ライフサイエンスコーパス: RGS protein

1 known as regulators of G protein signaling (RGS proteins).

2 Pases in the intracellular trafficking of an RGS protein.

3 one Galpha, one Gbeta, three Ggamma, and one RGS protein.

4 t reversible small-molecule inhibitors of an RGS protein.

5 ied the first small-molecule inhibitor of an RGS protein.

6 urface expression and through recruitment of RGS proteins.

7 the Galpha subunit, a reaction catalyzed by RGS proteins.

8 Rs (MOR and D2R) on the G protein bias of R7 RGS proteins.

9 g G protein and GPCR selectivity of striatal RGS proteins.

10 ervous system, is mediated exclusively by R7 RGS proteins.

11 maintaining proteolytic stability of the R7 RGS proteins.

12 ctivity, to mimic in cis the GAP function of RGS proteins.

13 ise from the consensus GoLoco motif found in RGS proteins.

14 terization of cancer-associated mutations in RGS proteins.

15 face between Gbeta5 and the N terminus of R7 RGS proteins.

16 lated to differential protein dynamics among RGS proteins.

17 d pathway under strong inhibitory control by RGS proteins.

18 the extent of inhibition by the R4 family of RGS proteins.

19 subfamilies consisting of over 20 different RGS proteins.

20 f Galpha12, a behavior consistent with other RGS proteins.

21 cs and inhibitor potency for three different RGS proteins.

22 olecule inhibitors targeting a subset of the RGS proteins.

23 rotein cycle is regulated by the activity of RGS proteins.

24 s, and the REGULATOR OF G-PROTEIN SIGNALING (RGS) protein.

25 amily of "regulator of G protein signaling" (RGS) proteins.

26 eract with regulator of G protein signaling (RGS) proteins.

27 ivity of "regulator of G-protein signaling" (RGS) proteins.

28 rolled by regulator of G protein signalling (RGS) proteins.

29 led by the regulator of G protein signaling (RGS) proteins.

30 led by the regulator of G-protein signaling (RGS) proteins.

31 Expression of RGS2, but not other RGS proteins, abolished androgen-independent AR activity

32 RGS proteins accelerate the intrinsic GTPase activity of

33 Regulator of G-protein signaling (RGS) proteins accelerate GTP hydrolysis by heterotrimeri

34 Regulator of G protein signaling (RGS) proteins accelerate the endogenous GTPase activity

35 including nucleotide binding, intrinsic and RGS protein-accelerated GTP hydrolysis, and interactions

36 Regulators of G-protein signaling (RGS) proteins act directly on Galpha subunits to increas

37 Regulator of G protein signaling (RGS) proteins act to temporally modulate the activity of

38 enuated by regulator of G protein signaling (RGS) proteins acting as GTPase-activating proteins for G

39 d blunting of sensitivity also engendered by RGS protein action in trans.

40 Septin organization is dependent on RGS protein activity.

41 s there are concomitant, independent LSEs of RGS proteins along with an extraordinary diversification

42 Many RGS proteins also bind additional signaling partners tha

43 rotein is readily inactivated by its cognate RGS protein and forms a stable, GDP-bound, heterotrimeri

44 protein-coupled receptors, Galpha subunits, RGS proteins and downstream effectors in mammalian syste

45 We explore the role of RGS proteins and G alpha(i2) in the physiologic regulati

46 RGS proteins and G alpha(i2) signaling play important ro

47 RGS2 is a member of the R4 subfamily of RGS proteins and is unique in that it is selective for G

48 endrites by varying the concentration of key RGS proteins and measuring the impact on transmission of

49 provide a brief overview of the discovery of RGS proteins and of the gradual and continuing discovery

50 NFR1 interacts with RGS proteins and phosphorylates them.

51 he catalytic activity of all canonical human RGS proteins and their selectivity for a complete set of

52 at the spatiotemporal-specific expression of RGS proteins and their target components, as well as the

53 th Loco, a regulator of G-protein signaling (RGS) protein and a known effector of glia specification.

54 lso binds regulators of G protein signaling (RGS) proteins and the third intracellular loop (3iL) of

55 o still bind the N-terminal DEP domain of R7 RGS proteins, and mutant Gbeta5-R7 RGS complexes initial

56 nteract with all members of the R7 family of RGS proteins, and palmitoylation of R7BP can target R7 R

57 rs involved in ACD, including GoLoco motifs, RGS proteins, and RIC-8.

58 protein inactivation, which is modulated by RGS proteins, and the rate of G protein activation, whic

59 including Regulator of G protein Signaling (RGS) proteins, and has been implicated in membrane targe

60 ypothesize Regulator of G-Protein Signaling (RGS) proteins, and specifically RGS5, are endogenous rep

61 RGS proteins are best understood as negative regulators

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 R7 subfamily RGS proteins are stabilized by the G-protein subunit Gbe

66 RGS proteins are subject to posttranslational modificati

67 Our results show that RGS proteins are widely distributed in the monocot linea

68 Regulator of G-protein signaling (RGS) proteins are a family of molecules that control the

69 Regulator of G-protein signaling (RGS) proteins are an integral part of the G-protein netw

70 Regulator of G-protein signaling (RGS) proteins are critical modulators of GPCR activity,

71 Regulators of G protein signaling (RGS) proteins are critical modulators of GPCR signaling

72 Regulators of G protein signaling (RGS) proteins are emerging as potentially important drug

73 Regulators of G-protein signaling (RGS) proteins are important components of signal transdu

74 The regulator of G-protein signaling (RGS) proteins are key interactors and critical modulator

75 Regulator of G protein signaling (RGS) proteins are multifunctional proteins expressed in

76 Regulator of G protein signaling (RGS) proteins are negative modulators of G protein signa

77 Regulator of G protein signaling (RGS) proteins are negative regulators of G protein-coupl

78 Regulator of G protein signaling (RGS) proteins are negative regulators of signal transduc

79 Regulator of G-protein signaling (RGS) proteins are potent inhibitors of heterotrimeric G-

80 Regulators of G protein signaling (RGS) proteins are potent negative modulators of G protei

81 Regulator of G protein signaling (RGS) proteins are signal transduction modulators, expres

82 Regulator of G protein signaling (RGS) proteins are united into a family by the presence o

83 Regulators of G protein signaling (RGSs, or RGS proteins) are responsible for the subsecond turn off

84 Our results strongly support a role for RGS proteins as negative regulators of opioid supraspina

85 indings reveal a hitherto overlooked role of RGS proteins as noise suppressors and demonstrate an abi

86 nd also reveal a potential novel function of RGS proteins as positive regulators of opioid spinal ant

87 entify RGS6, a member of the R7 subfamily of RGS proteins, as a key regulator of GABA(B)R signaling i

88 f these small-molecule inhibitors against 12 RGS proteins, as well as against the cysteine-null mutan

89 Regulators of G-protein signaling (RGS proteins) belong to a diverse protein family that wa

90 Specifically, RGS proteins bind to activated Galpha subunits in G-prot

91 Members of the RZ subfamily of RGS proteins bind to activated Galpha(o), Galpha(z), and

92 cytes with a Galphai2 mutation that disables RGS protein binding accumulated in the perivascular chan

93 alpha(i2) with a G184S mutation that blocks RGS protein binding and GTPase acceleration.

94 Additionally, KB-1753 interferes with RGS protein binding and resultant GAP activity.

95 The RGS7 (R7) family of RGS proteins bound to the divergent Gbeta subunit Gbeta5

96 GTPase-accelerating protein activity of the RGS protein by using small molecules.

97 , we reveal these differences in dynamics of RGS proteins by partitioning the protein structural spac

98 uss a rationale for therapeutic targeting of RGS proteins by regulation of expression or allosteric m

99 RGS proteins can be regulated by altering their GAP acti

100 Although RGS proteins canonically function as G-protein regulator

101 , to learn whether the loss of some of these RGS proteins causes the absence of the ERG b-wave.

102 Regulator of G-protein signaling (RGS) proteins classically function as negative modulator

103 All four R7 RGS proteins co-precipitate with R7BP from brain extract

104 With hundreds of GPCRs and dozens of RGS proteins, compartmentalization plays a key role in e

105 we highlight the diverse mechanisms by which RGS protein complexes control plasticity in response to

106 annel assembly with allosterically regulated RGS protein complexes, which provide a target for modula

107 e are key to controlling the stability of R7 RGS protein complexes.

108 family of regulators of G protein signaling (RGS) proteins, comprising RGS6, RGS7, RGS9, and RGS11, r

109 For example, members of the R7 family of RGS proteins contain a DEP, GGL, and novel DHEX domain a

110 However, many RGS proteins contain additional domains that serve other

111 which is responsible for GAP activity, most RGS proteins contain other distinct structural motifs.

112 R7 RGS proteins contain several distinct domains and form o

113 y a role in pathophysiological processes and RGS proteins could represent novel cardiovascular therap

114 r homolog Ste3alpha, Gbeta subunit Gpb1, and RGS protein Crg1.

115 In a previous study, we identified the RGS protein Crg2 involved in regulating the pheromone re

116 The R7 subfamily of RGS proteins critically regulates neuronal G protein-sig

117 However, RGS proteins differ widely in size and the organization

118 RGS proteins display remarkable selectivity and specific

119 to cholinergic stimulation, possibly due to RGS protein downregulation.

120 at loss of RSBP-1 phenocopies loss of the R7 RGS protein EAT-16, but does not disrupt function of the

121 does not disrupt function of the related R7 RGS protein EGL-10.

122 Neutrophil RGS proteins establish a threshold for Galpha(i) activat

123 RGS proteins exert their effect by directly binding to t

124 CCG-4986, lack of inhibition indicates that RGS proteins exhibit fundamental differences in their re

125 s and that RGS4 was by far the most abundant RGS protein expressed by these cells.

126 se and heart rate regulation, and changes in RGS protein expression and/or function are believed to p

127 "Regulator of G-protein signaling" (RGS) proteins facilitate the termination of G protein-co

128 The mammalian RGS protein family has more than 20 members and they sha

129 etics, the regulator of G-protein signaling (RGS) protein family modulates the timing of GIRK activit

130 of the R7 regulators of G protein signaling (RGS) protein family of neuronal RGS, is a critical regul

131 ber of the Regulator of G protein Signaling (RGS) protein family, as a nuclear factor that suppresses

132 ber of the regulator of G protein signaling (RGS) protein family.

133 ongly suggests a causal relationship between RGS protein flexibility and covalent inhibitor potency.

134 r Galpha(i)G203A), as well as GRK2NT-GFP (an RGS protein for G(q/11)) but neither p115RhoGEFRGS-GFP (

135 ich has the largest complement of Galpha and RGS proteins for any eukaryote, provides new insights in

136 of the regulators of G-protein signaling (R7 RGS) proteins form multi-subunit complexes that play cru

137 Most studies searching for modulators of RGS protein function have been focused on inhibiting the

138 ors have been identified; however, enhancing RGS protein function is often more clinically desirable

139 may prove to be an effective way to enhance RGS protein function.

140 Recent findings have established that R7 RGS proteins function as macromolecular complexes with t

141 t is unclear which of the more than 20 known RGS proteins function to negatively regulate and thereby

142 In this study, we show that RGS protein/Galphai2 interactions are essential for norm

143 ai2 (G184S/G184S) mutation that disables all RGS protein/Galphai2 interactions exhibit an unexpectedl

144 Although the R4 subfamily of RGS proteins generally accepts both Galphai/o and Galpha

145 Therefore, while RGS proteins generally act to downregulate signaling, lo

146 Several RGS proteins have a multidomain architecture that adds f

147 In a cellular context, RGS proteins have also been shown to speed up the onset

148 Several RGS proteins have been implicated in the cardiac remodel

149 , while G-proteins are widespread in plants, RGS proteins have been reported to be missing from the e

150 A variety of RGS proteins have been reported to modulate opioid recep

151 In vitro, RGS proteins have been shown to inhibit signaling by ago

152 targeting conserved cysteine residues among RGS proteins have emerged as potential candidates to inh

153 Several RGS proteins have reduced expression or function in path

154 ctions between activated Galpha subunits and RGS proteins have yielded a substantial number of inhibi

155 Endogenous regulator of G-protein signaling (RGS) proteins have been implicated as key inhibitors of

156 y, several regulator of G protein signaling (RGS) proteins have emerged as critical modulators of PD

157 mid-1990s, regulator of G protein signaling (RGS) proteins have emerged as key regulators of signalin

158 ears ago, regulators of G protein-signaling (RGS) proteins have received considerable attention as po

159 thway-selective manner, and (3) suggest that RGS proteins help to prevent unwarranted platelet activa

160 These results reveal the existence of RGS protein homo-oligomers and show regulation of their

161 Analysis of phosphorylated RGS protein identifies specific amino acids that, when p

162 ering promotes downregulation by placing the RGS protein in proximity to its substrate (receptor-acti

163 o downregulate signaling, loss of a specific RGS protein in sensory neurons can lead to defective res

164 nd signal transduction pathways regulated by RGS proteins in addiction and analgesia circuits.

165 an essential role for modulatory actions of RGS proteins in adult cerebellum.

166 ese findings establish an essential role for RGS proteins in B cell chemoattractant signaling and for

167 Our analysis of endogenous R7 RGS proteins in C. elegans neurons reveals key differenc

168 5 that selectively destabilize one of the R7 RGS proteins in Caenorhabditis elegans.

169 little is known about the role of endogenous RGS proteins in cardiac function.

170 were used to evaluate the role of endogenous RGS proteins in chronotropic regulation.

171 To determine the role of endogenous RGS proteins in functional responses to mu-opioid agonis

172 The 2 most abundant RGS proteins in human and mouse platelets are RGS10 and

173 g findings on the regulation and function of RGS proteins in models of analgesia and addiction.

174 ss reports on the regulation and function of RGS proteins in models of psychostimulant addiction.

175 evidence has revealed key roles for specific RGS proteins in multiple signaling pathways at neuronal

176 However, whether endogenous R7 RGS proteins in neurons require R7BP or membrane localiz

177 ervations (1) demonstrate an active role for RGS proteins in regulating platelet responsiveness, (2)

178 he role of regulator of G protein signaling (RGS) proteins in the modulation of these pathways in hum

179 Selective inhibition of RGS proteins increases G-protein activity and may provid

180 By contrast, Rgs proteins inhibit Gi/q-coupled GPCRs to negatively re

181 Rgs proteins inhibit the release of digestive enzymes ev

182 Regulator of G protein signaling (RGS) proteins inhibit G protein signaling by activating

183 Several small molecule RGS protein inhibitors have been identified; however, en

184 RGS proteins interact with, and affect the activity of,

185 Regulator of G protein signaling (RGS) proteins interact with activated Galpha subunits vi

186 or screening for modulators of the G protein-RGS protein interaction by assaying the amount of produc

187 Identification of the specific RGS proteins involved might permit their consideration a

188 s of SSRIs, but the identity of the specific RGS proteins involved remains unknown.

189 The characteristic hallmark of RGS proteins is a conserved approximately 120-aa RGS reg

190 identified that the binding site for R7BP in RGS proteins is formed by pairing of the DEP (Disheveled

191 The relevance of these mechanisms to other RGS proteins is not fully understood.

192 , the first biochemical function ascribed to RGS proteins, is sufficient to explain the activation ki

193 ident than the phenotype seen for individual RGS protein knockouts.

194 RGS proteins limit the duration that Galphai subunits re

195 After injury, the complex gradually releases RGS proteins, limiting platelet activation and providing

196 In contrast to other RGS proteins, little is known about RZ subfamily structu

197 ent evidence has raised the possibility that RGS proteins may interact directly with G-protein-couple

198 ized that regulators of G protein signaling (RGS) proteins may be involved.

199 Alternatively, RGS proteins might also have a direct role in regulating

200 on that Galpha(i) subunits remain GTP bound, RGS proteins modulate chemoattractant receptor signaling

201 ummarize findings on the mechanisms by which RGS proteins modulate functional responses to opioids in

202 This study reveals how RGS proteins modulate Galphai2 signaling to facilitate t

203 Despite many investigations, whether RGS proteins modulate GIRK activity in neurons by mechan

204 In the striatum, members of the R7 family of RGS proteins modulate signaling via D2 dopamine and mu-o

205 ation has emerged on the mechanisms by which RGS proteins modulate the efficacy of opioid analgesics

206 Regulator of G protein signaling (RGS) proteins modulate G protein-coupled receptor (GPCR)

207 Regulators of G-protein signaling (RGS) proteins modulate receptor signaling by binding to

208 r findings reveal that a sizable fraction of RGS protein mutations leads to a loss of function throug

209 izes with regulators of G protein signaling (RGS) proteins of the R7 family instead of Ggamma.

210 Regulators of G protein signaling (RGS) proteins of the R7 subfamily limit signaling by neu

211 ane and facilitating Gi/o deactivation by R7 RGS proteins on GIRK channels.

212 truncated regulator of G protein signaling (RGS) protein or a Gbetagamma-sequestering domain to a se

213 t for the adaptive coevolution of the Galpha:RGS protein pair based on single amino acid substitution

214 At present, it remains unknown whether RGS proteins play a role in regulating insulin release.

215 Regulators of G-protein signaling (RGS) proteins play a central role in modulating signalin

216 Regulator of G-protein-signaling (RGS) proteins play a key role in the regulation of G-pro

217 Regulator of G protein signaling (RGS) proteins play essential roles in the regulation of

218 al mushrooms show LSEs of Galphas but not of RGS proteins pointing to the probable differentiation of

219 Thus, endogenous RGS proteins potently reduce the actions of Galpha(i/o)-

220 RGS proteins primarily act as GTPase accelerators for ac

221 m that almost completely inhibits the Galpha-RGS protein-protein interaction.

222 20-residue RGS homology domain or "RGS box." RGS proteins regulate signaling via G protein-coupled re

223 Animals rendered insensitive to RGS protein regulation through a mutation in G(alpha)i2

224 ignal transduction, but the in vivo roles of RGS proteins remain poorly defined.

225 iological functions of Gbeta5-S and other R7 RGS proteins remain unclear.

226 in vitro, but the physiological function of RGS proteins remains poorly defined in part because of f

227 Accordingly, these RGS proteins represent novel therapeutic targets for the

228 As such, RGS proteins represent novel therapeutic targets in PD.

229 Regulator of G protein signaling (RGS) proteins represent an exciting class of novel drug

230 neficial effects of serotonin, inhibition of RGS proteins represents a therapeutic approach for the t

231 Lower or higher expression of RGS proteins results in fewer or more nodules, respectiv

232 However, unlike other RGS proteins, RGS14 also contains a G protein regulatory

233 specificity, and expression of R4 subfamily RGS proteins (RGS2, -3, -4, -5, and -8).

234 highlight the current knowledge of specific RGS proteins (RGS2, RGS4, RGS7, RGS9-2, and RGS14) that

235 In contrast, only one RGS protein, RGS2, is known to be selective for Galphaq/

236 Among the over 20 known RGS proteins, RGS2 has received increasing interest as a

237 e regulators of G protein-coupled signaling (RGS) proteins RGS4 and RGS5.

238 The R7 family of RGS proteins (RGS6, -7, -9, -11) is characterized by the

239 R7 family regulators of G protein signaling (RGS) proteins (RGS6, RGS7, RGS9, and RGS11) instead of G

240 ntains two Regulator of G-protein Signaling (RGS) proteins RGS7 and RGS11 that directly act on Go and

241 In neurons of the striatum, two RGS proteins, RGS7 and RGS9-2, regulate signaling by mu-

242 ruits the regulators of G-protein signaling (RGS) proteins, RGS7 and RGS11, to the dendritic tips of

243 conditions two equally abundant striatal R7 RGS proteins, RGS9-2 and RGS7, are unequally coupled to

244 ence that regulators of G-protein signaling (RGS) proteins serve this role in platelets, using mice w

245 All RGS proteins share a common RGS domain that interacts wi

246 Regulators of G protein signaling (RGS proteins) speed the turn-off of G protein signals an

247 The yeast RGS protein Sst2 is regulated at both the transcriptiona

248 We found that the RGS protein Sst2 limits variability in transcription and

249 The regulator of G protein signaling (RGS) protein Sst2 acts by accelerating GTP hydrolysis an

250 the yeast regulator of G protein signaling (RGS) protein Sst2 and demonstrate that the DEP domains i

251 RGS proteins stimulate the deactivation of heterotrimeri

252 of the R7 regulator of G-protein signaling (RGS) protein subfamily are versatile regulators of G-pro

253 midbrain expression and trafficking of other RGS proteins such as RGS4 and RGS8.

254 The regulators of G protein signaling (RGS) protein superfamily negatively controls G protein-c

255 RK2 and p63RhoGEF respond similarly to these RGS proteins supports the hypothesis that GRK2 is a bona

256 NRB bind all members of the R4 subfamily of RGS proteins tested (RGS1, RGS2, RGS4, RGS16) and GAIP.

257 , a palmitoylated allosteric modulator of R7 RGS proteins that accelerate deactivation of Gi/o class

258 Several RGS proteins that can act as negative regulators of G pr

259 understanding of the molecular diversity of RGS proteins that control MOR signaling, their circuit s

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 ded by the regulator of G protein signaling (RGS) proteins that deactivate G protein alpha subunits (

263 rolled by regulators of G protein signaling (RGS) proteins that shape the duration and extent of the

264 However, unlike other RGS proteins, that of axin (axinRGS) does not affect int

265 Regulators of G-protein signaling (RGS) proteins, through their GTPase activating protein (

266 EP domain in mediating the interaction of an RGS protein to the C-terminal tail of a GPCR, thus placi

267 yses and homology modeling of the Galpha and RGS proteins to address their expansion and its potentia

268 ing that RGS2 arose from the R4-subfamily of RGS proteins to have specialized activity as a potent an

269 brane anchoring subunit or further modulates RGS proteins to increase their GAP activity.

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 leic acid downregulation of IKACh-inhibiting RGS proteins was present at 16 weeks.

278 ion-based adaptive coevolution of the Galpha:RGS proteins was proposed to enable the loss of RGS in m

279 rs bind to conserved cysteine residues among RGS proteins, we have previously suggested [J. Am.

280 Several RGS proteins were expressed in mast cells including RGS1

281 These regulators of G-protein signaling (RGS) proteins were viewed by many as nodes downstream of

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 Regulator of G protein signaling (RGS) proteins, whether primarily expressed in SNc DA neu

285 ) is a member of a family of proteins called RGS proteins, which function as GTPase-activating protei

286 ve NFR1 receptors phosphorylate and activate RGS proteins, which help maintain the Galpha proteins in

287 ns and the regulator of G-protein signaling (RGS) proteins, which accelerate the inherent GTPase acti

288 ) bound by regulator of G-protein signaling (RGS) proteins, which function as GTPase-activating prote

289 Regulator of G protein signaling (RGS) proteins, which function to inactivate G proteins,

290 ped by the regulator of G protein signaling (RGS) proteins, which promote G protein deactivation.

291 Rgs6(-/-) mice is attributable to another R7 RGS protein whose influence on M2R-IKACh signaling is ma

292 They show selectivity among RGS proteins with a potency order of RGS 4 > 19 = 16 > 8

293 The soybean genome encodes two chimeric RGS proteins with an N-terminal seven transmembrane doma

294 vity, and provide principles for engineering RGS proteins with defined selectivity.

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