ライフサイエンスコーパス: GTP-gamma-S

1 GTP gamma S does not affect vesicle binding to chromatin

2 GTP gamma S-activated cytosol stimulated PLD activity an

3 GTP gamma S-stimulated intrinsic fluorescence changes we

4 GTP gamma S.Mg2+-bound complex of Gi alpha 1, with a sim

5 GTP-gamma-S [guanosine-5'-0-(2-thiotriphosphate)] (2 mM)

6 GTP-gamma-S enhanced the amplitude of glycine-induced cu

7 GTP-gamma-S functional assays showed 13 to be a selectiv

8 GTP-gamma-S produced persistent excitation after a flash

9 ligand of the gamma-phosphate of Gi alpha 1.GTP gamma S.Mg2+.

10 In particular, Mg(2+)GTP gamma S and Mg(2+)ATP gamma S inhibited cyclase acti

11 [35S]GTP gamma S autoradiography revealed that most of this a

12 ithout any significant changes on basal [35S]GTP gamma S binding (152.1 +/- 10.7 for control, 147.4 +

13 Release of bound [35S]GTP gamma S from ARF3 required the presence of both GEP

14 ivation of G-proteins was determined by [35S]GTP gamma S autoradiography of brain and spinal cord.

15 In spinal cord membranes, [35S]GTP gamma S binding was stimulated by agonists of severa

16 ist UK14304 to stimulate the binding of [35S]GTP gamma S to the modified G proteins was measured.

17 onist-induced stimulation of binding of [35S]GTP gamma S to the mutant G proteins also correlated wit

18 ere no effects of morphine treatment on [35S]GTP gamma S stimulation in spinal cord by other receptor

19 affinity shift in the binding of GTP (or[35S]GTP gamma S) versus GDP to the G protein and by the numb

20 g against [3H] NC), functional potency ([35S]GTP gamma S), and efficacy (as compared to NC) were perf

21 in the KD values of agonist-stimulated [35S]GTP gamma S binding between high efficacy agonists (DAMG

22 ne treatment decreased DAMGO-stimulated [35S]GTP gamma S binding in laminae I and II at all levels of

23 ion analysis of net CP55,940 stimulated [35S]GTP gamma S binding in SPM showed that the Bmax of canna

24 ical specificity of CP55,940 stimulated [35S]GTP gamma S binding in SPM was examined with CB1 recepto

25 of basal and opioid receptor-stimulated [35S]GTP gamma S binding in the presence of excess GDP.

26 atchard analysis of net agon stimulated [35S]GTP gamma S binding revealed two major components respon

27 dies indicated that CP55,940 stimulated [35S]GTP gamma S binding was blocked by SR141716A with a decr

28 dicate that the net CP55,940 stimulated [35S]GTP gamma S binding was increased with increasing concen

29 is net CP55,940 (1.5 microM) stimulated [35S]GTP gamma S binding was reduced significantly (-25%) in

30 in the Bmax value of agonist-stimulated [35S]GTP gamma S binding were observed between DAMGO and morp

31 This method is rapid compared to the [35S]GTP gamma S binding assay in that (i) the bound ligand d

32 nosine-5'-O-(3-[35S]thio)-triphosphate ([35S]GTP gamma S) binding in SPM from mouse.

33 anosine-5'-O-(gamma-thio)-triphosphate ([35S]GTP gamma S) binding to membranes in the presence of exc

34 nosine 5'-[gamma[35S]thio]triphosphate ([35S]GTP gamma S) by ARF1 and ARF3 was equally high without a

35 a mu-, delta-, and kappa-antagonist in [35S]GTP-gamma-S assays and was approximately 50 times more p

36 h measured stimulation or inhibition of [35S]GTP-gamma-S binding, we show that the trans-cinnamyl ana

37 and C6G analogues was examined with the [35S]GTP-gamma-S assay.

38 kappa opioid receptor antagonist in the [35S]GTP-gamma-S in vitro functional test.

39 al agonist activity for D3 receptor (EC(50) (GTP gamma S); D3 = 0.52 nM; D2/D3 (EC(50)): 223).

40 the ligand dissociation kinetics or induce a GTP gamma S-sensitive state of the phosphorylated FPR.

41 In response to a GTP gamma S stimulus we found that the time integral of

42 Supporting this notion, G beta h accelerated GTP gamma S release from G alpha h and changes the affin

43 rom cells exposed to the G protein activator GTP-gamma-S exhibited an approximately 2-fold increase i

44 beta-S) or irreversible G protein activator (GTP-gamma-S) suggesting a G protein-independent mechanis

45 er stimulation with the G-protein activators GTP gamma S and AlF(4) and with the second messenger 1,2

46 eceptor-G protein coupling (GTPase activity, GTP gamma S binding), tetGS alpha can facilitate the stu

47 he rates of transducin activation (GT(alpha)-GTP gamma S complex formation) were measured for all the

48 The GTP analog GTP gamma S potently inhibits nuclear envelope assembly

49 Under similar conditions, the GTP analogs GTP-gamma-S and GDP-beta-S failed to block endocytosis,

50 d by the nonhydrolyzable nucleotide analogue GTP gamma S, whereas the second stage is nucleotide inde

51 ted by GTP and its non-hydrolysable analogue GTP-gamma-S, but not by GDP.

52 Application of E2-BSAout and GTP gamma S(in) potentiated kainate-induced currents.

53 t I/-46GUS with oat phytochrome A (phyA) and GTP gamma S, an activator of heterotrimeric G proteins.

54 ivation of adenylyl cyclase by receptors and GTP gamma S (a non-hydrolyzable GTP analogue) is reduced

55 0 nM) inhibited both the actions of 5-HT and GTP-gamma-S.

56 renol in the presence of a PKA inhibitor and GTP-gamma-S in LDS but not VEDS cardiomyocytes, suggesti

57 guanine nucleotide analogues (GDP-beta-S and GTP-gamma-S) and pertussis toxin (PTX) treatment demonst

58 The mutants bound GTP gamma S with high affinity and showed only modest ch

59 as bypassed and the channel was activated by GTP gamma S.

60 NTES-induced PLD activation was augmented by GTP gamma S, but not GDP beta S, and inhibited by the pr

61 The displacement of specific binding by GTP gamma S suggests that the prokineticin receptor may

62 ilar effects on the cation current evoked by GTP gamma S.

63 ed) the acute Ca2+ sensitization of force by GTP gamma S, AIF-4, phenylephrine, and endothelin, but n

64 Endosome fusion was strongly inhibited by GTP gamma S, N-ethylmaleimide, and AIF4-.

65 Fusion inhibition by GTP gamma S is mediated by a soluble factor, initially n

66 Mn(2+) blocked AC inhibition by GTP gamma S/GppNHp in S49 cyc(-) membranes but enhanced

67 surements to 1.3 microM during regulation by GTP gamma S.

68 generation, even when this was sustained by GTP gamma S and ATP levels reduced far below the K(m) of

69 When G proteins are maximally activated by GTP-gamma-S, the action of ethanol was partially occlude

70 stant to ethanol and G-protein activation by GTP-gamma-S.

71 it was blocked by barium in the bath and by GTP-gamma-S in the pipette, suggesting activation of a G

72 tor greatly reduced the excitation caused by GTP-gamma-S injection.

73 release is stimulated by either Ca(++) or by GTP-gamma-S.

74 inositol (PI) stimulated by phospholipase C, GTP-gamma-S, NaF, and neurotransmitter receptor agonists

75 D-induced current whilst photolysis of caged GTP gamma S inside neurones irreversibly potentiated thi

76 Caged GTP-gamma-S released by flash photolysis reduced the sHV

77 min after patch rupture by photolysing caged GTP-gamma-S included in the pipette solution.

78 on is irreversible when the pipette contains GTP-gamma-S.

79 red (broken) 3T3L1 adipocytes also displayed GTP gamma S and sodium orthovanadate stimulation of acti

80 of exocytosis induced by infusion of either GTP gamma S or Ca2+, suggesting both stimuli involve G-p

81 Moreover exchange of GDP for GTP gamma S was also monitored by PWR spectroscopy.

82 ed by a soluble factor, initially named GSF (GTP gamma S-dependent soluble factor).

83 modified either by cytosolic Na+, ATP, GTP, GTP gamma S, dithiothreitol or TEA (10 mM) or by extrace

84 However, GTP gamma S binding induced by CCK-8 and vasoactive inte

85 In GTP gamma S binding assays, both regions exhibit guanine

86 By contrast, in GTP-gamma-S-loaded cells, R(N) was consistently decrease

87 ma S/MANT-GppNHp non-competitively inhibited GTP gamma S/GppNHp-, AlF(4)(-)-, beta(2)-adrenoceptor pl

88 At -60 mV, internal GTP-gamma-S led to the generation of spontaneous activit

89 e potentiated and prolonged by intracellular GTP gamma S.

90 entional whole-cell recordings intracellular GTP-gamma-S caused current up-regulation, an effect inhi

91 MANT-GTP gamma S and MANT-GppNHp competitively inhibited fors

92 MANT-GTP gamma S was much less effective than GTP gamma S at

93 MANT-GTP gamma S/MANT-GppNHp had lower affinities for G alpha

94 MANT-GTP gamma S/MANT-GppNHp non-competitively inhibited GTP

95 AC inhibition by MANT-GTP gamma S/MANT-GppNHp was not due to G alpha(s) inhibi

96 Collectively, MANT-GTP gamma S/MANT-GppNHp bind to G alpha(s)- and G alpha(

97 Instead, MANT-GTP gamma S/MANT-GppNHp constitute a novel class of pote

98 ) membranes but enhanced the potency of MANT-GTP gamma S/MANT-GppNHp at inhibiting AC by approximatel

99 -guanosine 5'-[gamma-thio]triphosphate (MANT-GTP gamma S) and MANT-guanosine 5'-[beta,gamma-imido]tri

100 ce signal from binding of methylanthraniloyl-GTP gamma S (mGTP gamma S).

101 by either 0.5 microM carbachol or 100 microM GTP gamma S.

102 Incubation of membranes with 100 microM GTP-gamma-S did not alter the IC(50) for CD in the prebi

103 ice, amylase secretion induced by 100 microM GTP-gamma-S was enhanced by 150%, and 10 microM Ca2+-sti

104 g.ATP, 1.2 mM free [Mg(2+)](i) or 100 microM GTP-gamma-S, allowing investigations on these currents i

105 Activation of G proteins with 2 mM GTP-gamma-S attenuated, but did not eliminate, ethanol-i

106 h interfere with nuclear pore assembly, NEM, GTP gamma S, and the Ca++ chelator, BAPTA.

107 TPA, but not GTP-gamma-S, also increased insulin release when [Ca2+]

108 ced by 28.6 +/- 6.8 % 5-HT-mediated, but not GTP-gamma-S-induced, inhibition of Ca(2+) current, where

109 and PTX-sensitive inhibition of ICa but not GTP-gamma-S-mediated voltage-independent inhibition.

110 (-)-alprenolol and inhibited by addition of GTP gamma S, and [125I]IAS migrated at the same position

111 Intracellular application of GTP gamma S (10 microM) opened the Ca2+V-activated K+ ch

112 The GRPr-catalyzed binding of GTP gamma S is selective for G alpha q, since we did not

113 used it to measure GRPr-catalyzed binding of GTP gamma S to purified G protein alpha subunits.

114 q showed that receptor-catalyzed binding of GTP gamma S was dependent on agonist (GRP) and G beta ga

115 The time course of GTP gamma S-driven secretion was concentration-independe

116 The mant derivative of GTP gamma S, mGTP gamma S, is synthesized and purified b

117 Intracellular dialysis of GTP gamma S (100 microM) also reduced NMDA whole-cell cu

118 e of exocytosis following rapid elevation of GTP gamma S by photolysis of a caged precursor was depen

119 f Ca(2+)-driven secretion was independent of GTP gamma S concentration, whereas the K(d) of the GTP g

120 The inhibition of GTP gamma S binding with the ternary complex requires a

121 We conclude that the loss of GTP gamma S- and agonist-induced Ca2+ sensitization thro

122 The presence of GTP gamma S blocks pore assembly at two distinct steps,

123 ilar values were obtained in the presence of GTP gamma S, suggesting GTP does not alter the sensitivi

124 sed from +63 mV to +48 mV in the presence of GTP gamma S.

125 one affinity (8.1 nmol/l) in the presence of GTP gamma S.

126 te of GDP binding was much less than that of GTP gamma S with and without GEP.

127 roteins Gi and G(o) is comparable to that of GTP gamma S.

128 oxytocin could be blocked by the addition of GTP-gamma-S to the recording pipette, suggesting activat

129 zed beta-cells was stimulated by addition of GTP-gamma-S, or by addition of a phorbol ester, 12-O-tet

130 (100 microM) or intracellular application of GTP-gamma-S.

131 Intracellular dialysis of GTP-gamma-S did not cause an up-regulation of persistent

132 The effects of GTP-gamma-S on R(N), V(th) and I(h) were partly countera

133 However, the inability of GTP-gamma-S (or GDP-beta-S) to eliminate completely the

134 Inclusion of GTP-gamma-S (500 microM) in the internal solution led to

135 Introduction of GTP-gamma-S into alpha1B cells greatly enhanced the exte

136 inergic receptor agonist) in the presence of GTP-gamma-S stimulated equivalent responses in the two g

137 phosphorylated equally well in their GDP- or GTP gamma S-bound forms.

138 GTP or GTP gamma S produced a concentration-dependent increase

139 he presence of both GEP and unlabeled GTP or GTP gamma S; GDP was much less effective.

140 E2 had no effect on either normal or GTP gamma S-increased Ca2+ sensitivity of the regulatory

141 r show that regardless of stimuli (Ca(++) or GTP-gamma-S) serotonin and hexosaminidase release requir

142 t 1 microm Ca2+ after incubation with GTP or GTP-gamma-S could mobilize approximately 90% of the tota

143 of the calcium chelator BAPTA, GDP-beta-S or GTP-gamma-S blocked the 5-HT-induced facilitation of the

144 y intracellular perfusing with GDP-beta-S or GTP-gamma-S.

145 The presence of purified GTP gamma S-activated alpha 11 subunits of heterotrimeri

146 We showed further that Rac2-GTP gamma S and to a lesser extent Rac2-GDP beta S could

147 alternative to assays based on radiolabeled GTP gamma S binding or ADP-ribosylation with pertussis t

148 beta ARK1 peptide reduced GTP-gamma-S-induced voltage-dependent and PTX-sensitive

149 Unexpectedly, PITP was also found to restore GTP gamma S-dependent secretion.

150 g and [(35)S]guanosine triphosphate gamma S (GTP gamma S) binding studies were performed.

151 (50) of opioid-induced stimulation of [(35)S]GTP gamma S binding by 3- to 10-fold to the left.

152 t G-protein activation as measured by [(35)S]GTP gamma S binding can be regulated by DAMGO and EGF by

153 ahydrocannabinol, failed to stimulate [(35)S]GTP gamma S binding in CB(1)(-/-) membranes.

154 nd I-TAC were agonists in stimulating [(35)S]GTP gamma S binding in recombinant cell and PBL membrane

155 The antibody attenuated [(35)S]GTP gamma S binding in response to IP-10 but not to I-TA

156 ocked subsequent DAMGO stimulation of [(35)S]GTP gamma S binding membranes, whereas [(35)S]GTP gamma

157 or WIN55212-2-induced stimulation of [(35)S]GTP gamma S binding only at concentrations greater than

158 concentration-dependent inhibition of [(35)S]GTP gamma S binding only in membranes prepared from cell

159 TP gamma S binding membranes, whereas [(35)S]GTP gamma S binding to membranes from cells expressing m

160 [(35)S]GTP gamma S binding was stimulated by anandamide and WIN

161 mide and 67% of WIN55212-2 stimulated [(35)S]GTP gamma S binding with an affinity appropriate for med

162 line receptor-mediated stimulation of [(35)S]GTP gamma S binding, suggesting a broader role for sigma

163 ated mu opioid-induced stimulation of [(35)S]GTP gamma S binding.

164 ssessed by the maximal stimulation of [(35)S]GTP gamma S binding.

165 tibody on I-TAC- and IP-10-stimulated [(35)S]GTP gamma S binding.

166 antagonists significantly stimulated [(35)S]GTP gamma S binding.

167 Finally, PTH stimulated [(35)S]GTP gamma S incorporation into G alpha(s) in a time- and

168 ine 5'-O-(3-[(35)S]thio)triphosphate ([(35)S]GTP gamma S) binding to membranes from cells expressing

169 ine 5'-O-(3-[(35)S]thio)triphosphate ([(35)S]GTP gamma S) binding, by sigma(1) receptors.

170 and selective kappa antagonism in the [(35)S]GTP-gamma-S assay using cloned opioid receptors (kappa K

171 ectivity at human CB2 receptors using [(35)S]GTP-gamma-S assays.

172 or functional activity in vitro using [(35)S]GTP-gamma-S binding assays in brain tissues and bioassay

173 In the [(35)S]GTP-gamma-S binding assays, most of these pyridomorphina

174 ntracellular calcium mobilization and [(35)S]GTP-gamma-S binding while enhancing [(3)H]CP55,940 bindi

175 Evaluation of 6a-g in the [(35)S]GTP-gamma-S in vitro functional assay showed that they w

176 ndicated by stimulation of binding of [(35)S]GTP-gamma-S.

177 tep in pore assembly occurs after the second GTP gamma S-sensitive step.

178 receptor as determined by agonist-stimulated GTP gamma S binding and GTPase activity.

179 ANT-GTP gamma S was much less effective than GTP gamma S at disrupting the ternary complex between th

180 ffinities for G alpha(s) and G alpha(i) than GTP gamma S/GppNHp as assessed by inhibition of GTP hydr

181 These results suggest that GTP-gamma-S and ethanol share the same pathway of activa

182 The GTP gamma S binding and GTPase activity of G alpha h are

183 The GTP gamma S binding by the ternary complex, consisting o

184 Down-regulation also abolished the GTP gamma S-induced increase in myosin light chain phosp

185 mma S concentration, whereas the K(d) of the GTP gamma S-driven response decreased from 63 to 31 micr

186 refrontal cortex (10), but not in (8/9), the GTP-gamma-S concentration-dependent stimulation of [3H]P

187 ase in [Ca++] but failed to block either the GTP-gamma-S-induced increase in I(K), the activation of

188 lmodulin with micromolar affinity, while the GTP-gamma-S-loaded catalytic domain of K-Ras4B may inter

189 analog guanosine 5'-0-(3 thiotriphosphate) (GTP gamma S) was diminished.

190 either guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S) or AlF-4 to stimulate G proteins resulted i

191 of GTP, guanosine-5'-O-(3-thiotriphosphate) (GTP gamma S), or [Ca(2+)](i) enhanced the amplitude and

192 such as guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S).

193 ation of guanosine 5-O-(3-thiotriphosphate) (GTP gamma S, 500 microM) evoked a 'noisy' inward current

194 uced by guanosine 5'-O-(3-thiotriphosphate) (GTP-gamma-S) in rat mast cells, introducing the protein

195 which cells lose their ability to respond to GTP-gamma-S.

196 as the guanosine 5'-3-O-(thio)triphosphate (GTP gamma S) sensitivity of the complex, as recently des

197 in a guanosine 5'-[gamma-thio]triphosphate (GTP gamma S) and sodium orthovanadate stimulation of act

198 ed by guanosine 5'-[gamma-thio]triphosphate (GTP gamma S) stimulation of adenosine diphosphate (ADP)-

199 with guanosine 5'-[gamma-thio]triphosphate (GTP gamma S; 5-16 h, 50 microM) of smooth muscle permeab

200 ce of guanosine 5'-O-(3-thio-trisphosphate) (GTP gamma S); they shifted to a model of one affinity (8

201 stigated under whole-cell patch clamp, using GTP-gamma-S (G-protein activator) or GDP-beta-S (G-prote

202 ir functional activities were measured using GTP-gamma-S accumulation and intracellular calcium mobil

203 To order the positions at which GTP gamma S and BAPTA interfere with pore assembly, a no

204 sociated from G alpha h upon activation with GTP gamma S or AlF4-.

205 Intracellular dialysis with GTP gamma S led to spontaneous inhibition and a slowing

206 Dialysis with GTP gamma S prevented reversal of the modulation, sugges

207 During intracellular dialysis with GTP gamma S to activate G-proteins, ionic currents demon

208 s were examined by EM after incubations with GTP gamma S.

209 t detected when the TGase is pre-loaded with GTP gamma S.

210 unaffected in cells internally perfused with GTP gamma S.

211 viously showed that vesicles pretreated with GTP gamma S plus recombinant mammalian ARF1 were inhibit

212 clear vesicle fusion after pretreatment with GTP gamma S.

213 omo-cAMP and by activation of G-protein with GTP gamma S.

214 cytosol-depleted cells when stimulated with GTP gamma S plus Ca2+.

215 (FMLP) or permeabilized PMNs stimulated with GTP gamma S, C2-ceramide did not inhibit RhoA translocat

216 lls to become refractory to stimulation with GTP gamma S plus 10 microM Ca2+ with regard to secretion

217 nsitization through prolonged treatment with GTP gamma S is not due to a decrease in the total conten

218 Perfusion of cells with GTP-gamma-S enhanced the facilitation of N-type channels

219 In cells dialyzed with GTP-gamma-S, bradykinin produced a total and irreversibl

220 , introducing recombinant Rab27A loaded with GTP-gamma-S into sperm elicited a remarkable increase in

221 t vesicle depletion after preincubation with GTP-gamma-S, whereas preincubation with GDP-beta-S left