ライフサイエンスコーパス: GTPgammaS

1 GTPgammaS pretreatment blocked GRK6/AGS3/Galphai2 format

2 GTPgammaS produced a slight Ca(2+) sensitizing effect in

3 GTPgammaS-stimulated activation of MMP14 also results in

4 u(2+) enters the active site within a Cu(2+)*GTPgammaS or Cu(2+)*GTP chelation complex, and that Cu(2

5 purified G(i1) alpha:beta4gamma11 with Mg+2/GTPgammaS following reconstitution into lipid vesicles a

6 [35S]GTPgammaS binding was stimulated by morphine and ET-1 in

7 oid 2-arachidonoyl glycerol (2-AG), for [35S]GTPgammaS binding and cAMP inhibition (5-10 fold).

8 CaM decreases 5-HT2A receptor-mediated [35S]GTPgammaS binding to NIH-3T3 cell membranes, supporting

9 ctive compounds, maximum stimulation of [35S]GTPgammaS binding decreased in the order kappa > ORL1 >

10 oteins reconstituted agonist-loading of [35S]GTPgammaS for each receptor.

11 promoting agonist-dependent binding of [35S]GTPgammaS to either alpha(q) or alpha(i1).

12 n the potency of compounds to stimulate [35S]GTPgammaS binding between cortex and thalamus, with the

13 at the ability of agonists to stimulate [35S]GTPgammaS binding relates to the receptor distribution o

14 onality by alpha2-AR agonist-stimulated [35S]GTPgammaS autoradiography.

15 U69,593 stimulated [35S]GTPgammaS binding in a concentration-dependent manner an

16 A (PKA) activity and agonist-stimulated [35S]GTPgammaS binding was assayed using tissue homogenates f

17 3H]SR141716A and WIN55,212-2-stimulated [35S]GTPgammaS binding were decreased in both regions 1 day a

18 B(1)) subunits, and baclofen-stimulated [35S]GTPgammaS binding, a measure of GABA(B) receptor functio

19 ptors as measured by agonist-stimulated [35S]GTPgammaS binding.

20 In the [35S]GTPgammaS assay full agonism was observed.

21 tors and their relative efficacy in the [35S]GTPgammaS assay.

22 eptive actions was determined using the [35S]GTPgammaS binding assay in membrane homogenates from the

23 mGlu2/3 receptors to G-proteins in the [35S]GTPgammaS binding assay.

24 inhibitory potency (Ke = 0.1 nM) in the [35S]GTPgammaS functional assay with delta opioid receptor se

25 anosine 5'-O-(3-[35S]thiotriphosphate) ([35S]GTPgammaS) to membranes containing M1 to M3 receptors, b

26 anosine 5'-O-(3-[35S]thio)triphosphate ([35S]GTPgammaS binding), respectively, in hippocampus and str

27 osine 5'-([gamma-35S]thio)triphosphate ([35S]GTPgammaS) binding in Gialpha immunoprecipitates from me

28 onists for both D2 and D3 receptors (EC(50) (GTPgammaS); D2 = 4.51 and 1.69 nM and D3 = 1.58 and 0.74

29 (1) to late endosomal vesicles and activated GTPgammaS(35) binding and pERK to similar maxima, only A

30 Activating GTPgammaS coupling with 12-(S)-HETE proved to be both re

31 onstitutive activity the G-protein activator GTPgammaS inhibited channel activity which was reversed

32 and Gln-14 significantly enhanced Gt(alpha)*-GTPgammaS activation of cone Pgamma truncation variants.

33 9-18) that reduces the ability of Gt(alpha)*-GTPgammaS to activate the reconstituted PDE6.

34 tivated transducin alpha-subunit (Gt(alpha)*-GTPgammaS).

35 rod or cone Pgamma contribute to Gt(alpha)*-GTPgammaS-mediated activation of PDE6.

36 d cells and is sensitive to the GTP analogue GTPgammaS.

37 ives of GTP and GDP and of the GTP analogues GTPgammaS and GMPPNP.

38 n formation of the GDP.AlF(4)(-)/Mg(2+)- and GTPgammaS/Mg(2+)-bound states.

39 that binds selectively to GDP x AlF4(-)- and GTPgammaS-bound states of G alpha(i) subunits.

40 incubated with the full complex, Arf1p, and GTPgammaS.

41 had no observable effect, but ATPgammaS and GTPgammaS, nucleotide triphosphate analogues resistant t

42 ion equilibrium in solution were derived and GTPgammaS was detected to increase the enthalpic stabili

43 ibited by the dynamin inhibitor dynasore and GTPgammaS introduced through the patch pipette, suggesti

44 tures of free spPH and Rac2 bound to GDP and GTPgammaS.

45 ision protein FtsZ, as the citrate, GDP, and GTPgammaS complexes, determined at 1.89, 2.60, and 2.08A

46 hares similarities with the heterotrimer and GTPgammaS/Mg(2+)-bound ChiT.

47 ver, upon activation of alpha with MgCl2 and GTPgammaS under nondenaturing conditions, the beta4 and

48 3 receptor-mediated calcium mobilization and GTPgammaS binding.

49 Intracellularly applied GTPgammaS (20 microM) during dual dendritic recordings s

50 s unproductive as the mutants failed to bind GTPgammaS and become activated.

51 guanosine 5'-O-(3-thio)triphosphate binding (GTPgammaS)] were assessed.

52 rization of Galpha(olf) showed that it binds GTPgammaS at a rate marginally slower than Galpha(s shor

53 beled GTP analogue, BODIPY-FL GTPgammaS (BOD-GTPgammaS), that binds to the alpha subunit of transduci

54 ese findings suggest that the binding of BOD-GTPgammaS to transducin causes it to adopt a distinct co

55 f rhodopsin and Gbetagamma from alpha(T)-BOD-GTPgammaS complexes, relative to their rates of dissocia

56 Nevertheless, the BOD-GTPgammaS-bound alpha(T) subunit is able to bind with hi

57 NS4B resulted in decreased affinity for both GTPgammaS and ATPgammaS as well as decreased ATP hydroly

58 ice displayed a significant increase in both GTPgammaS incorporation and migration as compared with w

59 nded lattice of the GMPCPP-MT, the EB3-bound GTPgammaS-MT has a compacted lattice that differs in lat

60 o evidence of DN properties, is activated by GTPgammaS, and has reduced GTPase activity.

61 The I(Cl,ATP) persistently activated by GTPgammaS, was inhibited by glibenclamide but not by DID

62 MMP14 activation by GTPgammaS is pertussis toxin-sensitive.

63 MMP14 activation by GTPgammaS occurs in a concentration- and time-dependent

64 uced in vitro adenylyl cyclase activation by GTPgammaS suggests that they cause constitutive adaptati

65 Gsalpha-R265E has facilitated activation by GTPgammaS, a slightly facilitated activation by GTP but

66 a-subunit that is resistant to activation by GTPgammaS, is devoid of resident nucleotide, and has dom

67 can be locked onto the trans-Golgi matrix by GTPgammaS, indicating that its association is regulated

68 Assembly is also supported by GTPgammaS.

69 tubulation activity of OPA1 is suppressed by GTPgammaS.

70 re indicative of a hexamer and unaffected by GTPgammaS.

71 hosphate) (GTPgammaS) in solution, and caged GTPgammaS or caged GTP loaded on the RhoA.RhoGDI complex

72 trast, in the presence of a divalent cation, GTPgammaS adopts an extended conformation, and the Walke

73 Furthermore, VAMP2 bound both GST-Cdc42-GTPgammaS and GST-Cdc42-GDP, indicating that the Cdc42-V

74 ivity by hypotonic cell swelling, cisplatin, GTPgammaS, or the cytokines TNF or interleukin-1 increas

75 In experiments with GTP analogs (commonly GTPgammaS), the extent of G-protein activation is predic

76 the identification of mutations that confer GTPgammaS sensitivity to agonist binding.

77 Conversely, GTPgammaS stimulated a low activity pool of PI4KIIalpha

78 A partial agonist molecule (-)-34 (EC50 (GTPgammaS); D2 = 21.6 (Emax = 27%) and D3 = 10.9 nM) was

79 = 1.15 nM) and full agonist activity (EC50 (GTPgammaS); D2 = 3.23 and D3 = 1.41 nM) at both D2 and D

80 with preferential D3 agonist activity (EC50(GTPgammaS); D3 = 0.10 nM; D2/D3 (EC50): 159).

81 en artery restored PDBu-induced and enhanced GTPgammaS-induced Ca(2+) sensitization.

82 alpha-Catenin enhanced GTPgammaS binding by ARF6 in vitro in the presence of p1

83 rophoresis buffer contained 250 nM BODIPY FL GTPgammaS.

84 luorescently labeled GTP analogue, BODIPY-FL GTPgammaS (BOD-GTPgammaS), that binds to the alpha subun

85 on with the activated receptor and following GTPgammaS binding.

86 teractions because they are not observed for GTPgammaS/Mg(2+)-bound ChiT generated independently of R

87 al catalysis of thiophosphoryl transfer from GTPgammaS.

88 In the functional GTPgammaS binding assay, (-)-34 exhibited full agonist a

89 Galpha(GDP)betagamma heterotrimer and Galpha(GTPgammaS) conformations are consistent with the local e

90 Galphai1(GTPgammaS) has no effect, whereas Galphai1(GDP) closes t

91 lphai1*GDP and lower (0.67-0.75) in Galphai1*GTPgammaS, although in crystal structures, switch segmen

92 0 is slower in Galphai1*GDP than in Galphai1*GTPgammaS.

93 rodimer and production of functional Galphaq-GTPgammaS monomer.

94 observed in the crystal structure of Galphas-GTPgammaS.

95 The 3.0 A resolution structure of Galphas.GTPgammaS/forskolin-activated VC1:IIC2 crystals soaked i

96 g a far Western method for examining Galphat-GTPgammaS proteolytic digestion patterns.

97 PDEgamma C-terminal positions to the Galphat-GTPgammaS N terminus, particularly from PDEgamma residue

98 xa 488 (C5) fluorescent dye (Ax) in the GDP, GTPgammaS (collectively, GXP), and Ric-8A-bound states.

99 NTS1-catalyzed GDP/GTPgammaS nucleotide exchange at Galphaq in the presence

100 Line widths observed for R*-generated GTPgammaS/Mg(2+)-bound (15)N-ChiT, however, indicated th

101 correlation (HSQC) spectrum of R*-generated GTPgammaS/Mg(2+)-bound ChiT revealed (1)HN, (15)N chemic

102 3.5 A or better resolution, bound to GMPCPP, GTPgammaS, or GDP, either decorated with kinesin motor d

103 ity of phosphate production assays (GTPase) >GTPgammaS-binding assays >cAMP inhibition assays.

104 h and without a nonhydrolysable form of GTP (GTPgammaS).

105 5, and -275 cal x mol(-1) x K(-1), with GTP, GTPgammaS, GDPNP, and GDP, respectively), associated wit

106 Importantly, GTPgammaS binding studies revealed that there is no dete

107 In GTPgammaS-loaded cells, I(Cl,ATP) was irreversibly activ

108 )(1), inhibiting both the exchange of GDP in GTPgammaS binding assays and the AlF(4)(-)-stimulated en

109 The increased GTPgammaS incorporation was blocked by G alpha(i3) prote

110 55) and potent antagonism of agonist-induced GTPgammaS binding.

111 uced basal recombinant S1P1 receptor-induced GTPgammaS binding and S1P-induced GTPgammaS binding in m

112 or-induced GTPgammaS binding and S1P-induced GTPgammaS binding in membranes.

113 ime of approximately 10 s with intracellular GTPgammaS and approximately 14 s with intracellular GTP

114 14),Arg(19)), binds to the PTHR in a largely GTPgammaS-resistant fashion, suggesting selective bindin

115 The affinity of eIF5B for mant-GTPgammaS was about 2 times lower (Kd approximately 6.9

116 Crystal structures, MANT-GTPgammaS binding, thermal denaturation, biochemical ass

117 e to vertebrate transducin by light-mediated GTPgammaS-binding assays.

118 cant effect on the rate of receptor-mediated GTPgammaS binding).

119 teins were incubated in the presence of 1 mm GTPgammaS, Myo5a tail and Rab3A formed a complex and a d

120 Addition of NaCl/GTPgammaS produced a steepening (slope 0.95+/-0.06, n=3)

121 (gp61) primase subunit, and nonhydrolyzable GTPgammaS.

122 binding of six NTPs (or six nonhydrolyzable GTPgammaS analogues) that are located at and stabilize t

123 hospholipids, Arf1p, and the nonhydrolyzable GTPgammaS.

124 Of note, GTPgammaS loading and time-resolved FRET assays with pur

125 brane fractions was inhibited by addition of GTPgammaS (IC(50) 21 +/- 1.8 nM).

126 Addition of GTPgammaS to Ric-8A-supplemented WGE Galphaq translation

127 Upon addition of GTPgammaS, the activated Galphai1(GTP) subunit dissociat

128 A tiny amount of GTPgammaS stabilizes polymers assembled in GTP and inhib

129 ely occluded by intracellular application of GTPgammaS, suggesting that endogenous neuromodulators in

130 mplex but does not interfere with binding of GTPgammaS to purified recombinant Galpha, suggesting tha

131 ints such as ligand occupancy and binding of GTPgammaS.

132 GDP release and slows its rate and extent of GTPgammaS uptake.

133 on of carbachol or intracellular infusion of GTPgammaS, demonstrating its effectiveness on native TRP

134 cts are incurred by cytoplasmic perfusion of GTPgammaS or the actin cytoskeleton disruptor latrunculi

135 ophila atlastin dimerizes in the presence of GTPgammaS but is monomeric with GDP or without nucleotid

136 RepX filaments assembled in the presence of GTPgammaS were more stable than those assembled in the p

137 udoknot core were altered in the presence of GTPgammaS, indicating donor-induced folding.

138 elicase "initiation complex." Replacement of GTPgammaS with GTP permits the completion of the helicas

139 creases in ligand-independent stimulation of GTPgammaS binding versus wild type CB(1), although basal

140 In M2 cells DAMGO stimulation of GTPgammaS binding was significantly greater than in A7 c

141 ., it decreased DAMGO-induced stimulation of GTPgammaS binding.

142 2, and IL-8/CXCL8 by binding, stimulation of GTPgammaS exchange, and chemotaxis of mCXCR1-transfected

143 binding isotherms, a minimal E(max) based on GTPgammaS binding analysis, and defective localization r

144 ide-depleted RhoA relative to either GDP- or GTPgammaS-bound forms.

145 f the heterotrimer in the absence of GTP (or GTPgammaS).

146 32 amino acids buried upon binding of GTP or GTPgammaS, respectively, and 15-19 amino acids upon bind

147 ent manner, similar to the binding of GTP or GTPgammaS, with an apparent dissociation constant of 100

148 Moreover in the latter patches GTPgammaS and OAG caused marked increases in NP(o).

149 both, and activation by a full agonist plus GTPgammaS reduced the oligomeric size of Gi1 without aff

150 lphai1 by the receptor-mimic mastoparan plus GTPgammaS, and constitutively active eGFP-Galphai1 was p

151 lators of the GABAB receptor by potentiating GTPgammaS stimulation induced by GABA at 2.5 and 25 muM

152 he MT1 receptor, and a full agonist profile (GTPgammaS test), being the most potent MT2-selective ful

153 Hypoxia also relaxed GTPgammaS contractures but importantly, arteries could n

154 termined the structure of the PRG-DH.PH-RhoA.GTPgammaS (guanosine 5'-O-[gamma-thio]triphosphate) comp

155 ence of AC activators forskolin or Galpha(s)-GTPgammaS as evidenced by a more rapid BATP turnover to

156 cted EC50 values for forskolin and Galpha(s)-GTPgammaS of 27 +/- 6 microM and 317 +/- 56 nM, respecti

157 ith 2.5 microM forskolin and 25 nM Galpha(s)-GTPgammaS, the amount of BcAMP formed was 3.4 times high

158 e functional assay was performed using (35)S-GTPgammaS (GTP is guanosine triphosphate) in primate bra

159 CUMI-101 did not stimulate (35)S-GTPgammaS binding in primate brain, in contrast to 8-OH-

160 sis toxin-sensitive manner, stimulated (35)S-GTPgammaS binding, and promoted the inhibition of forsko

161 dently inhibiting 8-OH-DPAT-stimulated (35)S-GTPgammaS binding.

162 a number of analogues of 1 using a [ (35) S]GTPgammaS binding assay.

163 (q) protein activation was probed by [(35) S]GTPgammaS incorporation followed by G(q) immunoprecipita

164 ation (measured by agonist-stimulated [(35)S]GTPgammaS (guanylyl-5'-[O-thio]-triphosphate) binding) i

165 55,940 displacement and its effect on [(35)S]GTPgammaS accumulation is substantially lower compared w

166 Cannabinoid-stimulated [(35)S]GTPgammaS and [(3)H]ligand autoradiography were assessed

167 DAMGO-stimulated [(35)S]GTPgammaS and [(3)H]naloxone binding reveals that the an

168 or the affinity difference, involving [(35)S]GTPgammaS and cAMP synthesis.

169 vitro measures of efficacy using the [(35)S]GTPgammaS assay are predictive of the in vivo profile.

170 formationally constrained series in a [(35)S]GTPgammaS assay showed that structural rigid compounds h

171 ipode proved to be an H4R antagonist ([(35)S]GTPgammaS assay).

172 full kappa agonistic activity in the [(35)S]GTPgammaS assay, and high selectivity over mu, delta, si

173 ent kappa-receptor antagonists in the [(35)S]GTPgammaS assay.

174 utive activity was identified using a [(35)S]GTPgammaS assay.

175 d its analogs were potent agonists in [(35)S]GTPgammaS assays at the mu opioid receptor but failed to

176 etermined and compared to JDTic using [(35)S]GTPgammaS assays.

177 Immunofluorescence and in vitro [(35)S]GTPgammaS autoradiography of rat tissue sections contain

178 CR2, SX-517 antagonized CXCL8-induced [(35)S]GTPgammaS binding (IC50 = 60 nM) and ERK1/2 phosphorylat

179 and binding and signaling properties ([(35)S]GTPgammaS binding and beta-arrestin recruitment) of 22 p

180 pit had comparable potencies for both [(35)S]GTPgammaS binding and beta-arrestin recruitment, suggest

181 We measured G protein activation by [(35)S]GTPgammaS binding and G(alpha) subtype-specific immunopr

182 Data from standard [(35)S]GTPgammaS binding and immunoprecipitation (G(alphai1-3))

183 ssic pharmacological methods, such as [(35)S]GTPgammaS binding and inhibition of cyclic AMP productio

184 as evident in both agonist-stimulated [(35)S]GTPgammaS binding and opioid analgesic assays; however,

185 n of the two compounds in an in vitro [(35)S]GTPgammaS binding assay showed that neither compound sho

186 aluation of these 28 compounds in the [(35)S]GTPgammaS binding assay showed that several of the analo

187 on, 84 had an EC(50) of 942 nM in the [(35)S]GTPgammaS binding assay using mouse striatal membranes b

188 oligand displacement binding assay, a [(35)S]GTPgammaS binding assay, and in a competition associatio

189 t MOR and full agonists at KOR in the [(35)S]GTPgammaS binding assay.

190 to MOR) and was a full agonist in the [(35)S]GTPgammaS binding assay.

191 the kappa and micro receptors in the [(35)S]GTPgammaS binding assay.

192 eceptor functional antagonism using a [(35)S]GTPgammaS binding assay.

193 these compounds were measured in the [(35)S]GTPgammaS binding assay.

194 gated for H(2)R agonism in GTPase and [(35)S]GTPgammaS binding assays at guinea pig (gp) and human (h

195 Ligand and [(35)S]GTPgammaS binding assays of the 5HT(1A) and EDG(1) GPCRs

196 Receptor binding and [(35)S]GTPgammaS binding assays were used to characterize the a

197 antagonists (5 and 27) were tested in [(35)S]GTPgammaS binding assays, and their RTs appeared correla

198 protein, determined using GTPase and [(35)S]GTPgammaS binding assays, did not show a difference betw

199 termination, washout experiments, and [(35)S]GTPgammaS binding assays, then validated 17b as the cova

200 ced desensitization as assessed using [(35)S]GTPgammaS binding assays.

201 was obtained using [(3)H]CP55940 and [(35)S]GTPgammaS binding assays.

202 using membrane-based [(3)H]DPCPX and [(35)S]GTPgammaS binding experiments.

203 2)-Met(5)-Glyol-enkephalin-stimulated [(35)S]GTPgammaS binding following fentanyl pretreatment was no

204 ovine serum albumin reduced the basal [(35)S]GTPgammaS binding in a concentration-dependent manner an

205 adulthood by measuring DOP-R-mediated [(35)S]GTPgammaS binding in brain membranes and DOP-R-mediated

206 o tissues: it attenuated MOR-mediated [(35)S]GTPgammaS binding in CPu but enhanced it in CHO-HA-rMOR.

207 t decrease in WIN 55,212-2-stimulated [(35)S]GTPgammaS binding in membranes prepared from the rostral

208 t not JNJ7777120, were able to induce [(35)S]GTPgammaS binding in membranes prepared from U2OS-H(4) c

209 r as well as enhancing AEA-stimulated [(35)S]GTPgammaS binding in mouse brain membranes and beta-arre

210 sults showed reduced DAMGO-stimulated [(35)S]GTPgammaS binding in the thalamus and PAG of CCI mice, w

211 tional when tested for stimulation of [(35)S]GTPgammaS binding in vitro and in patch-clamp electrophy

212 7777120 were both able to inhibit the [(35)S]GTPgammaS binding induced by clobenpropit.

213 d tested for their ability to inhibit [(35)S]GTPgammaS binding stimulated by the selective kappa opio

214 In cell membrane [(35)S]GTPgammaS binding studies, the presence of the EP(1) com

215 MIS significantly increased [(35)S]GTPgammaS binding to ovarian membranes, confirming that

216 2)-Met(5)-Glyol-enkephalin-stimulated [(35)S]GTPgammaS binding to spinal cord membranes from morphine

217 of selected compounds in stimulating [(35)S]GTPgammaS binding was assessed in CHO cells expressing e

218 pitation studies showed the increased [(35)S]GTPgammaS binding was associated with Galpha(i1-3) prote

219 -molecule GPR40 antagonist, and basal [(35)S]GTPgammaS binding was prevented by the selective Galpha(

220 ly5-OH] enkephalin (DAMGO)-stimulated [(35)S]GTPgammaS binding was then conducted at this time point

221 e compounds had no inverse agonism in [(35)S]GTPgammaS binding, a characteristic that is often though

222 le potencies in calcium mobilization, [(35)S]GTPgammaS binding, and cAMP assays, whereas substitution

223 ic agonist-induced cAMP accumulation, [(35)S]GTPgammaS binding, and CB(1) receptor internalization.

224 nds on CB(1) receptor agonist-induced [(35)S]GTPgammaS binding, inhibition, and stimulation of forsko

225 the lack of significant decreases in [(35)S]GTPgammaS binding.

226 s and desensitized agonist-stimulated [(35)S]GTPgammaS binding.

227 [(35)S]GTPgammaS binding/Galpha(q/11) immunoprecipitation assay

228 assessed DYN A peptide expression and [(35)S]GTPgammaS coupling assays were performed to assess KOR f

229 Competitive binding and [(35)S]GTPgammaS functional assays identified compound (-)-9b a

230 f the maximum functional efficacy (in [(35)S]GTPgammaS G protein binding assay) of the A(3)AR agonist

231 Measurement of [(35)S]GTPgammaS incorporation at D(2S) coexpressed with G-prot

232 surement of D(2L)- and D(2S)-mediated [(35)S]GTPgammaS incorporation in the presence of coexpressed G

233 , this detergent is compatible with a [(35)S]GTPgammaS radionucleotide exchange assay measuring guani

234 Using the antibody-capture [(35)S]GTPgammaS scintillation proximity assay, we demonstrated

235 ine 5'-O-(3-[(35)S]thio)triphosphate ([(35)S]GTPgammaS) binding assays.

236 ine 5'-O-(3-[(35)S]thio)triphosphate ([(35)S]GTPgammaS) binding, simulation (Galpha(s)-mediated), and

237 cell membranes (radioligand binding, [(35)S]GTPgammaS, or GTPase assays) and in part in luciferase a

238 We first demonstrate, via a [(35)S]GTPgammaS-binding assay, that drug activity is retained

239 f the mGlu receptor 2 (mGluR2) in a [(3)(5)S]GTPgammaS binding assay and were able to displace an mGl

240 ntable antagonist of PGD2-stimulated [(35)S]-GTPgammaS activation, and its effects were not fully rev

241 uanosine 5'(gamma-thio)triphosphate ([(35)S]-GTPgammaS) into sections of the PBN.

242 -8BDelta9 isoform stimulated Galpha(s short) GTPgammaS binding only.

243 Stimulated GTPgammaS binding indicated that alpha2-adrenergic recep

244 -HETE efficiently and selectively stimulated GTPgammaS coupling in the membranes of 12-HETER-transfec

245 assay of selected compounds for stimulating GTPgammaS binding was carried out with CHO cells express

246 ctivity of selected compounds in stimulating GTPgammaS binding was assessed with CHO cells expressing

247 ture was further exhibited when both alpha(t)GTPgammaS and Palphabeta were present and competing for

248 Furthermore, alpha(t)GTPgammaS co-immunoprecipitated with PDE6 and vice versa

249 Either Palphabeta or alpha(t)GTPgammaS could be pulled down by the Btn-Pgamma molecul

250 guanosine 5'-3-O-(thio)triphosphate (alpha(t)GTPgammaS) in comparison with the central region, wherea

251 albeit less efficiently compared to alpha(T)-GTPgammaS.

252 to their rates of dissociation from alpha(T)-GTPgammaS.

253 e to more extensive interactions between the GTPgammaS and the enzyme.

254 inity conformation (R(0)), distinct from the GTPgammaS-sensitive conformation (RG).

255 34 nM, respectively) and high potency in the GTPgammaS assay (EC 50 = 1.6 and 4.1 nM, respectively) a

256 In the GTPgammaS assay, while all of the cyclic analogues exhib

257 with wild type but similar stability in the GTPgammaS-bound state.

258 ndent of any potential interactions with the GTPgammaS thiophosphoryl group.

259 n is found to form a stable complex with the GTPgammaS/Mg(2+)-exchanged heterotrimer.

260 elease of guanosine 5'-O-3-thiotriphosphate (GTPgammaS)/Mg(2+)-bound ChiT.

261 ne, caged guanosine 5'-O-(thiotriphosphate) (GTPgammaS) in solution, and caged GTPgammaS or caged GTP

262 Hp) and guanosine 5'-(3-O-thiotriphosphate) (GTPgammaS).

263 binding was up to 20-fold more sensitive to GTPgammaS than G(i1) alpha:beta4gamma2-induced high-affi

264 TGase 3 transamidation activity, similar to GTPgammaS and GDP.

265 ollows: guanosine 5'-3-O-(thio)triphosphate (GTPgammaS) (0.4 microm), GTP (0.6 microm), GDP (1.0 micr

266 gs, guanosine 5'-O-(gamma-thio)triphosphate (GTPgammaS) and guanosine 5'-(beta,gamma-imido)-triphosph

267 hibited guanosine 5'-3-O-(thio)triphosphate (GTPgammaS) binding to purified G(i)alpha(1).

268 mulated guanosine 5'-3-O-(thio)triphosphate (GTPgammaS) binding to these subunits and Galpha(olf), wh

269 ion and guanosine 5'-3-O-(thio)triphosphate (GTPgammaS) incorporation.

270 P), and guanosine 5'-3-O-(thio)triphosphate (GTPgammaS) is enhanced substantially by gain of function

271 it with guanosine 5'-3-O-(thio)triphosphate (GTPgammaS) results in partial dissociation of Galpha fro

272 of the guanosine 5'-3-O-(thio)triphosphate (GTPgammaS) that is already bound to the Galpha(s).

273 ysis of guanosine 5'-3-O-(thio)triphosphate (GTPgammaS), suggesting a direct interaction of ML204 wit

274 anosine 5'-Omicron-(gamma-thio)triphosphate (GTPgammaS)-bound) form of Tr*, we found that Tr* activat

275 ted and guanosine 5'-3-O-(thio)triphosphate (GTPgammaS)-loaded ARF6 (active form) added to permeabili

276 nalogue guanosine 5'-3-O-(thio)triphosphate (GTPgammaS).

277 f guanosine 5[prime]-O-(3-thio)triphosphate (GTPgammaS).

278 ide and guanosine 5'-3-O-(thio)triphosphate (GTPgammaS)/Mg(2+)-bound (15)N-ChiT.

279 und to guanosine 5'-O-(3-thio)-triphosphate (GTPgammaS) using a series of full-length PDEgamma photop

280 lerated guanosine 5[gamma-thio]triphosphate (GTPgammaS) binding by ARF6, which participates in protei

281 bind guanosine 5'-[gamma-thio]triphosphate (GTPgammaS), and stimulate appropriate G protein effector

282 to guanosine 5'-O-[gamma-thio]triphosphate (GTPgammaS)-stabilized MTs, which mimic the EB1-preferred

283 and guanosine 5'-O-[gamma-thio]triphosphate (GTPgammaS).

284 ve a 'curved' conformation for gamma-tubulin-GTPgammaS, similar to that seen for GDP-bound, unpolymer

285 ese results (with our previous gamma-tubulin:GTPgammaS structure) support the lattice model by demons

286 d binding studies in ovarian membranes using GTPgammaS and PTX demonstrated that the MIS binds a rece

287 domain, relative to GDP-bound RhoC, whereas GTPgammaS-bound RhoC exhibits differences in both its sw

288 in the presence (with GTP) and absence (with GTPgammaS) of Tr* inactivation, PDE activation required

289 nilide and equilibrium binding analyses with GTPgammaS and ATPgammaS show that both GTP and ATP are b

290 vation state of NS3 helicase in complex with GTPgammaS, in which the triphosphate adopts a compact co

291 ated receptor 2, intracellular dialysis with GTPgammaS, or application of the synthetic diacylglycero

292 o FtsZ, and NMR competition experiments with GTPgammaS showed chrysophaentin A and GTP to bind compet

293 polymerization, and substitution of GTP with GTPgammaS stabilized the filaments.

294 Gt(e) retained its ability to interact with GTPgammaS.

295 e, which repletes intracellular GTP, or with GTPgammaS.

296 y of selected compounds was carried out with GTPgammaS binding assay.

297 h other Galpha subunits and was similar with GTPgammaS- and GDP-liganded Galpha(12).

298 However, treatment with GTPgammaS to inhibit G protein coupling diminished the a

299 and-independent, active form, treatment with GTPgammaS was used to inhibit G protein coupling.

300 direct activation of G proteins in vivo with GTPgammaS in the absence of exogenous Wnt will disrupt G