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 d cells and is sensitive to the GTP analogue GTPgammaS.

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

34 SNAP-23 significantly inhibited Ca(2+)- and GTPgammaS-stimulated surfactant secretion from permeabil

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

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

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

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

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

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

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

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

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

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

45 3 receptor-mediated calcium mobilization and GTPgammaS binding.

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

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

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

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

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

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

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

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

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

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

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

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

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

59 MMP14 activation by GTPgammaS is pertussis toxin-sensitive.

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

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

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

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

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

65 Furthermore, regulation of HA release by GTPgammaS or M2 expression was unaffected by cytosolic d

66 Assembly is also supported by GTPgammaS.

67 tubulation activity of OPA1 is suppressed by GTPgammaS.

68 re indicative of a hexamer and unaffected by GTPgammaS.

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

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

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

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

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

74 Conversely, GTPgammaS stimulated a low activity pool of PI4KIIalpha

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

76 = 1.15 nM) and full agonist activity (EC50 (GTPgammaS); D2 = 3.23 and D3 = 1.41 nM) at both D2 and D

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

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

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

80 d to detection of G proteins using BODIPY FL GTPgammaS as the fluorescent probe.

81 rophoresis buffer contained 250 nM BODIPY FL GTPgammaS.

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

83 on with the activated receptor and following GTPgammaS binding.

84 ructs, co-immunoprecipitation and assays for GTPgammaS binding.

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

86 al catalysis of thiophosphoryl transfer from GTPgammaS.

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

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

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

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

91 0 is slower in Galphai1*GDP than in Galphai1*GTPgammaS.

92 rodimer and production of functional Galphaq-GTPgammaS monomer.

93 observed in the crystal structure of Galphas-GTPgammaS.

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

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

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

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

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

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

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

101 3.5 A or better resolution, bound to GMPCPP, GTPgammaS, or GDP, either decorated with kinesin motor d

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

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

104 5, and -275 cal x mol(-1) x K(-1), with GTP, GTPgammaS, GDPNP, and GDP, respectively), associated wit

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

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

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

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

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

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

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

112 Because of their ability to inhibit GTPgammaS binding, preincubation of Cu(2+) or Zn(2+) wit

113 PM7 currents are suppressed by intracellular GTPgammaS, suggesting the involvement of heterotrimeric

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

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

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

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

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

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

120 ce and absence of 120 mM NaCl and 100 microM GTPgammaS.

121 o Ca(2+) (6.6 microm), Ca(2+) (0.2 microm) + GTPgammaS (1 mM), or in the absence of Ca(2+) after trea

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

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

124 (gp61) primase subunit, and nonhydrolyzable GTPgammaS.

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

126 hospholipids, Arf1p, and the nonhydrolyzable GTPgammaS.

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

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

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

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

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

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

133 ints such as ligand occupancy and binding of GTPgammaS.

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

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

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

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

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

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

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

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

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

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

144 2, and IL-8/CXCL8 by binding, stimulation of GTPgammaS exchange, and chemotaxis of mCXCR1-transfected

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

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

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

148 32 amino acids buried upon binding of GTP or GTPgammaS, respectively, and 15-19 amino acids upon bind

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

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

151 2+) or Zn(2+) with Galpha(s) does not permit GTPgammaS to activate Galpha(s) and stimulate AC activit

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

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

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

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

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

157 o kinase inhibitor Y27632 (1 microm) relaxed GTPgammaS and Ca(2+) contractures; but the latter requir

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

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

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

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

162 structures of the complex between Galpha(s).GTPgammaS and the catalytic C1 and C2 domains from type

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

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

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

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

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

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

169 55,940 displacement and its effect on [(35)S]GTPgammaS accumulation is substantially lower compared w

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

206 N/OFQ stimulated [(35)S]GTPgammaS binding in dog and CHO(hNOP) cell membranes co

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

238 -8BDelta9 isoform stimulated Galpha(s short) GTPgammaS binding only.

239 Stimulated GTPgammaS binding indicated that alpha2-adrenergic recep

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

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

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

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

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

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

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

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

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

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

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

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

252 34 nM, respectively) and high potency in the GTPgammaS assay (EC 50 = 1.6 and 4.1 nM, respectively) a

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

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

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

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

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

258 ited by guanosine 5'-O-(3-thiotriphosphate) (GTPgammaS) as well as under conditions known to negative

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

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

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

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

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

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

265 ns with guanosine 5'-3-O-(thio)triphosphate (GTPgammaS) and were facilitated nearly normally by depol

266 mulated guanosine 5'-3-O-(thio)triphosphate (GTPgammaS) binding and GIRK1/4 channel current effects i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

296 However, preincubation of Galpha(s) with GTPgammaS followed by addition of Cu(2+) or Zn(2+) did n

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