with the highly homologous α1B- or α1D-ARs, and RGS16 does not interact with any α1-AR. GST pulldown (in vitro), confocal fluorescence imaging of RGS2 recruitment, phosphoinositide hydrolysis assay, site-directed mutagenesis of receptor i3 loop The Journal of biological chemistry High 15917235
2005 RGS2 interacts with Gsα and adenylyl cyclase (AC) isoforms in living cells. Co-expression of AC isoforms (ACI, ACII, ACV, ACVI) recruits GFP-RGS2 to the plasma membrane. BRET signals were detected between RGS2-Rluc and Gsα-GFP, and between GFP-RGS2 and ACII-Rluc or ACVI-Rluc. Purified RGS2 selectively bound the third intracellular loop of the β2-AR in GST pulldown, and a BRET signal between GFP-RGS2 and β2-AR-Rluc was detected only when AC was co-expressed, suggesting AC stabilizes or promotes RGS2–receptor binding. GFP-RGS2 confocal localization, BRET (bioluminescence resonance energy transfer), GST pulldown with purified proteins Cellular signalling Medium 16095880
2006 RGS2 directly interacts with the NH2-terminal domain of TRPV6 (identified by yeast two-hybrid and GST pulldown). RGS2 overexpression reduces Na+ and Ca2+ current through TRPV6 but not TRPV5 in HEK293 cells. The ΔN-RGS2 deletion mutant lacking the NH2-terminal domain does not inhibit TRPV6 current. Cell surface biotinylation showed the inhibitory effect is not mediated by altered TRPV6 trafficking. The scaffolding protein spinophilin does not affect RGS2–TRPV6 binding or electrophysiology, indicating a GPCR-independent mechanism. Yeast two-hybrid, GST pulldown, whole-cell patch clamp electrophysiology, cell surface biotinylation, deletion mutagenesis The Journal of biological chemistry High 16895908
2006 RGS2 directly interacts with tubulin via amino acids 41–60 at its N-terminus and enhances microtubule polymerization in vitro. The tubulin binding region is necessary and sufficient for this activity. In Vero cells, microinjection of peptides containing the tubulin-binding region stimulated microtubule polymerization. Endogenous RGS2 localizes to the termini of neurites in differentiated PC12 cells. RGS2 overexpression enhanced NGF-induced neurite outgrowth, while RGS2 knockdown suppressed it. Co-immunoprecipitation with tubulin, in vitro microtubule polymerization assay, peptide microinjection in Vero cells, immunocytochemistry, PC12 neurite outgrowth assay with overexpression and siRNA knockdown Cellular signalling Medium 16820281
2006 RGS2 determines short-term synaptic plasticity in hippocampal neurons by downregulating Gi/o-mediated presynaptic Ca2+ channel inhibition, thereby increasing synaptic vesicle release. This was established by comparing electrophysiological recordings from RGS2 knockout and wild-type mice. Electrophysiological recordings from hippocampal neurons in RGS2 knockout vs. wild-type mice Neuron High 16950156
2007 RGS2 modulates the coupling efficiency between GABA(B) receptors and GIRK channels in dopamine neurons of the ventral tegmental area. In DA neurons, low coupling efficiency reflects selective expression of heteromeric GIRK2/3 channels and is dynamically modulated by RGS2. Repetitive exposure to GHB increases GABA(B) receptor–GIRK channel coupling efficiency through downregulation of RGS2. Electrophysiology in VTA DA and GABA neurons from mice, RGS2 knockdown/downregulation experiments with GHB exposure Nature neuroscience High 17965710
2007 cGMP-dependent protein kinase type Iα (cGKIα) phosphorylates RGS2, promoting its association with the plasma membrane (via its cGKIα phosphorylation sites) and increasing its GAP activity. RGS2 is degraded in vascular smooth muscle cells via the proteasome. Inhibition of cGK activity blunts RGS2 degradation, but inactivation of the cGKIα phosphorylation sites in RGS2 does not stabilize the protein, indicating cGK regulates RGS2 degradation through other mechanisms. RGS2 is required for cGMP-mediated inhibition of vasoconstrictor-elicited PLCβ activation, Ca2+ store release, and capacitative Ca2+ entry. Phosphorylation assay, confocal microscopy of RGS2 plasma membrane association, proteasome inhibitor treatment, Ca2+ signaling assays in VSMCs from RGS2-deficient and wild-type mice The Journal of biological chemistry High 17681944
2008 A human hypertension-associated RGS2 missense mutation R44H (within the N-terminal amphipathic α-helix) results in decreased plasma membrane association and weaker inhibition of receptor-mediated Gq signaling compared to wild-type RGS2. Tryptophan fluorescence and circular dichroism studies showed that R44H prevents proper entrenchment of hydrophobic residues into the lipid bilayer without disrupting helix-forming capacity. The R44H protein does not act as a dominant-negative. Confocal microscopy (YFP-tagged constructs), tryptophan fluorescence spectroscopy, circular dichroism, Gq signaling functional assay Molecular pharmacology High 18230714
2009 RGS2 binds eIF2Bε (eukaryotic initiation factor 2B epsilon subunit) and inhibits mRNA translation. This effect was not observed for other RGS proteins tested. The translation-inhibitory function maps to a 37-amino acid stretch within the conserved RGS domain and is distinct from RGS2's G protein GAP activity. RGS2 interferes with the eIF2–eIF2B GTPase cycle required for initiation of mRNA translation. Co-immunoprecipitation (RGS2–eIF2Bε binding), in vitro translation assay, domain mapping with deletion constructs, comparison across multiple RGS family members The Journal of cell biology High 19736320
2009 Structural determinants of RGS2 Gα selectivity were identified by x-ray crystallography. A trio of point mutations in RGS2 confers Gαi-directed binding and GAP activities without perturbing Gαq association. Crystal structure of the triple-mutant RGS2 in complex with transition-state Gαi was solved at 2.8 Å resolution. These three amino acids are evolutionarily conserved among organisms with modern cardiovascular systems, suggesting RGS2 specialized as a potent Gαq GAP. X-ray crystallography (2.8 Å), site-directed mutagenesis, in vitro GAP activity assay, Gα binding assays The Journal of biological chemistry High 19478087
2010 ANP/GC-A/cGMP signaling selectively suppresses Ang II (Gαq-mediated) but not isoproterenol (Gαs-mediated) Ca2+ currents and transients in cardiomyocytes. This suppression is abolished in cardiomyocytes deficient in GC-A, PKG I, or RGS2 (a target of PKG I), establishing RGS2 as a required downstream effector of the PKG I-mediated pathway that antagonizes Ang II/AT1 signaling. Voltage-clamp recordings, fluorescence Ca2+ imaging in isolated cardiomyocytes, cardiomyocyte-conditional GC-A KO mice, PKG I KO and RGS2 KO mice Basic research in cardiology High 20352235
2011 RGS2 is required for LABA-induced bronchoprotection. In primary human airway smooth muscle cells, glucocorticoid/LABA combinations synergistically induce RGS2 expression. RGS2 reduced intracellular free Ca2+ flux elicited by histamine, methacholine, leukotrienes, and other spasmogens. Protection against spasmogen-increased Ca2+ following 6 h of LABA plus corticosteroid treatment was dependent on RGS2. Rgs2-deficient mice showed enhanced bronchoconstriction to spasmogens and absence of LABA-induced bronchoprotection. Ca2+ flux assay in human airway smooth muscle cells, RGS2 siRNA knockdown, Rgs2-/- mouse bronchoconstriction assay, gene expression analysis Proceedings of the National Academy of Sciences of the United States of America High 22080612
2014 RGS2 is a novel interacting partner of LRRK2 in vivo and regulates both the GTPase and kinase activities of LRRK2. RGS2 regulates LRRK2-dependent control of neuronal process length in mammalian neurons, and is protective against neuronal toxicity of the LRRK2 G2019S mutation. RGS2 regulation of LRRK2 function occurs through effects on kinase activity independently of GTPase activity. Co-immunoprecipitation (in vivo interaction), kinase and GTPase activity assays, neuronal process length measurement, toxicity assay in mammalian neurons Human molecular genetics Medium 24794857
2014 RGS2 interacts with PAR1 (protease-activated receptor 1) in a Gαq/11-dependent manner in live cells. Very little BRET activity is observed between PAR1 and RGS2 in the absence of Gα, but is markedly enhanced by Gαq/11. PAR1 mutant R205A (eliminating Gq/11 coupling) blocks this interaction. The purified intracellular third loop of PAR1 binds directly to purified His-RGS2. RGS2 inhibits PAR1/Gα-mediated calcium and MAPK/ERK signaling but not RhoA signaling. BRET in live COS-7 cells, GST pulldown with purified proteins, Ca2+ signaling assay, ERK phosphorylation assay, RhoA activity assay, site-directed mutagenesis PloS one Medium 24743392
2015 RGS2 protein is degraded through the ubiquitin-proteasome system via a novel E3 ligase complex containing cullin 4B (CUL4B), DDB1, and F-box protein 44 (FBXO44). The more typical SCF complex (CUL1/Skp1/FBXO44) can bind FBXO44 but does not bind RGS2 and is not involved in its degradation. Genome-wide siRNA screen, co-immunoprecipitation, proteasome inhibitor assays, knockdown experiments PloS one Medium 25970626
2015 RGS2 protein is polyubiquitinated at residue K71 and undergoes proteasomal degradation. The deubiquitinase MCPIP1 stabilizes RGS2 protein; a dominant-negative MCPIP1 mutant (C157A) does not affect RGS2 levels. MG-132 treatment increased both endogenous and exogenous RGS2, indicating proteasomal regulation. Ubiquitination assay with K71 mutagenesis, proteasome inhibitor (MG-132) treatment, MCPIP1 overexpression and dominant-negative mutant, immunoblotting Journal of cellular biochemistry Medium 25187114
2019 RGS2 promotes translation of ATF4 and CHOP by a mechanism involving its eIF2B-interacting domain (RGS2eb). Expression of full-length RGS2 or RGS2eb significantly increases ATF4 and CHOP protein levels. These effects are translationally regulated and independent of eIF2α phosphorylation. RGS2 and domain overexpression, immunoblotting for ATF4/CHOP, translation assay, eIF2α phosphorylation analysis Cellular signalling Medium 30826455
2021 RGS2 causes prolonged translational arrest in slow-cycling/dormant cancer cells (SCCs) through persistent eIF2α phosphorylation via proteasome-mediated degradation of ATF4 (activating transcription factor 4). RGS2 antagonism or phosphodiesterase 5 inhibitors promoted ER stress-induced apoptosis in SCCs under stressed conditions. Proliferation-sensitive dye labeling, chemotherapeutic selection, lentiviral RGS2 overexpression/knockdown, eIF2α phosphorylation assay, ATF4 protein stability assay with proteasome inhibitors, in vitro and in vivo apoptosis assays The Journal of clinical investigation Medium 33393490
2011 RGS2 downregulation in striatal neurons of Huntington's disease models is a compensatory response. Silencing RGS2 in cultured rat primary striatal neurons reduced mutant huntingtin fragment toxicity and enhanced ERK activation, establishing a link between RGS2 inhibition and neuroprotective ERK signaling. Lentiviral shRNA knockdown in primary striatal neurons, cell viability assay, ERK phosphorylation assay, lentiviral RGS2 overexpression PloS one Medium 21779398
2014 PKG (but not PKA) phosphorylates RGS2 at Ser46 and Ser64 in gastrointestinal smooth muscle and enhances association of Gαi3-GTP with RGS2, thereby accelerating Gαi GTPase activity, enhancing Gαβγi trimer reassembly, and inhibiting Gβγi-dependent PLCβ3 activity. Expression of phosphorylation-site-deficient RGS2 (S46A/S64A) or RGS2 siRNA partially reversed the effect of GSNO on PI hydrolysis. PKG phosphorylation assay, co-immunoprecipitation of Gαi3 and RGS2, PI hydrolysis assay, phosphorylation-site mutagenesis (S46A/S64A), siRNA knockdown Cell biochemistry and biophysics Medium 24777815
2006 RGS2 directly binds STAT3 in the nucleus and represses STAT3-mediated transcriptional activation of Nox1. A GFP-tagged RGS2 concentrates in the nucleus and directly binds STAT3, inhibiting its transcriptional activity. RGS2 expression is itself repressed by TLR2 signaling. Co-immunoprecipitation (RGS2–STAT3 binding), GFP-RGS2 confocal localization, Nox1 reporter assay, siRNA knockdown Cellular signalling Medium 22120521
1999 RGS2 accelerates the speed of ACh-mediated activation and deactivation of GIRK1/2 and GIRK1/4 currents in Xenopus oocytes. Two point mutations in RGS2 (N109S and L180F) reduced the acceleration of current amplification after ACh application on GIRK1/4 channels compared with wild-type RGS2. Pertussis toxin completely abolished ACh-mediated current amplification with or without RGS2, indicating RGS2 acts on Gi/o. Xenopus oocyte whole-cell electrophysiology, RGS2 co-expression with GIRK and mAChR subunits, site-directed mutagenesis, pertussis toxin treatment The Journal of physiology Medium 10332086
2003 Loss of RGS2 in mice increases agonist potency and efficacy for P2Y receptor-mediated Ca2+ signaling in vascular smooth muscle cells and slows the kinetics of signal termination, resulting in prolonged vasoconstriction and hypertension. RGS2-/- and RGS2+/- mouse model; in vivo blood pressure telemetry; in vitro vascular smooth muscle cell Ca2+ imaging The Journal of clinical investigation High 12588882
2010 Renal RGS2 is sufficient to control blood pressure: kidney cross-transplantation in RGS2-deficient mice showed that loss of renal RGS2 was sufficient to cause hypertension, whereas absence of RGS2 from all extrarenal tissues (including peripheral vasculature) did not significantly alter blood pressure. Kidney cross-transplantation in total body RGS2-deficient and wild-type mice, blood pressure measurement Journal of the American Society of Nephrology High 20847141
2023 RGS2 enhances estradiol biosynthesis in trophoblasts by promoting proteasomal degradation of HAND1 (a trans-inactivator of the aromatase gene) through suppression of USP14-mediated deubiquitination of HAND1, thereby increasing aromatase expression and E2 production. However, aromatase binds to RGS2 and represses its GAP activity. JEG-3 cell overexpression/knockdown, protein stability assays, co-immunoprecipitation (RGS2–aromatase, RGS2–USP14), ubiquitination assay for HAND1, E2 ELISA, reporter assays Experimental & molecular medicine Medium 36653442

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1997 RGS2/G0S8 is a selective inhibitor of Gqalpha function. Proceedings of the National Academy of Sciences of the United States of America 303 9405622
1998 Dynamic regulation of RGS2 suggests a novel mechanism in G-protein signaling and neuronal plasticity. The Journal of neuroscience : the official journal of the Society for Neuroscience 253 9736641
2003 Hypertension and prolonged vasoconstrictor signaling in RGS2-deficient mice. The Journal of clinical investigation 246 12588882
2000 Regulation of T cell activation, anxiety, and male aggression by RGS2. Proceedings of the National Academy of Sciences of the United States of America 232 11027316
2004 RGS2 binds directly and selectively to the M1 muscarinic acetylcholine receptor third intracellular loop to modulate Gq/11alpha signaling. The Journal of biological chemistry 188 14976183
2007 RGS2 modulates coupling between GABAB receptors and GIRK channels in dopamine neurons of the ventral tegmental area. Nature neuroscience 177 17965710
1999 G protein selectivity is a determinant of RGS2 function. The Journal of biological chemistry 152 10567399
2002 RGS2: a multifunctional regulator of G-protein signaling. The international journal of biochemistry & cell biology 129 11906816
2005 Spinophilin regulates Ca2+ signalling by binding the N-terminal domain of RGS2 and the third intracellular loop of G-protein-coupled receptors. Nature cell biology 118 15793568
2006 Reduced expression of regulator of G-protein signaling 2 (RGS2) in hypertensive patients increases calcium mobilization and ERK1/2 phosphorylation induced by angiotensin II. Journal of hypertension 115 16685212
2003 Recruitment of RGS2 and RGS4 to the plasma membrane by G proteins and receptors reflects functional interactions. Molecular pharmacology 114 12920194
1999 A novel regulator of G protein signalling in yeast, Rgs2, downregulates glucose-activation of the cAMP pathway through direct inhibition of Gpa2. The EMBO journal 114 10523302
2003 Identification of RGS2 and type V adenylyl cyclase interaction sites. The Journal of biological chemistry 111 12604604
2001 Mechanisms governing subcellular localization and function of human RGS2. The Journal of biological chemistry 108 11278586
2005 RGS2 interacts with Gs and adenylyl cyclase in living cells. Cellular signalling 104 16095880
2008 Influence of RGS2 on anxiety-related temperament, personality, and brain function. Archives of general psychiatry 98 18316676
2005 Selective loss of fine tuning of Gq/11 signaling by RGS2 protein exacerbates cardiomyocyte hypertrophy. The Journal of biological chemistry 88 16380388
2005 Selective inhibition of alpha1A-adrenergic receptor signaling by RGS2 association with the receptor third intracellular loop. The Journal of biological chemistry 85 15917235
2000 Protein kinase C phosphorylates RGS2 and modulates its capacity for negative regulation of Galpha 11 signaling. The Journal of biological chemistry 85 11063746
2006 Regulator of G-protein signaling 2 (RGS2) inhibits androgen-independent activation of androgen receptor in prostate cancer cells. Oncogene 81 16449965
2005 Autonomic nervous system and blood pressure regulation in RGS2-deficient mice. American journal of physiology. Regulatory, integrative and comparative physiology 81 15661972
2000 Specific regulation of RGS2 messenger RNA by angiotensin II in cultured vascular smooth muscle cells. Molecular pharmacology 81 10692485
2008 Variant in RGS2 moderates posttraumatic stress symptoms following potentially traumatic event exposure. Journal of anxiety disorders 73 19162436
2006 RGS2 determines short-term synaptic plasticity in hippocampal neurons by regulating Gi/o-mediated inhibition of presynaptic Ca2+ channels. Neuron 71 16950156
2011 β2-Adrenoceptor agonist-induced RGS2 expression is a genomic mechanism of bronchoprotection that is enhanced by glucocorticoids. Proceedings of the National Academy of Sciences of the United States of America 67 22080612
2010 Novel insights into the mechanisms mediating the local antihypertrophic effects of cardiac atrial natriuretic peptide: role of cGMP-dependent protein kinase and RGS2. Basic research in cardiology 66 20352235
2009 Structural determinants of G-protein alpha subunit selectivity by regulator of G-protein signaling 2 (RGS2). The Journal of biological chemistry 66 19478087
2004 RGS2 is an important target gene of Flt3-ITD mutations in AML and functions in myeloid differentiation and leukemic transformation. Blood 65 15536149
1997 Comparison of mRNA expression of two regulators of G-protein signaling, RGS1/BL34/1R20 and RGS2/G0S8, in cultured human blood mononuclear cells. DNA and cell biology 61 9174164
2004 Dopamine receptor-mediated regulation of RGS2 and RGS4 mRNA differentially depends on ascending dopamine projections and time. The European journal of neuroscience 56 15090051
2011 Rgs2 mediates pro-angiogenic function of myeloid derived suppressor cells in the tumor microenvironment via upregulation of MCP-1. PloS one 55 21494556
2000 Dynamic regulation of RGS2 in bone: potential new insights into parathyroid hormone signaling mechanisms. Endocrinology 55 10614620
2015 RGS2 suppresses breast cancer cell growth via a MCPIP1-dependent pathway. Journal of cellular biochemistry 52 25187114
2010 RGS2 inhibits beta-adrenergic receptor-induced cardiomyocyte hypertrophy. Cellular signalling 52 20362664
2009 RGS2 and generalized anxiety disorder in an epidemiologic sample of hurricane-exposed adults. Depression and anxiety 51 18833580
2021 RGS2-mediated translational control mediates cancer cell dormancy and tumor relapse. The Journal of clinical investigation 50 33393490
2009 Translational control by RGS2. The Journal of cell biology 49 19736320
2011 Identification of a cAMP-response element in the regulator of G-protein signaling-2 (RGS2) promoter as a key cis-regulatory element for RGS2 transcriptional regulation by angiotensin II in cultured vascular smooth muscles. The Journal of biological chemistry 48 22057271
2009 Evidence for enhanced M3 muscarinic receptor function and sensitivity to atrial arrhythmia in the RGS2-deficient mouse. American journal of physiology. Heart and circulatory physiology 48 19966055
2002 Expression of RGS2, RGS4 and RGS7 in the developing postnatal brain. The European journal of neuroscience 48 11906535
2006 RGS2 is upregulated by and attenuates the hypertrophic effect of alpha1-adrenergic activation in cultured ventricular myocytes. Cellular signalling 47 16517124
2011 Decreased striatal RGS2 expression is neuroprotective in Huntington's disease (HD) and exemplifies a compensatory aspect of HD-induced gene regulation. PloS one 46 21779398
2014 A Parkinson's disease gene regulatory network identifies the signaling protein RGS2 as a modulator of LRRK2 activity and neuronal toxicity. Human molecular genetics 45 24794857
1999 New roles for RGS2, 5 and 8 on the ratio-dependent modulation of recombinant GIRK channels expressed in Xenopus oocytes. The Journal of physiology 45 10332086
2022 Fatty acid metabolism is related to the immune microenvironment changes of gastric cancer and RGS2 is a new tumor biomarker. Frontiers in immunology 43 36591293
2001 Oxidative stress and heat shock stimulate RGS2 expression in 1321N1 astrocytoma cells. Archives of biochemistry and biophysics 42 11488592
2007 Regulation of RGS2 and second messenger signaling in vascular smooth muscle cells by cGMP-dependent protein kinase. The Journal of biological chemistry 41 17681944
2006 RGS2 promotes formation of neurites by stimulating microtubule polymerization. Cellular signalling 39 16820281
2006 RGS2 inhibits the epithelial Ca2+ channel TRPV6. The Journal of biological chemistry 39 16895908
2002 Characterization and comparison of RGS2 and RGS4 as GTPase-activating proteins for m2 muscarinic receptor-stimulated G(i). Molecular pharmacology 39 12181442
2002 Opposite modulation of regulators of G protein signalling-2 RGS2 and RGS4 expression by dopamine receptors in the rat striatum. Neuroscience letters 39 12419501
1995 Differential expression of a basic helix-loop-helix phosphoprotein gene, G0S8, in acute leukemia and localization to human chromosome 1q31. Leukemia 39 7643615
2017 Epigenetic regulation of RGS2 (Regulator of G-protein signaling 2) in chemoresistant ovarian cancer cells. Journal of chemotherapy (Florence, Italy) 37 28102109
2010 Deregulation of RGS2 in cardiovascular diseases. Frontiers in bioscience (Scholar edition) 36 20036967
2006 RGS2 is regulated by angiotensin II and functions as a negative feedback of aldosterone production in H295R human adrenocortical cells. Endocrinology 35 16627589
2007 Association of RGS2 gene polymorphisms with suicide and increased RGS2 immunoreactivity in the postmortem brain of suicide victims. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 34 17728697
2007 RGS5, RGS4, and RGS2 expression and aortic contractibility are dynamically co-regulated during aortic banding-induced hypertrophy. Journal of molecular and cellular cardiology 34 18207159
2002 Analysis of regulator of G-protein signaling-2 (RGS-2) expression and function in osteoblastic cells. Journal of cellular biochemistry 34 11968023
2011 RGS2 is a primary terminator of β₂-adrenergic receptor-mediated G(i) signaling. Journal of molecular and cellular cardiology 33 21291891
2016 Upregulation of RGS2: a new mechanism for pirfenidone amelioration of pulmonary fibrosis. Respiratory research 32 27549302
2007 Association of the RGS2 gene with extrapyramidal symptoms induced by treatment with antipsychotic medication. Pharmacogenetics and genomics 32 17558307
2005 Angiotensin II-evoked enhanced expression of RGS2 attenuates Gi-mediated adenylyl cyclase signaling in A10 cells. Cardiovascular research 32 15914115
2004 RGS2-mediated regulation of Gqalpha. Methods in enzymology 32 15488171
2008 Further evidence for association of the RGS2 gene with antipsychotic-induced parkinsonism: protective role of a functional polymorphism in the 3'-untranslated region. The pharmacogenomics journal 31 18347610
2004 Role of regulator of G protein signaling 2 (RGS2) in Ca(2+) oscillations and adaptation of Ca(2+) signaling to reduce excitability of RGS2-/- cells. The Journal of biological chemistry 31 15292238
2023 Long noncoding RNA HITT coordinates with RGS2 to inhibit PD-L1 translation in T cell immunity. The Journal of clinical investigation 30 37014700
2005 NO-dependent blood pressure regulation in RGS2-deficient mice. American journal of physiology. Regulatory, integrative and comparative physiology 30 16269576
2019 Reduced mRNA Expression of RGS2 (Regulator of G Protein Signaling-2) in the Placenta Is Associated With Human Preeclampsia and Sufficient to Cause Features of the Disorder in Mice. Hypertension (Dallas, Tex. : 1979) 28 31865781
2015 FBXO44-Mediated Degradation of RGS2 Protein Uniquely Depends on a Cullin 4B/DDB1 Complex. PloS one 28 25970626
2014 Regulation of Gβγi-dependent PLC-β3 activity in smooth muscle: inhibitory phosphorylation of PLC-β3 by PKA and PKG and stimulatory phosphorylation of Gαi-GTPase-activating protein RGS2 by PKG. Cell biochemistry and biophysics 27 24777815
2008 Association of RGS2 and RGS5 variants with schizophrenia symptom severity. Schizophrenia research 27 18262772
2016 RGS2 expression predicts amyloid-β sensitivity, MCI and Alzheimer's disease: genome-wide transcriptomic profiling and bioinformatics data mining. Translational psychiatry 26 27701409
2015 RGS2 ggenetic variation: association analysis with panic disorder and dimensional as well as intermediate phenotypes of anxiety. American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics 26 25740197
2013 Influence of RGS2 on sertraline treatment for social anxiety disorder. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 26 24154666
2018 Analysis of regulator of G-protein signalling 2 (RGS2) expression and function during prostate cancer progression. Scientific reports 25 30467386
2014 Regulator of G protein signaling 2 (RGS2) and RGS4 form distinct G protein-dependent complexes with protease activated-receptor 1 (PAR1) in live cells. PloS one 25 24743392
2011 Resistance to age-related, normal body weight gain in RGS2 deficient mice. Cellular signalling 25 21447383
2001 RGS2: regulation of expression and nuclear localization. Biochemical and biophysical research communications 24 11322774
2000 RGS4 and RGS2 bind coatomer and inhibit COPI association with Golgi membranes and intracellular transport. Molecular biology of the cell 24 10982407
2012 RGS2 mediates the anxiolytic effect of oxytocin. Brain research 23 22459044
2001 Second messengers regulate RGS2 expression which is targeted to the nucleus. Biochimica et biophysica acta 23 11755214
2020 Regulators of G-protein signaling, RGS2 and RGS4, inhibit protease-activated receptor 4-mediated signaling by forming a complex with the receptor and Gα in live cells. Cell communication and signaling : CCS 22 32517689
2014 RGS2 regulates urotensin II-induced intracellular Ca2+ elevation and contraction in glomerular mesangial cells. Journal of cellular physiology 22 24105430
2009 Ischemia induces regulator of G protein signaling 2 (RGS2) protein upregulation and enhances apoptosis in astrocytes. American journal of physiology. Cell physiology 22 20032508
2008 The RGS2 gene product from a candidate hypertension allele shows decreased plasma membrane association and inhibition of Gq. Molecular pharmacology 22 18230714
2018 A bronchoprotective role for Rgs2 in a murine model of lipopolysaccharide-induced airways inflammation. Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology 21 30305828
2017 Protective Roles for RGS2 in a Mouse Model of House Dust Mite-Induced Airway Inflammation. PloS one 21 28107494
2016 Digoxin-Mediated Upregulation of RGS2 Protein Protects against Cardiac Injury. The Journal of pharmacology and experimental therapeutics 21 26941169
2015 MicroRNA hsa-miR-4717-5p regulates RGS2 and may be a risk factor for anxiety-related traits. American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics 21 25847876
2014 Regulator of G protein signaling 2 (RGS2) deficiency accelerates the progression of kidney fibrosis. Biochimica et biophysica acta 21 24973550
2011 RGS2 is a negative regulator of STAT3-mediated Nox1 expression. Cellular signalling 21 22120521
2010 Renal actions of RGS2 control blood pressure. Journal of the American Society of Nephrology : JASN 21 20847141
2002 Oxytocin stimulation of RGS2 mRNA expression in cultured human myometrial cells. American journal of physiology. Endocrinology and metabolism 21 11832360
2023 RGS2 promotes estradiol biosynthesis by trophoblasts during human pregnancy. Experimental & molecular medicine 20 36653442
2014 Expression and regulation of regulator of G-protein signaling protein-2 (RGS2) in equine and bovine follicles prior to ovulation: molecular characterization of RGS2 transactivation in bovine granulosa cells. Biology of reproduction 20 25339105
2006 Cellular stress increases RGS2 mRNA and decreases RGS4 mRNA levels in SH-SY5Y cells. Neuroscience letters 20 16733081
2017 Increased fear learning, spatial learning as well as neophobia in Rgs2-/- mice. Genes, brain, and behavior 19 28846187
2019 RGS2 promotes the translation of stress-associated proteins ATF4 and CHOP via its eIF2B-inhibitory domain. Cellular signalling 18 30826455
2013 Valproic acid substantially downregulated genes folr1, IGF2R, RGS2, COL6A3, EDNRB, KLF6, and pax-3, N-acetylcysteine alleviated most of the induced gene alterations in chicken embryo model. Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie 18 24398995
2012 RGS2 is a component of the cellular stress response. Biochemical and biophysical research communications 18 22922103

Missed literature

Know a paper Affinage missed for RGS2? Flag it for the maintainers and the community.

No submissions yet.