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1  known as regulators of G protein signaling (RGS proteins).
2 t reversible small-molecule inhibitors of an RGS protein.
3 ied the first small-molecule inhibitor of an RGS protein.
4 Pases in the intracellular trafficking of an RGS protein.
5 one Galpha, one Gbeta, three Ggamma, and one RGS protein.
6 ctivity, to mimic in cis the GAP function of RGS proteins.
7 ise from the consensus GoLoco motif found in RGS proteins.
8 face between Gbeta5 and the N terminus of R7 RGS proteins.
9 d pathway under strong inhibitory control by RGS proteins.
10 the extent of inhibition by the R4 family of RGS proteins.
11  subfamilies consisting of over 20 different RGS proteins.
12 f Galpha12, a behavior consistent with other RGS proteins.
13 ates RGS18 and RGS14 without modifying other RGS proteins.
14  may generally extend to other receptors and RGS proteins.
15 rotein cycle is regulated by the activity of RGS proteins.
16 urface expression and through recruitment of RGS proteins.
17  the Galpha subunit, a reaction catalyzed by RGS proteins.
18 Rs (MOR and D2R) on the G protein bias of R7 RGS proteins.
19 g G protein and GPCR selectivity of striatal RGS proteins.
20 ervous system, is mediated exclusively by R7 RGS proteins.
21  maintaining proteolytic stability of the R7 RGS proteins.
22 s, and the REGULATOR OF G-PROTEIN SIGNALING (RGS) protein.
23 ivity of "regulator of G-protein signaling" (RGS) proteins.
24 rolled by regulator of G protein signalling (RGS) proteins.
25 led by the regulator of G protein signaling (RGS) proteins.
26 led by the regulator of G-protein signaling (RGS) proteins.
27 ction with regulator of G-protein signaling (RGS) proteins.
28 r of the "regulator of G protein signaling" (RGS) proteins.
29 ression of regulator of G protein signaling (RGS) proteins.
30 amily of "regulator of G protein signaling" (RGS) proteins.
31 eract with regulator of G protein signaling (RGS) proteins.
32            Expression of RGS2, but not other RGS proteins, abolished androgen-independent AR activity
33                                              RGS proteins accelerate the intrinsic GTPase activity of
34            Regulator of G-protein signaling (RGS) proteins accelerate GTP hydrolysis by heterotrimeri
35            Regulator of G protein signaling (RGS) proteins accelerate the endogenous GTPase activity
36  including nucleotide binding, intrinsic and RGS protein-accelerated GTP hydrolysis, and interactions
37           Regulators of G-protein signaling (RGS) proteins act directly on Galpha subunits to increas
38            Regulator of G protein signaling (RGS) proteins act to temporally modulate the activity of
39 enuated by regulator of G protein signaling (RGS) proteins acting as GTPase-activating proteins for G
40 d blunting of sensitivity also engendered by RGS protein action in trans.
41 Galphaq, Galphaq-G188S, that is resistant to RGS protein action were sensitized to the development of
42          Septin organization is dependent on RGS protein activity.
43 s there are concomitant, independent LSEs of RGS proteins along with an extraordinary diversification
44                                         Many RGS proteins also bind additional signaling partners tha
45 rotein is readily inactivated by its cognate RGS protein and forms a stable, GDP-bound, heterotrimeri
46  protein-coupled receptors, Galpha subunits, RGS proteins and downstream effectors in mammalian syste
47                       We explore the role of RGS proteins and G alpha(i2) in the physiologic regulati
48                                              RGS proteins and G alpha(i2) signaling play important ro
49 endrites by varying the concentration of key RGS proteins and measuring the impact on transmission of
50                          NFR1 interacts with RGS proteins and phosphorylates them.
51 at the spatiotemporal-specific expression of RGS proteins and their target components, as well as the
52 th Loco, a regulator of G-protein signaling (RGS) protein and a known effector of glia specification.
53 lso binds regulators of G protein signaling (RGS) proteins and the third intracellular loop (3iL) of
54 o still bind the N-terminal DEP domain of R7 RGS proteins, and mutant Gbeta5-R7 RGS complexes initial
55 nteract with all members of the R7 family of RGS proteins, and palmitoylation of R7BP can target R7 R
56 rs involved in ACD, including GoLoco motifs, RGS proteins, and RIC-8.
57  protein inactivation, which is modulated by RGS proteins, and the rate of G protein activation, whic
58  including Regulator of G protein Signaling (RGS) proteins, and has been implicated in membrane targe
59 ypothesize Regulator of G-Protein Signaling (RGS) proteins, and specifically RGS5, are endogenous rep
60                                              RGS proteins are best understood as negative regulators
61                                          The RGS proteins are GTPase activating proteins that acceler
62         Previous studies have suggested that RGS proteins are more effective on less efficiently coup
63  regulator of Hh-mediated signaling and that RGS proteins are potential targets for novel therapeutic
64                              Because several RGS proteins are rapidly degraded by the N-end rule path
65 influence of RGS proteins on these pathways, RGS proteins are regulators of cardiovascular physiology
66                                 R7 subfamily RGS proteins are stabilized by the G-protein subunit Gbe
67                                              RGS proteins are subject to posttranslational modificati
68                        Our results show that RGS proteins are widely distributed in the monocot linea
69            Regulator of G-protein signaling (RGS) proteins are a family of molecules that control the
70            Regulator of G-protein signaling (RGS) proteins are critical modulators of GPCR activity,
71           Regulators of G protein signaling (RGS) proteins are emerging as potentially important drug
72           Regulators of G-protein signaling (RGS) proteins are important components of signal transdu
73        The regulator of G-protein signaling (RGS) proteins are key interactors and critical modulator
74            Regulator of G protein signaling (RGS) proteins are negative regulators of signal transduc
75            Regulator of G-protein signaling (RGS) proteins are potent inhibitors of heterotrimeric G-
76           Regulators of G protein signaling (RGS) proteins are potent negative modulators of G protei
77            Regulator of G protein signaling (RGS) proteins are united into a family by the presence o
78  Regulators of G protein signaling (RGSs, or RGS proteins) are responsible for the subsecond turn off
79      Our results strongly support a role for RGS proteins as negative regulators of opioid supraspina
80 indings reveal a hitherto overlooked role of RGS proteins as noise suppressors and demonstrate an abi
81 nd also reveal a potential novel function of RGS proteins as positive regulators of opioid spinal ant
82 entify RGS6, a member of the R7 subfamily of RGS proteins, as a key regulator of GABA(B)R signaling i
83 f these small-molecule inhibitors against 12 RGS proteins, as well as against the cysteine-null mutan
84           Regulators of G-protein signaling (RGS proteins) belong to a diverse protein family that wa
85           Regulators of G protein signaling (RGS) proteins bind to activated Galpha subunits, includi
86 cytes with a Galphai2 mutation that disables RGS protein binding accumulated in the perivascular chan
87  alpha(i2) with a G184S mutation that blocks RGS protein binding and GTPase acceleration.
88        Additionally, KB-1753 interferes with RGS protein binding and resultant GAP activity.
89                      The RGS7 (R7) family of RGS proteins bound to the divergent Gbeta subunit Gbeta5
90  GTPase-accelerating protein activity of the RGS protein by using small molecules.
91 uss a rationale for therapeutic targeting of RGS proteins by regulation of expression or allosteric m
92                                     However, RGS proteins can be highly regulated and can demonstrate
93                                              RGS proteins can be regulated by altering their GAP acti
94      These findings demonstrate that certain RGS proteins can directly interact with preferred G-prot
95                                         Most RGS proteins can serve as GAPs for multiple isoforms of
96                                     Although RGS proteins canonically function as G-protein regulator
97 spectroscopic probe to measure intrinsic and RGS protein-catalyzed nucleotide hydrolysis by Galphao.
98 , to learn whether the loss of some of these RGS proteins causes the absence of the ERG b-wave.
99            Regulator of G-protein signaling (RGS) proteins classically function as negative modulator
100                                  All four R7 RGS proteins co-precipitate with R7BP from brain extract
101         With hundreds of GPCRs and dozens of RGS proteins, compartmentalization plays a key role in e
102 annel assembly with allosterically regulated RGS protein complexes, which provide a target for modula
103 e are key to controlling the stability of R7 RGS protein complexes.
104 family of regulators of G protein signaling (RGS) proteins, comprising RGS6, RGS7, RGS9, and RGS11, r
105     For example, members of the R7 family of RGS proteins contain a DEP, GGL, and novel DHEX domain a
106                                However, many RGS proteins contain additional domains that serve other
107  which is responsible for GAP activity, most RGS proteins contain other distinct structural motifs.
108                                           R7 RGS proteins contain several distinct domains and form o
109 attendant regulators of G-protein signaling (RGS) proteins control both intercellular signaling and a
110 y a role in pathophysiological processes and RGS proteins could represent novel cardiovascular therap
111 r homolog Ste3alpha, Gbeta subunit Gpb1, and RGS protein Crg1.
112       In a previous study, we identified the RGS protein Crg2 involved in regulating the pheromone re
113                          The R7 subfamily of RGS proteins critically regulates neuronal G protein-sig
114                                     However, RGS proteins differ widely in size and the organization
115                                              RGS proteins display remarkable selectivity and specific
116  to cholinergic stimulation, possibly due to RGS protein downregulation.
117 at loss of RSBP-1 phenocopies loss of the R7 RGS protein EAT-16, but does not disrupt function of the
118  does not disrupt function of the related R7 RGS protein EGL-10.
119                                   Neutrophil RGS proteins establish a threshold for Galpha(i) activat
120                                              RGS proteins exert their effect by directly binding to t
121  CCG-4986, lack of inhibition indicates that RGS proteins exhibit fundamental differences in their re
122 s and that RGS4 was by far the most abundant RGS protein expressed by these cells.
123 se and heart rate regulation, and changes in RGS protein expression and/or function are believed to p
124          "Regulator of G-protein signaling" (RGS) proteins facilitate the termination of G protein-co
125                                The mammalian RGS protein family has more than 20 members and they sha
126 etics, the regulator of G-protein signaling (RGS) protein family modulates the timing of GIRK activit
127 of the R7 regulators of G protein signaling (RGS) protein family of neuronal RGS, is a critical regul
128 ber of the Regulator of G protein Signaling (RGS) protein family, as a nuclear factor that suppresses
129 ber of the regulator of G-protein signaling (RGS) protein family, possesses an N-terminal RGS domain,
130 ber of the regulator of G protein signaling (RGS) protein family.
131 r Galpha(i)G203A), as well as GRK2NT-GFP (an RGS protein for G(q/11)) but neither p115RhoGEFRGS-GFP (
132 ich has the largest complement of Galpha and RGS proteins for any eukaryote, provides new insights in
133 of the regulators of G-protein signaling (R7 RGS) proteins form multi-subunit complexes that play cru
134     Most studies searching for modulators of RGS protein function have been focused on inhibiting the
135  may prove to be an effective way to enhance RGS protein function.
136                                Specifically, RGS proteins function as GTPase accelerating proteins (G
137     Recent findings have established that R7 RGS proteins function as macromolecular complexes with t
138 t is unclear which of the more than 20 known RGS proteins function to negatively regulate and thereby
139                  In this study, we show that RGS protein/Galphai2 interactions are essential for norm
140 ai2 (G184S/G184S) mutation that disables all RGS protein/Galphai2 interactions exhibit an unexpectedl
141                 Although the R4 subfamily of RGS proteins generally accepts both Galphai/o and Galpha
142                             Therefore, while RGS proteins generally act to downregulate signaling, lo
143                                      Several RGS proteins have a multidomain architecture that adds f
144                       In a cellular context, RGS proteins have also been shown to speed up the onset
145                                      Several RGS proteins have been implicated in the cardiac remodel
146 , while G-proteins are widespread in plants, RGS proteins have been reported to be missing from the e
147                                 A variety of RGS proteins have been reported to modulate opioid recep
148                                    In vitro, RGS proteins have been shown to inhibit signaling by ago
149                                         Many RGS proteins have GAP-independent functions that influen
150                                      Several RGS proteins have reduced expression or function in path
151 ctions between activated Galpha subunits and RGS proteins have yielded a substantial number of inhibi
152 Endogenous regulator of G-protein signaling (RGS) proteins have been implicated as key inhibitors of
153 ears ago, regulators of G protein-signaling (RGS) proteins have received considerable attention as po
154 thway-selective manner, and (3) suggest that RGS proteins help to prevent unwarranted platelet activa
155        These results reveal the existence of RGS protein homo-oligomers and show regulation of their
156                   Analysis of phosphorylated RGS protein identifies specific amino acids that, when p
157 ering promotes downregulation by placing the RGS protein in proximity to its substrate (receptor-acti
158 o downregulate signaling, loss of a specific RGS protein in sensory neurons can lead to defective res
159 These findings highlight the central role of RGS proteins in [Ca(2+)](i) oscillations and reveal a pr
160  an essential role for modulatory actions of RGS proteins in adult cerebellum.
161 ese findings establish an essential role for RGS proteins in B cell chemoattractant signaling and for
162                Our analysis of endogenous R7 RGS proteins in C. elegans neurons reveals key differenc
163 5 that selectively destabilize one of the R7 RGS proteins in Caenorhabditis elegans.
164 little is known about the role of endogenous RGS proteins in cardiac function.
165 were used to evaluate the role of endogenous RGS proteins in chronotropic regulation.
166 cate that the level and functional status of RGS proteins in DCs significantly impact their response
167          To determine the role of endogenous RGS proteins in functional responses to mu-opioid agonis
168 evidence has revealed key roles for specific RGS proteins in multiple signaling pathways at neuronal
169               However, whether endogenous R7 RGS proteins in neurons require R7BP or membrane localiz
170 ervations (1) demonstrate an active role for RGS proteins in regulating platelet responsiveness, (2)
171 enes (rgsA, rgsB and rgsC) encoding putative RGS proteins in the genome of Aspergillus nidulans.
172                                       Mutant RGS proteins in which the conserved Cys-2 residue could
173 he role of regulator of G protein signaling (RGS) proteins in the modulation of these pathways in hum
174                                              Rgs proteins inhibit the release of digestive enzymes ev
175            Regulator of G protein signaling (RGS) proteins inhibit G protein signaling by activating
176 uld be useful in screening for and analyzing RGS protein inhibitory compounds.
177                                              RGS proteins interact with, and affect the activity of,
178            Regulator of G protein signaling (RGS) proteins interact with activated Galpha subunits vi
179 or screening for modulators of the G protein-RGS protein interaction by assaying the amount of produc
180               Identification of the specific RGS proteins involved might permit their consideration a
181 s of SSRIs, but the identity of the specific RGS proteins involved remains unknown.
182               The characteristic hallmark of RGS proteins is a conserved approximately 120-aa RGS reg
183 identified that the binding site for R7BP in RGS proteins is formed by pairing of the DEP (Disheveled
184   The relevance of these mechanisms to other RGS proteins is not fully understood.
185 ly of the regulators of G protein signaling (RGS) proteins is represented by four members broadly exp
186 , the first biochemical function ascribed to RGS proteins, is sufficient to explain the activation ki
187 ident than the phenotype seen for individual RGS protein knockouts.
188                               Alterations in RGS protein levels, in particular RGS2 and RGS4, produce
189                                              RGS proteins limit the duration that Galphai subunits re
190 After injury, the complex gradually releases RGS proteins, limiting platelet activation and providing
191   These data provide the first evidence that RGS proteins may be important modulators of cancer risk
192 ent evidence has raised the possibility that RGS proteins may interact directly with G-protein-couple
193 uggest that drug discovery efforts targeting RGS proteins may represent a novel mechanism to manipula
194 ized that regulators of G protein signaling (RGS) proteins may be involved.
195                               Alternatively, RGS proteins might also have a direct role in regulating
196 on that Galpha(i) subunits remain GTP bound, RGS proteins modulate chemoattractant receptor signaling
197                       This study reveals how RGS proteins modulate Galphai2 signaling to facilitate t
198         Despite many investigations, whether RGS proteins modulate GIRK activity in neurons by mechan
199               Recent reports have shown that RGS proteins modulate neuronal, cardiovascular, and lymp
200 In the striatum, members of the R7 family of RGS proteins modulate signaling via D2 dopamine and mu-o
201            Regulator of G protein signaling (RGS) proteins modulate G protein signaling by acting as
202            Regulator of G protein signaling (RGS) proteins modulate G protein-coupled receptor (GPCR)
203 fects caused by deletion of flbA encoding an RGS protein negatively controlling FadA-mediated vegetat
204                                              RGS proteins negatively regulate heterotrimeric G protei
205 izes with regulators of G protein signaling (RGS) proteins of the R7 family instead of Ggamma.
206           Regulators of G protein signaling (RGS) proteins of the R7 subfamily limit signaling by neu
207 ane and facilitating Gi/o deactivation by R7 RGS proteins on GIRK channels.
208 aling pathways and the profound influence of RGS proteins on these pathways, RGS proteins are regulat
209  truncated regulator of G protein signaling (RGS) protein or a Gbetagamma-sequestering domain to a se
210 t for the adaptive coevolution of the Galpha:RGS protein pair based on single amino acid substitution
211       At present, it remains unknown whether RGS proteins play a role in regulating insulin release.
212            Regulator of G-protein-signaling (RGS) proteins play a key role in the regulation of G-pro
213            Regulator of G protein signaling (RGS) proteins play essential roles in the regulation of
214 al mushrooms show LSEs of Galphas but not of RGS proteins pointing to the probable differentiation of
215                             Thus, endogenous RGS proteins potently reduce the actions of Galpha(i/o)-
216 m that almost completely inhibits the Galpha-RGS protein-protein interaction.
217 20-residue RGS homology domain or "RGS box." RGS proteins regulate signaling via G protein-coupled re
218              Animals rendered insensitive to RGS protein regulation through a mutation in G(alpha)i2
219 ignal transduction, but the in vivo roles of RGS proteins remain poorly defined.
220 iological functions of Gbeta5-S and other R7 RGS proteins remain unclear.
221  in vitro, but the physiological function of RGS proteins remains poorly defined in part because of f
222 neficial effects of serotonin, inhibition of RGS proteins represents a therapeutic approach for the t
223  encodes a regulator of G protein signaling (RGS) protein, restores chemosensation in Ce-grk-2 mutant
224                Lower or higher expression of RGS proteins results in fewer or more nodules, respectiv
225                        However, unlike other RGS proteins, RGS14 also contains a G protein regulatory
226 e show that unique among the known mammalian RGS proteins, RGS14 localizes in centrosomes.
227  specificity, and expression of R4 subfamily RGS proteins (RGS2, -3, -4, -5, and -8).
228  highlight the current knowledge of specific RGS proteins (RGS2, RGS4, RGS7, RGS9-2, and RGS14) that
229                        In contrast, only one RGS protein, RGS2, is known to be selective for Galphaq/
230 ecrease in RGS2 (but not other major cardiac RGS proteins (RGS3-RGS5)) that occurs prior to hypertrop
231 e regulators of G protein-coupled signaling (RGS) proteins RGS4 and RGS5.
232                             The R7 family of RGS proteins (RGS6, -7, -9, -11) is characterized by the
233 R7 family regulators of G protein signaling (RGS) proteins (RGS6, RGS7, RGS9, and RGS11) instead of G
234 ntains two Regulator of G-protein Signaling (RGS) proteins RGS7 and RGS11 that directly act on Go and
235              In neurons of the striatum, two RGS proteins, RGS7 and RGS9-2, regulate signaling by mu-
236 ruits the regulators of G-protein signaling (RGS) proteins, RGS7 and RGS11, to the dendritic tips of
237  conditions two equally abundant striatal R7 RGS proteins, RGS9-2 and RGS7, are unequally coupled to
238  loops of GPCRs selectively recruit specific RGS protein(s) via their N termini to regulate the linke
239 live cells, members of the B/R4 subfamily of RGS proteins selectively modulate G protein signaling de
240 ence that regulators of G-protein signaling (RGS) proteins serve this role in platelets, using mice w
241                                          All RGS proteins share a common RGS domain that interacts wi
242                                       Hence, RGS proteins should be considered multifunctional signal
243           Regulators of G protein signaling (RGS proteins) speed the turn-off of G protein signals an
244                                    The yeast RGS protein Sst2 is regulated at both the transcriptiona
245                            We found that the RGS protein Sst2 limits variability in transcription and
246        The regulator of G protein signaling (RGS) protein Sst2 acts by accelerating GTP hydrolysis an
247  the yeast regulator of G protein signaling (RGS) protein Sst2 and demonstrate that the DEP domains i
248                                              RGS proteins stimulate the deactivation of heterotrimeri
249  of the R7 regulator of G-protein signaling (RGS) protein subfamily are versatile regulators of G-pro
250 midbrain expression and trafficking of other RGS proteins such as RGS4 and RGS8.
251  and does not overlap with that used to bind RGS proteins such as RGS4.
252       The regulators of G protein signaling (RGS) protein superfamily negatively controls G protein-c
253 RK2 and p63RhoGEF respond similarly to these RGS proteins supports the hypothesis that GRK2 is a bona
254  NRB bind all members of the R4 subfamily of RGS proteins tested (RGS1, RGS2, RGS4, RGS16) and GAIP.
255                                   RGS2 is an RGS protein that shows preference toward Galpha(q).To be
256 , a palmitoylated allosteric modulator of R7 RGS proteins that accelerate deactivation of Gi/o class
257                                      Several RGS proteins that can act as negative regulators of G pr
258  understanding of the molecular diversity of RGS proteins that control MOR signaling, their circuit s
259               RGS7 belongs to a subfamily of RGS proteins that exist as dimers with the G protein bet
260 GS7 and RGS9-2 belong to the R7 subfamily of RGS proteins that form macromolecular complexes with R7-
261 as well as regulator of G protein signaling (RGS) proteins that contain a Ggamma-like subdomain.
262 rolled by regulators of G protein signaling (RGS) proteins that shape the duration and extent of the
263                        However, unlike other RGS proteins, that of axin (axinRGS) does not affect int
264           Regulators of G-protein signaling (RGS) proteins, through their GTPase activating protein (
265 EP domain in mediating the interaction of an RGS protein to the C-terminal tail of a GPCR, thus placi
266 yses and homology modeling of the Galpha and RGS proteins to address their expansion and its potentia
267 ing that RGS2 arose from the R4-subfamily of RGS proteins to have specialized activity as a potent an
268 brane anchoring subunit or further modulates RGS proteins to increase their GAP activity.
269 we examine whether GPCRs selectively recruit RGS proteins to modulate linked G protein signaling.
270 ings point to a critical role for endogenous RGS proteins to suppress the antidepressant-like effects
271 s to evaluate the contribution of endogenous RGS proteins to the antinociceptive effects of morphine
272                                 R7BP targets RGS proteins to the plasma membrane and augments their G
273 ns, and palmitoylation of R7BP can target R7 RGS proteins to the plasma membrane in cultured cells.
274 ility of a regulator of G protein signaling (RGS) protein to suppress noise.
275 ain GTP bound, and the loss of an individual RGS protein typically enhances chemokine receptor signal
276 n of gene transcription, can be regulated by RGS proteins via both allosteric and GAP mechanisms.
277            Stimulation of GTPase activity by RGS proteins was inhibited 38-81% by 40 mum YJ34, a prev
278 leic acid downregulation of IKACh-inhibiting RGS proteins was present at 16 weeks.
279 ion-based adaptive coevolution of the Galpha:RGS proteins was proposed to enable the loss of RGS in m
280  of these regulators of G protein signaling (RGS) proteins was perturbed either by hypoxia or in cell
281                                      Several RGS proteins were expressed in mast cells including RGS1
282 R7 family regulators of G protein signaling (RGS) proteins when purified from tissues.
283 (GAPs), both phospholipase C (PLC)-betas and RGS proteins, when assayed in solution under single turn
284  heterotrimeric G-protein-coupled receptors, RGS proteins, which act as GTPase-activating proteins fo
285 ne nucleotide exchange factors (GEFs) and by RGS proteins, which act as guanosine triphosphatase (GTP
286 ) is a member of a family of proteins called RGS proteins, which function as GTPase-activating protei
287 ve NFR1 receptors phosphorylate and activate RGS proteins, which help maintain the Galpha proteins in
288 ns and the regulator of G-protein signaling (RGS) proteins, which accelerate the inherent GTPase acti
289 ) bound by regulator of G-protein signaling (RGS) proteins, which function as GTPase-activating prote
290            Regulator of G protein signaling (RGS) proteins, which function to inactivate G proteins,
291 ped by the regulator of G protein signaling (RGS) proteins, which promote G protein deactivation.
292 Rgs6(-/-) mice is attributable to another R7 RGS protein whose influence on M2R-IKACh signaling is ma
293                  They show selectivity among RGS proteins with a potency order of RGS 4 > 19 = 16 > 8
294      The soybean genome encodes two chimeric RGS proteins with an N-terminal seven transmembrane doma
295 g 9-1 (RGS9-1) and RGS9-2 are highly related RGS proteins with distinctive C termini arising from alt
296           We propose that the interaction of RGS proteins with orphan GPCRs promotes signaling select
297 se findings argue that the association of R7 RGS proteins with the membrane environment provides a ma
298 mplexes of regulator of G-protein signaling (RGS) proteins with G-protein beta5 (Gbeta5) subunits are
299 regulation, and functional role of canonical RGS proteins, with a special focus on the healthy heart
300 At neuronal synapses, GPCRs, G proteins, and RGS proteins work in coordination to regulate key aspect

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