ライフサイエンスコーパス: Galphaq

1 amily member, was determined in complex with Galphaq.

2 iosensors, we demonstrate that H1R activates Galphaq.

3 ctivation requires allosteric activation via Galphaq.

4 ood pressure by decreasing signaling through Galphaq.

5 upt association with active Galpha13 but not Galphaq.

6 GTPase accelerating protein activity toward Galphaq.

7 eased during transgenic expression of mutant Galphaq.

8 tream target of the heterotrimeric G protein Galphaq.

9 s heart failure induced by overexpression of Galphaq.

10 GTPase accelerating protein activity toward Galphaq.

11 etion that was dependent on BBS-induced GPCR/Galphaq-(1)(2)/(1)(3)/Rho mediated activation of nuclear

12 the Hippo tumor suppressor pathway, via the Galphaq-11, PLCbeta/PKC, and Rho/ROCK signaling pathways

13 amygdala of fear-naive mice PAR1 couples to Galphaq/11 and Galphao proteins, while after fear condit

14 n adaptor/scaffold assembling CD3varepsilon, Galphaq/11 and PLCbeta3 into a complex that activates PL

15 mmunoprecipitation studies show that PECAM-1.Galphaq/11 binding is dramatically decreased by competit

16 duction, but not the regulated splicing, was Galphaq/11 dependent.

17 Galphaq/11 has an impact on LFA-1 expression at plasma m

18 A11, two highly homologous alpha subunits of Galphaq/11 heterotrimeric G proteins, and in PLCB4 (phos

19 Upstream, MCP1 activates CCR2 and Galphaq/11 in a time-dependent manner, and down-regulati

20 tory and complementary roles of Galpha12 and Galphaq/11 in basal vs evoked EC vWF secretion may provi

21 e findings, we hypothesized that ablation of Galphaq/11 in GnRH neurons would diminish but not comple

22 The nature of the PECAM-1.Galphaq/11 interaction is still unclear although it is l

23 ation assay, we show that endogenous PECAM-1.Galphaq/11 interactions in endothelial cells are disrupt

24 In summary vesicle-associated Galphaq/11 is required for the turnover of LFA-1 adhesio

25 d receptors, which is blunted in endothelial Galphaq/11 KO mice.

26 ether, our results indicate that the PECAM-1.Galphaq/11 mechanosensitive complex contains an endogeno

27 gnaling bias among the Galphas, Galphai, and Galphaq/11 pathways.

28 l cells, 20-HETE binding to GPR75 stimulated Galphaq/11 protein dissociation and increased inositol p

29 lateral nucleus of the amygdala through two Galphaq/11 protein-coupled signaling pathways, activated

30 ent at the postsynaptic site, are coupled to Galphaq/11 proteins and display an excitatory response u

31 his study we show that the separate class of Galphaq/11 proteins is required for the underlying abili

32 show increases in GPCR-mediated Galphas and Galphaq/11 signaling, as the consequence of reduced GRK2

33 weeks of age in shGRK2 mice due to enhanced Galphaq/11 signaling.

34 roteins generally accepts both Galphai/o and Galphaq/11 subunits as substrates, the R7 and R12 subfam

35 otrimeric G protein subunits Galphaq and 11 (Galphaq/11) are junctional proteins that have been indep

36 ls, GPR75-20-HETE pairing is associated with Galphaq/11- and GPCR-kinase interacting protein-1-mediat

37 Additionally, activation of FFA2 with Galphaq/11-biased agonists substantially increased beta

38 d that it could couple to and signal via non-Galphaq/11-coupled pathways.

39 KP signals via KISS1R, a Galphaq/11-coupled receptor, and mice bearing a global d

40 While KISS1R is best understood as a Galphaq/11-coupled receptor, we previously demonstrated

41 and, more importantly, while it establishes Galphaq/11-coupled signaling as a major conduit of GnRH

42 it also uncovers a significant role for non-Galphaq/11-coupled signaling in potentiating reproductiv

43 sponsiveness to KP and gonadotropins reflect Galphaq/11-independent GnRH secretion and activation of

44 y block KP-triggered GnRH secretion and that Galphaq/11-independent GnRH secretion would be sufficien

45 l fibrillation from enhanced activity in the Galphaq/11-IP3 pathway, resulting in abnormal Ca(2+) rel

46 t DeltaNT activation of NFAT is dependent on Galphaq/11-mediated or beta-arrestin-mediated signaling

47 ors that signal through both Galpha12/13 and Galphaq/11.

48 protein, RGS2, is known to be selective for Galphaq/11.

49 s, the R7 and R12 subfamilies select against Galphaq/11.

50 ly competed with effectors for engagement of Galphaq A representative peptide was specific for active

51 es in the signaling pathway of the G protein Galphaq, a protein that is essential for animal life and

52 We show that Galphaq activates FAK through TRIO-RhoA non-canonical Ga

53 fic desensitization, evident at the level of Galphaq activation, phosphatidylinositol 4,5-bisphosphat

54 Our results suggest that Galphaq activity is not involved in S1P-mediated regulat

55 arkable similarity between the effect of the Galphaq agonist and that of mechanical forces on cardiac

56 tive AVA firing and reversals require EGL-30/Galphaq, an mGluR5 effector.

57 CAM-1) and heterotrimeric G protein subunits Galphaq and 11 (Galphaq/11) are junctional proteins that

58 dent signal decrease mediated by blocking of Galphaq and 2) a mechanism involving phosphorylation of

59 Furthermore, MASS1 interacts with Galphas/Galphaq and activates PKA and PKC in response to extrace

60 elopmentally regulated genes associated with Galphaq and Ca(2+) signaling.

61 ase persists in mutants deficient for egl-30 Galphaq and egl-8 PLCbeta and requires DAG binding to UN

62 is mediated by a presynaptic pathway (egl-30 Galphaq and egl-8 PLCbeta) that produces DAG, and by DAG

63 ly contributes to pathological activation of Galphaq and ErbB receptor-dependent pathways in the hear

64 bind ERK5 thus acting as a scaffold between Galphaq and ERK5 upon GPCR activation.

65 o GRPR stimulated Gli through its downstream Galphaq and Galpha(1)(2)/(1)(3) GTPases, and consistentl

66 By using cells null for Galphaq and Galpha(1)(2)/(1)(3), we demonstrate that the

67 )(2)/(1)(3) GTPases, and consistently, other Galphaq and Galpha(1)(3) coupled receptors (such as musc

68 ic mutations in the G protein alpha subunits Galphaq and Galpha11 (encoded by GNAQ and GNA11, respect

69 level which was blocked by the knockdown of Galphaq and Galpha12.

70 ive signaling pathways most likely involving Galphaq and Galphai to induce degranulation.

71 For example, TA inhibition requires Galphaq and Galphas signaling in the peptidergic ASI sen

72 ntly different, and the apparent affinity of Galphaq and Gbeta(1)gamma(1) to activated NTS1 increased

73 Furthermore, interactions between Galphaq and GRK2 were associated with a prolongation of

74 RANKL binding to LGR4 activates the Galphaq and GSK3-beta signaling pathway, an action that

75 by alpha7 nicotinic receptor activation of a Galphaq and IP3 receptor pathway.

76 soform is activated by the G-protein subunit Galphaq and is required for normal rates of locomotion;

77 protein constitutively activates endogenous Galphaq and is unresponsive to stimulation by leukotrien

78 e find similar and significant population of Galphaq and one of its receptors, bradykinin type 2 rece

79 results indicate that the mechanism by which Galphaq and PLC-beta3 mutually regulate each other is fa

80 nduced interactions between STIM1 and TRPC1, Galphaq and PLCbeta1, which required STIM1 and TRPC1.

81 ivity and associations between TRPC1, STIM1, Galphaq and PLCbeta1, which were inhibited by STIM1 knoc

82 -TRPC1 complexes, which then associated with Galphaq and PLCbeta1.

83 hat staphylococcal enterotoxin B activates a Galphaq and PLCbeta2-dependent pathway in human T cells.

84 vation promotes a direct interaction between Galphaq and protein kinase C zeta (PKCzeta), leading to

85 lthough recent structural studies showed how Galphaq and Rac1 bind PLC-beta, there is a lack of conse

86 al component of caveolae, specifically binds Galphaq and stabilizes its activation state resulting in

87 the interaction between this novel region in Galphaq and the effector PKCzeta is a key event in Galph

88 engages these receptor complexes to activate Galphaq and thus phospholipase C.

89 nine nucleotide exchange factor for Galphai, Galphaq, and Galpha12/13 and as a molecular chaperone re

90 withstanding severe reduction in Galphai2/3, Galphaq, and Galpha13 proteins.

91 Galphai, Galphaq, and Galpha13, but not Galphas produced from Ric

92 receptor GAR-3, the heterotrimeric G protein Galphaq, and its effector, Trio RhoGEF.

93 etion induced interactions between TRPC1 and Galphaq, and TRPC1 and PLCbeta1.

94 mediates G-protein-coupled receptor (GPCR)-, Galphaq- and Galpha(1)(2)/(1)(3)-dependent Gli stimulati

95 d potentiated insulin secretion in a GPR43-, Galphaq-, and phospholipase C-dependent manner.

96 The G-protein inhibitor GDP-beta-S, anti-Galphaq antibodies, the PLC inhibitor U73122, and the PK

97 ta on differentiation appears independent of Galphaq as down-regulating Galphaq at constant PLCbeta d

98 RGS8 adopts the same pose on Galphaq as it does when bound to Galphai3, indicating th

99 (alpha7345-348A) abolishes interaction with Galphaq as well as Gbetagamma while having no effect on

100 wild type, and not the AKKAA mutant, induced Galphaq association with RGS3 via an AP-2-dependent mech

101 on due to flattening leads to a loss in Cav1-Galphaq association.

102 rs independent of Galphaq as down-regulating Galphaq at constant PLCbeta does not affect differentiat

103 o stabilize calcium signals mediated through Galphaq-B2R, but does not affect cAMP signals mediated t

104 presentative peptide was specific for active Galphaq because it did not bind inactive Galphaq or othe

105 R188H mutant had a significant reduction in Galphaq binding affinity (10-fold increase in Ki compare

106 lded Kd values of about 200 nm for PLC-beta3-Galphaq binding.

107 Active Galphaq binds its two major classes of effectors, the ph

108 ate functional couplings to both Galphas and Galphaq but also identify a Galphai component to CLR sig

109 and-binding site, blocking signaling through Galphaq but not Galpha13 in vitro and thrombus formation

110 we showed that FZD6 assembles with Galphai1/Galphaq (but not with Galphas, Galphao and Ga12/13), and

111 PAR1, where they selectively interfere with Galphaq, but not Galpha12/13.

112 We find that interactions of the Galphas and Galphaq C termini with the beta(2)-adrenergic receptor (

113 Interaction of Galphas or Galphaq C termini with the GPCR increases signaling pote

114 ificantly attenuate the alpha7 nAChR-induced Galphaq calcium signaling response as evidenced by a dec

115 ction, and that not only Gbetagamma but also Galphaq can target GRK2 to the membrane.

116 minant negative cDNA constructs or siRNA for Galphaq causes accumulation of LFA-1 adhesions and stall

117 This loss in Galphaq/Cav1 association due to osmotic stress results i

118 Additionally Galphaq co-localizes with LFA-1- and EEA1-expressing int

119 +) signals to assess the activity of PLCbeta-Galphaq complexes and measurements of the reversal of si

120 es to the plasma membrane upon activation of Galphaq coupled GPCRs, resembling the well-known activat

121 ses to a similar extent after stimulation of Galphaq coupled GPCRs.

122 type I cannabinoid receptor (CB(1)R) and the Galphaq-coupled AT1R.

123 model where both an increased expression of Galphaq-coupled CysLT1, and sustained intracellular calc

124 ough the angiotensin II receptor 1 and major Galphaq-coupled downstream pathways, including Rho kinas

125 ate G protein-coupled receptor 40 (GPR40), a Galphaq-coupled free fatty acid receptor linked to MAPK

126 duction pathways activate RhoA-for instance, Galphaq-coupled Histamine 1 Receptor signaling via Galph

127 ation, extracellular zinc, and activation of Galphaq-coupled muscarinic (M3) receptors, compared with

128 hippocampus slices, we show that endogenous Galphaq-coupled muscarinic acetylcholine receptors activ

129 mprise 5-HT2A, 5-HT2B, and 5-HT2C, which are Galphaq-coupled receptors and display distinct pharmacol

130 eptor types, cross-talk between Galphai- and Galphaq-coupled receptors is often thought to be oligome

131 Furthermore, multiple Galphaq-coupled receptors modulate phosphorylation by PK

132 spholipase C, and it remains unclear whether Galphaq-coupled receptors signal to PKA in their native

133 tyrosine phosphatase (STEP) is recruited by Galphaq-coupled receptors, including the M1 muscarinic a

134 ing the endothelial barrier by acting on H1R Galphaq-coupled receptors, which is blunted in endotheli

135 signaling in response to the large family of Galphaq-coupled receptors.

136 uires the expression of the adrenergic-like, Galphaq-coupled, TA receptor TYRA-3 on inhibitory monoam

137 Overexpression of the Galphaq coupling-deficient mutant GRK2-D110A suppressed

138 ve Galphaq inhibitor, thereby confirming the Galphaq-coupling of the GnRH receptor in pituitary alpha

139 -beta3 dissociation or PLC-beta3-potentiated Galphaq deactivation, is not sufficient to explain the o

140 (Ncr1-Cre-Gnaq(fl/fl)), we demonstrate that Galphaq deficiency leads to enhanced NK cell survival.

141 de flanked by fluorescent proteins inhibited Galphaq-dependent activation of PLC-beta3 at least as ef

142 q-coupled Histamine 1 Receptor signaling via Galphaq-dependent activation of RhoGEFs such as p63.

143 tro, M3Ri2, M3Ri3, and M3R/H8-CT potentiated Galphaq-dependent but not Gbetagamma-dependent PLCbeta3

144 with 5-HT2C receptors does not alter 5-HT2C Galphaq-dependent inositol phosphate signaling, 5-HT2A o

145 h cardiac myocyte-specific overexpression of Galphaq develop progressive left ventricular failure ass

146 of PKCzeta and a novel interaction module in Galphaq different from the classical effector-binding si

147 otential therapeutic target for UM and other Galphaq-driven pathophysiologies that involve unrestrain

148 f absolute FRET amplitudes demonstrated that Galphaq enhances the extent and stability of the GRK2-M3

149 pathway through Galphaq in NRVMs and via the Galphaq/ErbB receptor pathways in cardiac fibroblasts.

150 ighty percent of UMs harbor mutations in the Galphaq family members GNAQ and GNA11.

151 and GNA11 oncogenes, encoding heterotrimeric Galphaq family members, have been identified in approxim

152 articularly those coupled to the Galphas and Galphaq family members.

153 ynamics and kinetics of PLC-beta3 binding to Galphaq FRET and fluorescence correlation spectroscopy,

154 r treatment associates with TRAX rather than Galphaq Functional measurements of Ca(2+) signals to ass

155 Activating mutations in GNAQ/GNA11, encoding Galphaq G proteins, are initiating oncogenic events in u

156 duced vWF secretion was defective in both EC-Galphaq(-/-);Galpha11(-/-) and Galpha12(-/-) mice.

157 GDP-AlF4(-)-bound Galphai, Galphaq, Galpha13, and Galphas produced in mock-depleted

158 compound WIN55,212-2 for Galphai/o, Galphas, Galphaq, Gbetagamma, and beta-arrestin1 signaling follow

159 toinhibited, and several proteins, including Galphaq, Gbetagamma, and Rac1, directly engage distinct

160 We identify three hot spot residues (Galphas/Galphaq-Gln-384/Leu-349, Gln-390/Glu-355, and Glu-392/As

161 mutants with reduced binding affinity toward Galphaq [GRK2(D110A)] and Gbetagamma [GRK2(R587Q)] were

162 aq-mediated PLC-beta3 activation and for the Galphaq GTPase-activating protein activity of PLC-beta.

163 haq heterodimer and production of functional Galphaq-GTPgammaS monomer.

164 ation resulted in dissociation of the Ric-8A:Galphaq heterodimer and production of functional Galphaq

165 l filtered as a approximately 100 kDa Ric-8A:Galphaq heterodimer.

166 rt formation of preassembled apo-GHSR1a:DRD1:Galphaq heteromeric complexes in hippocampal neurons.

167 l hallucinogen-in complex with an engineered Galphaq heterotrimer by cryoelectron microscopy (cryo-EM

168 g peptides should effectively inhibit active Galphaq in cells and that these and genetically encoded

169 to monitor the spatiotemporal activation of Galphaq in cells.

170 This reveals an important role of Galphaq in efficient recruitment of GRK2 to M3-ACh recep

171 e induced PAR(2) coupling to Galphas but not Galphaq in HEK293 cells.

172 the activation of the ERK1/2 pathway through Galphaq in NRVMs and via the Galphaq/ErbB receptor pathw

173 ether, these findings reveal a dual role for Galphaq in RhoGEF activation, as it both recruits and al

174 omoted neuronal depolarization downstream of Galphaq in the mouse prefrontal cortex.

175 talyzed GDP/GTPgammaS nucleotide exchange at Galphaq in the presence of Gbeta(1)gamma(1) and NT was c

176 ted to synthesize peptides that bound active Galphaq in vitro with affinities similar to full-length

177 LCbeta increases 4-fold within 24 h, whereas Galphaq increases only 1.4-fold, and this increase occur

178 M8 is caused by a direct action of activated Galphaq independent of the phospholipase C pathway.

179 ruitment by these receptors, indicating that Galphaq influences signaling and desensitization.

180 on was completely abolished with a selective Galphaq inhibitor, thereby confirming the Galphaq-coupli

181 t the non-canonical interaction of RGS2 with Galphaq is due to unique features of RGS2.

182 However the influence of Galphaq is not confined to the vesicles that express it,

183 nted activation of PLC-beta3 or p63RhoGEF by Galphaq; it also prevented G protein-coupled receptor-pr

184 tor responses were intact in D2 receptor and Galphaq KO mice, as well as in knock-in mice expressing

185 mGluR1a and mGluR5) are coupled primarily to Galphaq, leading to the activation of phospholipase C an

186 pression resulted from eicosanoid binding to Galphaq-linked neuronal receptors.

187 Importantly, we discovered that Galphaq-linked prostaglandin E2 and leukotriene D4 recep

188 ct the mechanical deformation of caveolae to Galphaq-mediated Ca(2+) signals.

189 y via Galphas, we found that the H2R induces Galphaq-mediated calcium release.

190 phosphoinositol signaling pathway involving Galphaq-mediated PLC activity is responsible for driving

191 Kd is 50-100 times greater than the EC50 for Galphaq-mediated PLC-beta3 activation and for the Galpha

192 nd selectively potentiates mGlu5 coupling to Galphaq-mediated signaling but not mGlu5 modulation of N

193 rdered based on agonist stimulation strength Galphaq-mediated signaling.

194 G protein-coupled receptor kinase 2, a known Galphaq modulator, led to a complete abrogation of ERK5

195 hibition or knockdown, or expression of a DN-Galphaq mutant likewise blocked activation of both p38 M

196 FR900359 inhibited spontaneous Galphaq nucleotide exchange, while having little effect

197 In the current study, we address the role of Galphaq on the interaction of GRK2 with activated Gq-pro

198 Galphaq, on the other hand, signals through phospholipas

199 We were unable to detect Galphaq or Galpha11 protein coupling to homomers or hete

200 Interfering with Galphaq or Galpha11 using dominant negative cDNA constru

201 High concentrations of Galphaq or Gbeta1gamma2 did not activate purified PLC-be

202 ive Galphaq because it did not bind inactive Galphaq or other classes of active Galpha subunits and d

203 t compatible with SKF83959 signaling through Galphaq or through a D1/D2 heteromer and challenge the e

204 ultiple G proteins, including the C. elegans Galphaq ortholog, EGL-30, in rectal epithelial cells to

205 I (Ang)-induced cardiomyopathy as well as in Galphaq overexpressing mice with heart failure.

206 ially rescued the heart failure phenotype of Galphaq overexpressing mice.

207 roperties in female pathological hearts from Galphaq-overexpressing or pressure-overloaded mice after

208 ng from prolonged Ang stimulation as well as Galphaq overexpression, suggesting its potential clinica

209 sion in cardiomyopathic mice with myocardial Galphaq overexpression.

210 In Galphaq, p115 RhoGEF, and RhoA-depleted human umbilical

211 d RhoA-dependent gene expression through the Galphaq-p63RhoGEF signaling pathway.

212 through inhibitory effects on the downstream Galphaq-p63RhoGEF-RhoA signaling pathway.

213 e a previously unrecognized effect of NAC on Galphaq palmitoylation and phospholipase C beta-mediated

214 Similarly, NAC treatment also decreased Galphaq palmitoylation in ischemic and nonischemic hindl

215 ipase C beta-dependent fashion and decreased Galphaq palmitoylation.

216 ugh the alpha7 channel and activation of the Galphaq pathway are necessary for growth.

217 cally to treat for neoplastic disorders with Galphaq pathway mutations.

218 orm of phospholipase C as a component in the Galphaq pathway.

219 electrostatic interactions, whereas the V1AR/Galphaq peptide interactions are predominantly hydrophob

220 V1A receptor (V1AR)-Galphaq The Galphas and Galphaq peptides adopt different orientations in beta2-A

221 sed SOCs requires G protein alpha q subunit (Galphaq)/phospholipase C (PLC)beta1 activities and prote

222 proteins requires G protein alpha q subunit (Galphaq)/phospholipase C (PLC)beta1/protein kinase C (PK

223 lcium responses in cells are mediated by the Galphaq/phospholipase Cbeta (PLCbeta)/phosphatidylinosit

224 nhance calcium signals generated through the Galphaq/phospholipase Cbeta signaling pathway and that s

225 stress results in a significant reduction of Galphaq/phospholipase Cbeta-mediated Ca(2+) signals.

226 rogate ERK5 phosphorylation, indicating that Galphaq/PKCzeta association is required for the activati

227 report herein that the activation-dependent Galphaq/PKCzeta complex involves the basic PB1-type II d

228 Finally, we reveal that Galphaq/PKCzeta complexes link Galphaq to apoptotic cell

229 emains active for some time following either Galphaq-PLC-beta3 dissociation or PLC-beta3-potentiated

230 oduced non-canonical signal transduction via Galphaq-PLC-IP3-Ca(2+) at the expense of canonical DRD1

231 s a novel mechanochemical connection between Galphaq/PLCbeta /PI(4,5)P(2) that couples calcium respon

232 nduced calcium mobilization through the PAR1/Galphaq/PLCbeta signaling axis.

233 3PO diminishes Ca(2+) release in response to Galphaq/PLCbeta stimulation by 30 to 40%.

234 the behavior of individual components of the Galphaq/PLCbeta/PI(4,5)P(2) pathway during retraction an

235 h store depletion induces formation of TRPC1-Galphaq-PLCbeta1 complexes that lead to PKC stimulation

236 -operated STIM1-TRPC1 interactions stimulate Galphaq/PLCbeta1/PKC activity to induce channel gating.

237 Residue Glu-355 in Galphaq prevents this peptide from interacting strongly

238 ementation of WGE did not support functional Galphaq production.

239 Furthermore, we show that Galphaq promotes the YAP-dependent growth of uveal melan

240 es reveal determinants responsible for HTR2A-Galphaq protein interactions as well as the conformation

241 ons of GNAQ (encoding the T96S alteration of Galphaq protein) in 8.7% (11/127) of NKTCL patients, thr

242 In wild-type animals Ang II acting through Galphaq protein-coupled receptors down-regulates IK(Na)

243 y regulated by angiotensin II acting through Galphaq protein-coupled receptors.

244 nt on cell-intrinsic expression of NMUR1 and Galphaq protein.

245 Such Galphaq-protein coupled receptors trigger the release of

246 nnel is negatively regulated by oxytocin via Galphaq-protein-coupled receptor activation of protein k

247 rdium and arrhythmic events, suggesting that Galphaq-protein-coupled receptor activation provides ino

248 After Galphaq-protein-coupled receptor activation, Ca(2+) mobi

249 IP3Rs may be activated after Galphaq-protein-coupled receptor stimulation, affecting

250 The Galphaq-protein/coupled receptor/IP3R axis modulates the

251 ammation, signals through LPA2 receptors and Galphaq proteins of cultured proximal tubule cells to tr

252 osed to form hetero-oligomers that couple to Galphaq proteins, and SKF83959 has been proposed to act

253 Activating mutations in Galphaq proteins, which form the alpha subunit of certai

254 ion of TGR5 and Galphas (but not Galphai and Galphaq ) proteins was increased 2-fold to 3-fold in cys

255 to the plasma membrane when coexpressed with Galphaq Q209L compared with 67% for WT RGS2.

256 Point mutations in this Galphaq region completely abrogate ERK5 phosphorylation,

257 n alpha6 of the RGS domain and Switch III of Galphaq, regions of high sequence and conformational div

258 betagamma without altering basal activity or Galphaq response.

259 nit of the heterotrimeric G protein complex, Galphaq, resulting in inhibition of Galphaq signaling.

260 he crystal structure of RGS2 in complex with Galphaq revealed a non-canonical interaction that could

261 Instead, selectivity for Galphaq seems more likely determined by whether strong c

262 Constitutive activation of Galphaq signaling by mutations in GNAQ or GNA11 occurs i

263 oncogene and highlight the critical role of Galphaq signaling in uveal melanoma pathogenesis.

264 ium activity of the receptor channel and the Galphaq signaling pathway at the growth cone.

265 Activating mutations in the Galphaq signaling pathway at the level of GNAQ, GNA11, o

266 se ARF6 acts as a proximal node of oncogenic Galphaq signaling to induce all of these downstream path

267 The underlying canonical Galphaq signaling via production of inositol phosphates

268 tracellular calcium from local ER stores via Galphaq signaling, leading to IP3 receptor (IP3R) activa

269 olipase C beta4), the downstream effector of Galphaq signaling.

270 complex, Galphaq, resulting in inhibition of Galphaq signaling.

271 q and the effector PKCzeta is a key event in Galphaq signaling.

272 ptor regulation of APP expression depends on Galphaq-signaling and conventional protein kinase C isof

273 ctivates FAK through TRIO-RhoA non-canonical Galphaq-signaling, and genetic ablation or pharmacologic

274 We found that Galphaq stimulates YAP through a Trio-Rho/Rac signaling

275 Here, we show that prolonged Galphaq stimulation results in the retraction of neurite

276 Based on the RGS8-Galphaq structure, residues in RGS8 that contact a uniqu

277 The C terminus of either the Galphas or Galphaq subunit is sufficient to enhance Galpha subunit

278 in all UM cells with driver mutation in the Galphaq subunit or the upstream receptor.

279 tein betagamma subunits as well as activated Galphaq subunits, it can be considered as an effector fo

280 (A1R), tethered to Galphas-XL, Galphai2, or Galphaq subunits.

281 We also find that Galphaq suppresses tumor growth of NKTCL via inhibition

282 Moreover, the Galphaq T96S mutant may act in a dominant negative manne

283 supplementation of WGE allowed production of Galphaq that gel filtered as a approximately 100 kDa Ric

284 ies, such as Galphai1, Galphao, Galphas, and Galphaq The FZD4-G protein complex dissociates upon stim

285 r (beta2-AR)-Galphas and V1A receptor (V1AR)-Galphaq The Galphas and Galphaq peptides adopt different

286 embrane-dependent activation of PLC-beta3 by Galphaq Therefore, XY-69 can replace radioactive phospha

287 e reveal that Galphaq/PKCzeta complexes link Galphaq to apoptotic cell death pathways.

288 olinergic signaling works through downstream Galphaq to control oxidative stress and death of neurons

289 Phospholipase Cbeta1 is activated by Galphaq to generate calcium signals in response to hormo

290 ucing its cytosolic population by activating Galphaq to localize it to the plasma membrane returns di

291 eta1 dependent and involves translocation of Galphaq to the nucleus, where it interacts with PLC-beta

292 tion of GTPgammaS to Ric-8A-supplemented WGE Galphaq translation resulted in dissociation of the Ric-

293 gth PLC-beta3 for binding Gbetagamma but not Galphaq, Using sequence conservation, structural analyse

294 WGE-translated Galphaq was gel filtered and found to be an aggregate.

295 To test this, Gnaq (encodes Galphaq) was selectively inactivated in the GnRH neurons

296 ontact a unique alpha-helical domain loop of Galphaq were converted to those typically found in R12 s

297 on can be induced by extended stimulation of Galphaq where cells return to a spherical morphology and

298 pholipase Cbeta (PLCbeta) and its activator, Galphaq, which together mediate Ca(2+) release.

299 migration by facilitating the interaction of Galphaq with PLC-beta2.

300 us helix-turn-helix of the effectors engages Galphaq within its canonical binding site consisting of