ライフサイエンスコーパス: GTP

1 GTP binding to these sensors results in a ratiometric ch

2 GTP cyclohydrolase 1 (GCH1) and its product tetrahydrobi

3 GTP is a major regulator of multiple cellular processes,

4 GTP-bound Rab5 GTPases accumulate in the encasement, but

5 TC) with eukaryotic initiation factor (eIF)2-GTP scans the mRNA leader for an AUG codon in favorable

6 pability, although the affinities toward m(7)GTP are significantly reduced when compared with FluA PB

7 omplex with a 5'TOP motif, a cap analog (m(7)GTP), and a capped cytidine (m(7)GpppC), resolved to 2.6

8 Rab GTPase family comprises approximately 70 GTP-binding proteins, functioning in vesicle formation,

9 on the surface of proteins, but it is also a GTP binding protein.

10 the closed conformation that functions as a GTP-binding GTPase and is required for cancer stem cell

11 0(-11)), a variant of ARL15, which encodes a GTP-binding protein.

12 d revealing a distinct mode of control for a GTP-binding protein.

13 aining KIF21B tail displays preference for a GTP-type over a GDP-type microtubule lattice and contrib

14 the vertebrate orthologue of Sey1p, forms a GTP-hydrolysis-dependent network on its own, serving as

15 e found that Arl4C interacted with FLNa in a GTP-dependent manner and that FLNa IgG repeat 22 is both

16 in-like FtsZ protein, which polymerizes in a GTP-dependent manner to form the cytokinetic Z ring.

17 st that rapid 50S subunit joining involves a GTP- and fMet-tRNA(fMet)-dependent "activation" of IF2,

18 d from depolymerization by the presence of a GTP or GDP/Pi cap.

19 drial elongation in MFN1, probably through a GTP-loading-dependent domain rearrangement.

20 nt the crystal structure of N-Ras bound to a GTP analogue and interpret the kinetic data in terms of

21 he bacterial G protein FeoB that undergoes a GTP-driven conformational change.

22 nating between inactive GDP-bound and active GTP-bound conformation.

23 tching between inactive GDP-bound and active GTP-bound forms.

24 variants with known inactive GDP- and active GTP-bound RAB11B mutants, we modeled the variants on the

25 RNA in the context of translationally active GTP.EF-Tu.tRNA ternary complexes.

26 expressing wild type, constitutively active (GTP bound), or dominant-negative (GDP bound) rab17.

27 GTP levels and increased amounts of active (GTP-bound) RAC1, RHO-A and RHO-C.

28 hat Rab2 binds to HOPS, and that its active, GTP-locked form associates with autolysosomes.

29 ligands (intrabodies) that recognize active, GTP-bound K- and H-Ras.

30 ed peptides that bind selectively to active, GTP-bound Ral proteins and that compete with downstream

31 transglutaminase (tTG) is an acyltransferase/GTP-binding protein that contributes to the development

32 l overgrowth, but how these mutations affect GTP catalysis is poorly understood.

33 les around the IT, but mutations that affect GTP hydrolysis or GTP/GDP exchange modified this localiz

34 iments using a mutant form of ARF1 affecting GTP hydrolysis suggest that ARF1[GTP] is functionally re

35 ) 0.007 to 0.016 min(-1)], without affecting GTP or GDP dissociation kinetics [koff = 0.093 and 0.148

36 dissociation of GT into its component alphaT-GTP and beta1gamma1 subunit complex.

37 matic l-amino acid decarboxylase (AADC), and GTP cyclohydrolase I (GCH1) transcription; increases str

38 catalytic activity, substrate affinity, and GTP sensitivity and validated this finding in cells.

39 and AMP involved in the synthesis of ATP and GTP, prompting us to investigate ADS lyase in C. neoform

40 dY is a branched-chain amino acid (BCAA) and GTP sensor and a global regulator of transcription in lo

41 bation of UreG with nickel, bicarbonate, and GTP.

42 ction associated with EB protein binding and GTP hydrolysis.

43 aperones, termed cofactors A-E (TBCA-E), and GTP are required for the folding of alpha- and beta-tubu

44 in their GTP-binding, GDP/GTP-exchange, and GTP-hydrolysis activities, but the extent to which these

45 of Ca(2+)/CaM on the interaction of GDP- and GTP-loaded K-Ras4B with heterogeneous model biomembranes

46 itochondria via combined oligomerization and GTP hydrolysis.

47 ortant identifiers are phosphoinositides and GTP-bound GTPases, which provide well-defined but mutabl

48 ibitor binding at the transamidase site, and GTP binding is blocked because inhibitor interaction at

49 samidase site, inhibit both transamidase and GTP-binding activities.

50 1 affecting GTP hydrolysis suggest that ARF1[GTP] is functionally required for the tubules to form.

51 h the proposed GAP role for ELMOD1, the ARF6 GTP/GDP ratio was significantly elevated in rda/rda utri

52 ompared with controls, and the level of ARF6-GTP was correlated with the severity of the rda/rda phen

53 a-specific deletions of ARL13b in which ARL3-GTP formation is impaired.

54 Arl6*GTP does not affect these interactions, suggesting no di

55 Even though all impair GAP-assisted GTP --> GDP hydrolysis, the mutation frequencies of K-Ra

56 rements of a G-quadruplex that can both bind GTP and promote peroxidase reactions.

57 netochores using its TOG domains, which bind GTP-tubulin, a coiled-coil homodimerization domain, and

58 nical G-G-G-G tetrads in the context of both GTP-binding and peroxidase activity.

59 crossover conformational shift, catalyzed by GTP hydrolysis, that converts the dimer from a "prefusio

60 d lipid mixing are catalyzed concurrently by GTP hydrolysis but that the energy requirement for lipid

61 ivated by a conformational change induced by GTP-binding, allowing interactions with downstream effec

62 ted current by noradrenaline was mediated by GTP binding proteins, and was highly dependent on calciu

63 around bacterial Z-rings that is powered by GTP hydrolysis and guides correct septal cell wall synth

64 BH4 is regulated by GTP cyclohydrolase 1, the rate-limiting enzyme in BH4 bi

65 PDE activity is allosterically regulated by GTP, further linking c-di-GMP levels to nutrient availab

66 RalGDS-RBD as a bait to selectively capture GTP-bound active Rap1.

67 0/FOP complex and then specifically captures GTP-bound RABL2B, which is activated via its intrinsic n

68 The G-domain, which catalyzes GTP hydrolysis and mediates downstream signaling, is 95%

69 ecific affinity of Cdc11 for transient Cdc12*GTP drive assembly of distinct trimers, Cdc11-Cdc12-Cdc3

70 rization is associated with a focus of Cdc42*GTP which is thought to self sustain by recruiting a com

71 dimer-dimer association to solution changes (GTP/GDP, urea, and trimethylamine oxide).

72 one key residue difference in the consensus GTP-binding motifs.

73 Decreasing the cytosolic GTP:GDP ratio increases the incorporation of Shs1 vs Cdc

74 ut how fission is mediated is still debated: GTP energy could be spent in membrane constriction requi

75 l, enhanced binding to RABGDI, and decreased GTP loading of RAB7 and RAB8.

76 kinase that regulates PI(5)P levels, detects GTP concentration and converts them into lipid second me

77 Actin has a biphasic effect on Drp1 GTP hydrolysis, increasing at low actin:Drp1 ratio but r

78 ing, leading to a monomer-dimer cycle during GTP hydrolysis.

79 e MT surface is biased away from the dynamic GTP-rich MT tip.

80 We show that in fibroblasts, dynamin GTP hydrolysis occurs as stochastic bursts, which are ra

81 To follow dynamin GTP hydrolysis at endocytic pits, we generated a conform

82 eIF2-GTP binds Met-tRNAi to form the eIF2-GTP*Met-tRNAi terna

83 ion by restricting the levels of active eIF2-GTP/Met-tRNAi ternary complexes (TC).

84 P, reaction intermediates, apo-eIF2 and eIF2-GTP, and product, TC, with direct implications for the e

85 at eIF2B can compete with Met-tRNAi for eIF2-GTP and can destabilize TC.

86 for TC and identify that phosphorylated eIF2-GTP translation initiation intermediate complexes can be

87 eIF2-GTP binds Met-tRNAi to form the eIF2-GTP*Met-tRNAi ternary complex (TC), which is recruited t

88 re-initiation complex (PIC) bearing the eIF2.GTP.Met-tRNAi(Met) ternary complex (TC) scans the mRNA f

89 otein partner eIF2 via interaction with eIF2.GTP at an early step in translation initiation.

90 and characterization of genetically encoded GTP sensors, which we constructed by inserting a circula

91 s ARL2, and not beta-tubulin, that exchanges GTP in the trimer.

92 Following GTP hydrolysis, eIF2-GDP is recycled back to TC by its g

93 EF-Tu-GDP-Pi-Lys-tRNA(Lys) complex following GTP hydrolysis by EF-Tu.

94 kinetics [koff = 0.093 and 0.148 min(-1) for GTP and GDP, respectively).

95 d "undruggable" due to its high affinity for GTP and its lack of hydrophobic binding pockets.

96 hat revealed an increase in the affinity for GTP by ARL2 in the trimer.

97 troduced into FeoB to alter its affinity for GTP created a series of sensors with a wide dynamic rang

98 domain of the protein that are critical for GTP and receptor binding.

99 the GPCR catalyzing the exchange of GDP for GTP on the heterotrimeric G protein transducin (GT).

100 omplex or influence the affinity of MeaB for GTP but is required for transducing signals between MeaB

101 APs exhibit a distinctly high propensity for GTP misincorporation opposite dT, predicting frequent A-

102 oop of the 50S subunit, activating EF-Tu for GTP hydrolysis and enabling accommodation of the aminoac

103 Septins are filament-forming GTP-binding proteins involved in many essential cellular

104 side include tubulin-like FtsZ, which forms GTP-dependent protofilaments, and actin-like FtsA, which

105 ish conditions for efficient initiation from GTP to form the dinucleotide and subsequent intermediate

106 ation of dihydroneopterin 3'triphosfate from GTP, producing BH4 after two further steps catalyzed by

107 that combinatorial bioactive botanicals from GTPs and BSp are highly effective in inhibiting ERalpha-

108 the equilibrium binding of FtsZ-GDP and FtsZ-GTP to ZipA immobilized at controlled densities on the s

109 of oligomers of free FtsZ-GDP and free FtsZ-GTP formed in solution.

110 to be saturable, whereas in the case of FtsZ-GTP equilibrium binding appears to be saturable.

111 lized and bundled straight filaments of FtsZ-GTP, but also stabilized the highly curved filaments and

112 drives SNARE-mediated fusion, which is fully GTP-dependent.

113 Further GTP hydrolysis triggers local outer membrane fusion at t

114 Furthermore, GTP-bound Rap1 promoted tight junction assembly, and los

115 at binds with a KD of 2.1muM to H-Ras(G12V) (GTP), excellent state selectivity, and remarkable specif

116 een Gbetagamma-promoted adhesion and Galphai-GTP reversal of adhesion is important for this process.

117 ndicates that adhesion regulation by Galphai-GTP occurs downstream of Rap1a and Radil, but is upstrea

118 These data identify a novel role of Galphai-GTP in regulation of cell adhesion and migration.

119 Galphai1 expression, suggesting that Galphai-GTP also regulates adhesion in immune cells at the level

120 ental syndrome, likely caused by altered GDP/GTP binding that inactivate the protein and induce GEF b

121 subtle differences in their GTP-binding, GDP/GTP-exchange, and GTP-hydrolysis activities, but the ext

122 lexes activate Rab GTPases by catalyzing GDP/GTP nucleotide exchange.

123 report here that SmgGDS does not mediate GDP/GTP exchange on DiRas1.

124 ry structure, induced by the binding of GMP, GTP, or ATP to the GMPR CBS domain.

125 ly exclusive, as the closed conformation has GTP binding/GTPase activity, and the open conformation t

126 atypical beta subunit of the heterotrimeric GTP-binding proteins (Gbeta5).

127 1 in T-ALLs results in a constitutively high GTP-loading rate of Ras, which is constantly counterbala

128 s of its catalytic machinery and explain how GTP binding induces conformational changes to promote GT

129 Our findings explain how GTP hydrolysis controls septin assembly, and uncover mec

130 e a model of IF2 activation that reveals how GTP, fMet-tRNA(fMet), and specific structural elements o

131 as a nucleotide-free monomer that hydrolyzes GTP and readily binds its analog guanosine 5'-3-O-(thio)

132 lation of Rho GTPase (enzyme that hydrolyzes GTP) activity.

133 tent of this biopterin increases with age in GTP cyclohydrolase 1-deficient hyperphenylalaninemia-1 (

134 e for detection of spatiotemporal changes in GTP levels in living cells and for high-throughput scree

135 internally normalized response to changes in GTP levels while minimally perturbing those levels.

136 s at dynamic ends suggests no differences in GTP cap sizes.

137 amidase site-specific inhibitors can inhibit GTP binding/signalling by driving a conformation change

138 f MITF results in elevation of intracellular GTP levels and increased amounts of active (GTP-bound) R

139 signaling by stimulating the slow intrinsic GTP hydrolysis (GTPase) reaction.

140 Moreover, in vitro tRNase activity is GTP-dependent, suggesting that CdiA-CT(EC869) only cleav

141 We now reveal that INM targeting is GTP-dependent.

142 ivity of hTG2 and allosterically abolish its GTP binding ability with a high degree of selectivity an

143 ort that methylation of septin2 affected its GTP binding activity and formation of the septin2-6-7 co

144 ine nucleotide exchange factor (GEF) for its GTP-binding protein partner eIF2 via interaction with eI

145 (CRF1) is sex biased whereby coupling to its GTP-binding protein, Gs, is greater in females, whereas

146 to promote purine salvage pathways, maintain GTP homeostasis and ensure continued (p)ppGpp synthesis.

147 both GEF-mediated exchange and GAP-mediated GTP hydrolysis, consistent with NMR-detected structural

148 oughput screening of molecules that modulate GTP levels.

149 tubulin cofactors and Arl2 as a multisubunit GTP-hydrolyzing catalytic chaperone that cycles to promo

150 lso compounds found exclusively with the new GTP hydrolysis monitoring-based GTPase cycling assay.

151 the newly identified small GTPase, Nucleolar GTP-binding protein 1 (NOG1), functions for plant immuni

152 Addition of GTP or high levels of GMP induced a marked increase in a

153 siae form a tubular network upon addition of GTP.

154 NORD50A and SNORD50B increased the amount of GTP-bound, active K-Ras and hyperactivated Ras-ERK1/ERK2

155 We find that binding of GTP analogs leads to a rigid and closed arrangement of t

156 of GDP from Galpha and subsequent binding of GTP.

157 the three isoforms in intrinsic catalysis of GTP by Ras in the absence and presence of the Ras-bindin

158 ifically cleaves substrate in the context of GTP.EF-Tu.aa-tRNA complexes.

159 g to Rab3-GAP1, disrupting the conversion of GTP-Rab3a into GDP-Rab3a and thus impairing the docking

160 We find that cycles of GTP hydrolysis induce progressive formation of a docking

161 ut suggests they carry 25% of the energy of GTP hydrolysis as bending strain, enabling them to drive

162 ATLs harness the energy of GTP hydrolysis to initiate a series of conformational ch

163 es, but tools for quantitative evaluation of GTP levels in live cells have not been available.

164 ectly activated by cAMP promotes exchange of GTP in the small GTPase Rap1.

165 propose that EF-Ts promotes the formation of GTP.EF-Tu.tRNA ternary complexes, thereby accelerating s

166 itide 3-kinase enhancer (PIKE) is a group of GTP-binding proteins that belong to the subgroup of cent

167 ts the binding and induces the hydrolysis of GTP by the other.

168 lated proteins that couple the hydrolysis of GTP to specific molecular events on the ribosome.

169 RGS domains and accelerate the hydrolysis of GTP.

170 a high affinity, leading to an inhibition of GTP production.

171 ng BRAF mutants cause feedback inhibition of GTP-bound RAS, are RAS-independent and signal either as

172 Cell spreading and levels of GTP-bound RhoA were increased upon depletion of either R

173 Overexpression of GTP cyclohydrolase I (GCH1), the rate-limiting enzyme fo

174 Phosphorylation of ROC enhances its rate of GTP hydrolysis [from kcat (catalytic constant) 0.007 to

175 ng subunit, greatly accelerating the rate of GTP hydrolysis.

176 tric signal upon depletion or restoration of GTP pools.

177 a helical domain during different stages of GTP hydrolysis.

178 leotide, stabilizing the transition state of GTP hydrolysis and compensating for the lack of the aspa

179 romotes autolysosomal fusions unlike that of GTP-locked Rab7, suggesting that its amount is normally

180 e feature of Trl1 is its preferential use of GTP as phosphate donor for the RNA kinase reaction.

181 studies revealed the combinatorial diets of GTPs and BSp significantly inhibited breast tumor growth

182 in fission reaction is strictly dependent on GTP hydrolysis, but how fission is mediated is still deb

183 witch I mutations had only modest effects on GTP binding and on GTPase activity and did not perturb s

184 g activity of HflX on the 70S ribosome, only GTP can completely dissociate the 100S ribosome.

185 whereas it did not influence GDP binding or GTP hydrolysis.

186 but mutations that affect GTP hydrolysis or GTP/GDP exchange modified this localization.

187 LRRK2 from interacting with either Rab29 or GTP strikingly inhibit phosphorylation of a cluster of h

188 and suggests that CrSEPT may act as its own GTP-activating protein.

189 n-3-gallate (EGCG) in green tea polyphenols (GTPs) and sulforaphane (SFN) in broccoli sprouts (BSp) o

190 tial (GWP) and global temperature potential (GTP) metrics.

191 mbranes of dense-core vesicles, and prevents GTP-Rab3a from binding to Rab3-GAP1, disrupting the conv

192 RK2 R1441G/C and Y1699C mutants that promote GTP binding are more readily recruited to the Golgi and

193 Complementary proteoliposomes bearing a Rab:GTP and either the vacuolar R-SNARE or one of the three

194 these actions through interaction with Rab3A-GTP and synapsin proteins.

195 Rab6a-GTP, either in solution or bound to artificial liposomes

196 e endosome function under regulation of Rab7-GTP.

197 of MR in SMCs blunted the production of Rac1-GTP after IR.

198 , ischemic kidneys had higher levels of Rac1-GTP, required for NADPH oxidase activation, than sham co

199 nstruct the assembly of the full-length RagA(GTP):RagC(GDP) dimer bound to Ragulator at 16 A resoluti

200 ts different complexes, bound either to Ran (GTP/GDP) or tRNA or both.

201 Ran-GTP can promote microtubule nucleation near chromatin, b

202 linking viral RNAs to the cellular CRM1/Ran-GTP nuclear export machinery through the activity of Rev

203 We found that decreasing Ran-GTP levels or tethering active Ran to the equatorial mem

204 y upregulated by the chromatin-dependent Ran-GTP pathway.

205 suggest a molecular mechanism of how the Ran-GTP gradient can regulate TPX2-dependent MT formation.

206 ntrast, Galphai1(Q204L) did not reverse Rap1-GTP-interacting adaptor molecule (RIAM)-dependent increa

207 Rapid GTP hydrolysis by monomeric Cdc10 drives assembly of the

208 0E dimerization directly or by elevating RAS-GTP.

209 f inhibitor-induced formation of the RAF/RAS-GTP complex.

210 bind more tightly than wild-type BRAF to RAS-GTP, and their binding to and activation of wild-type CR

211 f SOS to the membrane through binding of Ras.GTP in the SOS allosteric binding site.

212 y, we also observe HVR-autoinhibited K-Ras4B-GTP states, with GDP-bound-like orientations of the heli

213 DeltaCTL also displays a reduced GTP hydrolysis rate compared with WT, but this altered a

214 se binds with high affinity to and regulates GTP hydrolysis in the cpSRP54.cpFtsY complex, suggesting

215 The mechanism of vinylphosphonate REM-GTP is discussed in detail for initiation and propagatio

216 observations suggest that the toxin remodels GTP.EF-Tu.aa-tRNA complexes to free the 3'-end of aa-tRN

217 In contrast, simvastatin did not change Rho-GTP loading in A549 and MDA-MB-231.

218 Simvastatin-induced Rho-GTP loading significantly increased in U251 cells which

219 indicate that Myo9b-RhoGAP accelerates RhoA GTP hydrolysis by a previously unknown dual-arginine-fin

220 bitory phosphorylation of RhoA, reduced RhoA GTP-loading and reversal of myosin light chain phosphory

221 Anillin contains a RhoA-GTP binding domain, which autoinhibits the NLS and the n

222 essed bradykinin-induced RhoA activity (RhoA-GTP content).

223 hboring microtubule-binding domain, and RhoA-GTP binding may relieve this inhibition during mitosis.

224 nhibition of ARF1 led to an increase in RhoA-GTP levels and triggered assembly of myosin-IIA filament

225 The increased RhoA-GTP results from AKT phosphorylating three serines (S298

226 hich interferes with the interaction of RhoA-GTP with the RhoGAP domain, reduces the hydrolysis of Rh

227 hoGAP domain, reduces the hydrolysis of RhoA-GTP, the binding of other DLC1 ligands, and the colocali

228 essed the effects of BK and TGF-beta on RhoA-GTP content, RhoA translocation and MYPT1 and MLC20 phos

229 on, but suppressed the effects of BK on RhoA-GTP content, SrcFK auto-phosphorylation and cofilin de-p

230 Additionally, we identified that RhoA-GTP could be a potential regulator in MSI1/TNS3-mediated

231 1, but independently of SrcFK and total RhoA-GTP content.

232 ainst disassembly in the absence of a robust GTP cap.

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

234 ious sizes as a lipid bilayer model, we show GTP-dependent membrane binding of hGBP1F In addition, we

235 We show GTP-induced dynamic rearrangements of the dynamin helix

236 SI-GTP is presented as a method for surface functionalizati

237 Lack of compaction might reflect slower GTP hydrolysis or a different degree of allosteric coupl

238 The ARL15 gene encodes a small GTP-binding protein whose function is currently unknown.

239 the post-translational prenylation of small GTP-binding proteins such as Rho and Rac, and their down

240 ASA1), a negative regulator of the Ras small GTP-binding protein.

241 tivating protein in hair cells for the small GTP-binding protein ARF6, known to participate in actin

242 The small GTP-binding protein Rab12 plays an important role in the

243 We now show that the small GTP-binding protein Rap2A is the obligate effector for,

244 n of the toxin domain onto previously solved GTP.EF-Tu.aa-tRNA structures reveals potential steric cl

245 1, but not ROCK2, was necessary to stabilize GTP-RhoA at the ZA, thereby sustaining junctional tensio

246 urs when a microtubule loses its stabilizing GTP cap.

247 ation, KRAS K104Q did not alter steady-state GTP-bound levels or the ability of the oncogenic KRAS G1

248 onformation change that disorganizes the TG2 GTP binding to reduce TG2-dependent signalling, and that

249 gnaling in exosome biogenesis, we found that GTP binding of K-Ras was dispensable for its packaging w

250 dSar1:T34N) mutants of LdSar1, we found that GTP-bound LdSar1 specifically binds to LdSec23, which bi

251 n an in vitro budding assay, indicating that GTP-bound LdSar1 is required for budding of Ldgp63-conta

252 We recently showed that GTP binding, but not transamidase activity, is required

253 Our findings suggest that GTP caps retain the filament helical structure and hydro

254 The GTP-binding domain of CrSEPT purified as a nucleotide-fr

255 We predicted that both variants alter the GTP/GDP binding pocket and show that they both have loca

256 yphosphate 5'-phosphatase E (INPP5E) and the GTP-binding protein (Rheb) that cargo sorting depends on

257 eliminates the energy difference between the GTP- and GDP-tubulin thermodynamic states.

258 ation of the ARF domain is essential for the GTP hydrolysis activity of TRIM23 and activation of TANK

259 n conformation to disorganize/inactivate the GTP binding/GTPase site.

260 Slower elongation led to erosion of the GTP cap and an increase in the frequency of catastrophe.

261 Arhgap1, which resulted in activation of the GTP-binding Rho family protein Cdc42 and accounted for h

262 cytoskeletal dynamics via activation of the GTP-binding Rho family protein Cdc42 by the guanine nucl

263 pled to GTPase activity, supporting that the GTP energy is primarily spent in constriction.

264 taphylococcus aureus We demonstrate that the GTP synthesis enzymes HprT and Gmk bind with a high affi

265 ipermeabilized cells and is sensitive to the GTP analogue GTPgammaS.

266 ; 2) antimorphic mutations, which map to the GTP binding site and intradimer and interdimer interface

267 lled dynab, that binds preferentially to the GTP hydrolytic state of dynamin-1.

268 tive site shows structural similarity to the GTP-binding site of MoaA, suggesting that the viperin su

269 , Exo70, and Sec5 bind preferentially to the GTP-bound form of Arl13b, consistent with the exocyst be

270 vated during catalytic turnover by using the GTP-binding energy to offload inactive cofactor.

271 Their GTP/GDP cycle is often tightly connected to a membrane/c

272 proteins exhibit subtle differences in their GTP-binding, GDP/GTP-exchange, and GTP-hydrolysis activi

273 only upon activation and conversion to their GTP-bound state are they anchored to membranes through m

274 We show that these GTP evaluators (GEVALs) are suitable for detection of sp

275 that this domain specifically contributed to GTP binding, whereas it did not influence GDP binding or

276 ysin, a subunit of BORC, promotes the GDP-to-GTP exchange of ARL-8 in vitro and recruits ARL-8 onto S

277 nt why the TS for guanosine 5'-triphosphate (GTP) hydrolysis is higher in energy when RhoA is complex

278 igands increase RhoA-guanosine triphosphate (GTP) in untransformed and transformed cell lines and det

279 that the binding of guanosine triphosphate (GTP) to one subunit inhibits the binding and induces the

280 P, which regenerates guanosine triphosphate (GTP), powers ribosomes, and promotes transcription of rR

281 hat TBSV co-opts the guanosine triphosphate (GTP)-bound active form of the endosomal Rab5 small GTPas

282 creased the level of guanosine triphosphate (GTP)-bound ARF1.

283 rmational change in response to beta-tubulin GTP hydrolysis [2, 3].

284 We demonstrate that using a unique GTP-specific antibody fragment to monitor GTPase cycling

285 Upon GTP hydrolysis, dynamin breaks these necks, a reaction c

286 face as seen for mammalian microtubules upon GTP hydrolysis.

287 P-bound states, while it forms monomers upon GTP binding, leading to a monomer-dimer cycle during GTP

288 y, and the ability of casein kinase 2 to use GTP as a phosphate donor, may be a source of differences

289 TOR ROP2 physically interacts with and, when GTP-bound, activates TOR in vitro TOR activation in resp

290 The tubules rapidly fragment when GTP hydrolysis of Sey1p is inhibited, indicating that ne

291 target of rapamycin complex 1 (mTORC1) when GTP loaded.

292 yltransferase domain into the cytosol, where GTP-binding proteins of the Rho/Ras family are mono-O-gl

293 ATP promotes octamer polymerization, whereas GTP promotes a compact, inactive conformation whose abil

294 f the coenzyme NADH alone or in concert with GTP results in a binary mixture in which the enzyme is i

295 celerating the replacement of bound GDP with GTP.

296 show the PBM directs interaction of p14 with GTP-Rab11.

297 The loading of Ran with GTP, which is mediated by RCC1, the guanine nucleotide e

298 average distances between turns reduce with GTP hydrolysis.

299 HOPS binding to Ypt7-GTP then drives SNARE-mediated fusion, which is fully GT

300 mbranes to which the R- or Qa-SNARE and Ypt7:GTP are integrally bound, and each of the other three SN