ライフサイエンスコーパス: GTP hydrolysis

1 ss dependent on self-assembly and coupled to GTP hydrolysis.

2 e observed movement of domain IV of EF-G and GTP hydrolysis.

3 dal directional cue therefore requires Cdc42 GTP hydrolysis.

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

5 lved by expenditure of energy in the form of GTP hydrolysis.

6 GTP and, at the same time, compromising its GTP hydrolysis.

7 h is a noncanonical interface that regulates GTP hydrolysis.

8 catalytic residue (e.g. Ras Q61L) to impair GTP hydrolysis.

9 o GTPase-activating proteins and the rate of GTP hydrolysis.

10 a helical domain during different stages of GTP hydrolysis.

11 tivation of Ras family proteins by impairing GTP hydrolysis.

12 ions found in Ras-like GTPases that abrogate GTP hydrolysis.

13 3 in Rap into the active site for catalyzing GTP hydrolysis.

14 s G83 as the key RNA residue that stimulates GTP hydrolysis.

15 nslocon in a multistep process controlled by GTP hydrolysis.

16 , which leads to impaired regulator-mediated GTP hydrolysis.

17 nal rigidity and relaxation before and after GTP hydrolysis.

18 idation of a glutamine, which is crucial for GTP hydrolysis.

19 gation factor-G (EF-G) to the ribosome after GTP hydrolysis.

20 mp activity, cytosolic proteins, and ATP and GTP hydrolysis.

21 agnesium ion contributes to the catalysis of GTP hydrolysis.

22 face as seen for mammalian microtubules upon GTP hydrolysis.

23 ubunit, presumably due to the stimulation of GTP hydrolysis.

24 became rigidly stabilized in the absence of GTP hydrolysis.

25 ps governed by k(cat) in the LRRK2-catalyzed GTP hydrolysis.

26 brane fission without direct energy from ATP/GTP hydrolysis.

27 ing within the A site, both before and after GTP hydrolysis.

28 uriously, mutating the Thr appears to reduce GTP hydrolysis.

29 average distances between turns reduce with GTP hydrolysis.

30 itochondria via combined oligomerization and GTP hydrolysis.

31 ely disrupt the proper geometry required for GTP hydrolysis.

32 he ribosome is catalyzed by EF-G binding and GTP hydrolysis.

33 inal domain, whose positioning is coupled to GTP hydrolysis.

34 aneous nucleotide exchange coupled with slow GTP hydrolysis.

35 inated movements associated with EF-G-driven GTP hydrolysis.

36 hanges of ADPR-eEF2 that are due strictly to GTP hydrolysis.

37 ction associated with EB protein binding and GTP hydrolysis.

38 me, factor-bound pre-GTP hydrolysis and post-GTP hydrolysis.

39 ATP cannot circumvent processes that require GTP hydrolysis.

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

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

42 a GTP-bound form and subsequently catalyzes GTP hydrolysis.

43 789/Q61 organization, impairing GAP-mediated GTP hydrolysis.

44 facilitate spontaneous membrane fission upon GTP hydrolysis.

45 nformation and are resistant to GAP-mediated GTP hydrolysis.

46 ide exchange, whereas F82V and T83P impaired GTP hydrolysis.

47 ird, dynamin catalyzes membrane fission upon GTP hydrolysis.

48 d retention of free Crm1 at RanBP2 after Ran-GTP hydrolysis.

49 st be retained for uncompromised activity in GTP hydrolysis.

50 Galpha subunits are turned off by GTP hydrolysis.

51 is critically involved in the activation of GTP hydrolysis.

52 oting an intermediate state generated during GTP hydrolysis.

53 ement of GTPase-activating protein (GAP) and GTP hydrolysis.

54 due for carrying out guanosine triphosphate (GTP) hydrolysis.

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

56 rates of GDP release, GTP binding [2-8], and GTP hydrolysis[9, 10].

57 Thus, YlxM appears to modulate GTP hydrolysis, a process necessary for proper recycling

58 protein substrates revealed highest in vitro GTP hydrolysis-activating activity with Rab32 and Rab33B

59 elay that included a lag phase followed by a GTP hydrolysis activation step, until reaction reached t

60 corpse removal, dynamin's self-assembly and GTP hydrolysis activities establish a precise dynamic co

61 The GTP hydrolysis activities of Rho GTPases are stimulated

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

63 tein prenylation of small GTPases relates to GTP hydrolysis activity and downstream signaling.

64 In the absence of FtsY, YlxM increased the GTP hydrolysis activity of Ffh alone and in complex with

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

66 nd V was shown to possess ribosome-dependent GTP hydrolysis activity that was not affected by the pre

67 e 28S subunit facilitating its assembly, and GTP hydrolysis acts as the release mechanism.

68 ation is gated by the departure of IF2 after GTP hydrolysis, allowing efficient arrival of elongator

69 f subunits from protofilament ends following GTP hydrolysis and (2) reversible association and dissoc

70 s active Galpha(i/o)-GTP subunits to promote GTP hydrolysis and a G protein regulatory (GPR) motif th

71 Oncogenic mutations in Ras and GAPs slow GTP hydrolysis and are a factor in many cancers.

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

73 e residue provided by Ffh (E277), triggering GTP hydrolysis and complex disassembly at the end of the

74 ering step and, if so, the potential role of GTP hydrolysis and cross-over in tethering remain unknow

75 s interface that disrupt assembly-stimulated GTP hydrolysis and dynamin-catalyzed membrane fission in

76 complex formation, in promoting eIF5-induced GTP hydrolysis and eIF2/GDP release from the initiation

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

78 that remodelling of the Z ring, mediated by GTP hydrolysis and exchange of subunits, is necessary fo

79 ling (RGS) protein Sst2 acts by accelerating GTP hydrolysis and facilitating pathway desensitization.

80 RP-SR targeting complex that activate it for GTP hydrolysis and for handover of the translating ribos

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

82 e cytoplasm is associated with its increased GTP hydrolysis and inactivation.

83 anoma RAC1(P29S) protein maintains intrinsic GTP hydrolysis and is spontaneously activated by substan

84 The activity cycle is coupled to GTP hydrolysis and is tightly controlled by regulatory p

85 l of T. gondii replication by mGBP2 requires GTP hydrolysis and isoprenylation thus, enabling reversi

86 can stimulate higher order assembly, enhance GTP hydrolysis and lead to membrane deformation into tub

87 n on the membrane at the onset of stimulated GTP hydrolysis and may function to couple dynamin's mech

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

89 tivities, including cardiolipin association, GTP hydrolysis and membrane tubulation.

90 he GTPase domain of Mfn2) not only abolishes GTP hydrolysis and mitochondrial membrane fusion but als

91 SRL inhibited EF-G binding, and consequently GTP hydrolysis and mRNA-tRNA translocation.

92 n is not coupled to but likely precedes both GTP hydrolysis and mRNA/tRNA translocation.

93 in sensing the on/off state and in mediating GTP hydrolysis and nucleotide exchange.

94 now to identify key residues of Galphai1 in GTP hydrolysis and nucleotide exchange.

95 ramework that helps explain how the rates of GTP hydrolysis and peptide bond formation are controlled

96 tructural elements required for irreversible GTP hydrolysis and peptide bond formation plays a key ro

97 Pase Associated Center (GAC), is followed by GTP hydrolysis and Pi release, and results in formation

98 we investigated the consequences of G31R on GTP hydrolysis and Pi release, and the effects of intrag

99 tional cycle: apo-ribosome, factor-bound pre-GTP hydrolysis and post-GTP hydrolysis.

100 after initial 70S ribosome formation follows GTP hydrolysis and precedes P(i) release, paralleling mo

101 tubule (MT) dynamic instability is driven by GTP hydrolysis and regulated by microtubule-associated p

102 is temporally regulated by vesicle-bound Rab-GTP hydrolysis and requires vesicle tethering by the exo

103 deletion constructs were designed and their GTP hydrolysis and ribosome binding properties assessed.

104 the rates of elongation factor-Tu-catalyzed GTP hydrolysis and ribosome-catalyzed peptide bond forma

105 levated the V(max) of Galpha(s) steady state GTP hydrolysis and the apparent K(m) values of GTP bindi

106 We report the KM, Vmax, and Ea values for GTP hydrolysis and the Kd value for nucleotide binding f

107 t the full-length AtRGS1 protein accelerates GTP hydrolysis and thereby counteracts the fast nucleoti

108 arge ribosomal subunit, altering the rate of GTP hydrolysis and/or interaction of the large subunit w

109 nding, intrinsic and RGS protein-accelerated GTP hydrolysis, and interactions with Gbetagamma dimers,

110 nd hydrolysis, subcellular Ran localization, GTP hydrolysis, and the interaction with import and expo

111 ng to the pretranslocation (PRE) complex and GTP hydrolysis are rapidly followed by formation of the

112 s of dynamin's basal and assembly-stimulated GTP hydrolysis are unknown, though both are indirectly i

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

114 Here, we have used 70S ribosome binding and GTP hydrolysis assays to study the effects of thiostrept

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

116 nding) and GAP-catalyzed H-Ras deactivation (GTP hydrolysis) at nanomolar protein concentrations.

117 try is rate-limiting in GAP(334)-facilitated GTP hydrolysis but only partially rate-limiting in the N

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

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

120 We found that tethering depended on GTP hydrolysis, but, unlike fusion, it did not depend on

121 Ras proteins accelerate GTP hydrolysis by a factor of 10(5) compared to GTP in w

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

123 to the fidelity of translation by modulating GTP hydrolysis by aminoacyl-tRNA * EF-Tu * GTP ternary c

124 CP targeting complex in vitro and stimulates GTP hydrolysis by cpSRP54 and cpFtsY in a strictly cpSRP

125 SC2 GTPase-activating protein (GAP)-mediated GTP hydrolysis by displacing the hydrolytic water molecu

126 codons CAA and CAG and increases the rate of GTP hydrolysis by E. coli EF-Tu by fivefold.

127 The contribution of the ribosome-stimulated GTP hydrolysis by EF-G to tRNA/mRNA translocation remain

128 in inhibition also promotes futile cycles of GTP hydrolysis by EF-G.

129 lvent isotope effects, and ion dependence of GTP hydrolysis by EF-Tu off and on the ribosome to disse

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

131 essential role of SBDS is to tightly couple GTP hydrolysis by EFL1 on the ribosome to eIF6 release.

132 Following subunit joining, GTP hydrolysis by eIF5B alters the conformation of the f

133 nly after subunit joining, is accelerated by GTP hydrolysis by eIF5B.

134 GTP hydrolysis by elongation factor Tu (EF-Tu), a transl

135 nistic insight into the coordination between GTP hydrolysis by eRF3 and subsequent peptide release by

136 two release factors, eRF1 and eRF3, in which GTP hydrolysis by eRF3 couples codon recognition with pe

137 s, eRF1 and eRF3, and the ribosome, in which GTP hydrolysis by eRF3 couples codon recognition with pe

138 Mutations that impair GTP hydrolysis by eukaryotic translation initiation fact

139 rs or at nonpolar locations, indicating that GTP hydrolysis by FlhF is required for proper flagellar

140 We used this system to test how GTP hydrolysis by FtsZ is involved in Z-ring constrictio

141 We observe that rapid GTP hydrolysis by IF2 drives the transition to the elong

142 GTP hydrolysis by IF2 induces opening of the L1 stalk an

143 Blocking GTP hydrolysis by IF2 results in 70S complexes formed in

144 Rapid GTP hydrolysis by monomeric Cdc10 drives assembly of the

145 that TBC1D16 enhances the intrinsic rate of GTP hydrolysis by Rab4A.

146 d regulates effector enzymes and facilitates GTP hydrolysis by repositioning the gamma-carbonyl of a

147 the plasma membrane, bind RhoA, and promote GTP hydrolysis by RhoA.

148 Added GTPase-activating protein promotes GTP hydrolysis by Ypt7p, and added GDI captures Ypt7p in

149 h14 in activating Guanosine-5'-triphosphate (GTP) hydrolysis by aminoacyl-tRNA * EF-Tu * GTP.

150 activation of G(t), but had no effect on the GTP-hydrolysis by Galpha(t1).

151 GTP hydrolysis catalyzed by EF-G does not affect the rel

152 lar in nature to the transition state of the GTP hydrolysis catalyzed by Ras alone.

153 sis reactions, we measured the (18)O KIEs in GTP hydrolysis catalyzed by Ras in the presence of GAP(3

154 Arf4 mutant I46D, impaired in ASAP1-mediated GTP hydrolysis, causes aberrant rhodopsin trafficking an

155 The strong defect in GTP hydrolysis conferred by M18V likely explains its bro

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

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

158 e conformational coupling of atlastin to its GTP hydrolysis cycle have been carried out largely on at

159 s dynamin on the membrane surface during the GTP hydrolysis cycle.

160 n binding and dissociation are governed by a GTP hydrolysis cycle.

161 changes in dynamin that alter control of the GTP hydrolysis cycle.

162 ing reactions of the guanosine triphosphate (GTP) hydrolysis cycle.

163 the expression of wild-type TGase-2 and the GTP hydrolysis-defective mutant was sustained.

164 h Drp1 to constrict lipid bilayers through a GTP hydrolysis-dependent mechanism.

165 he variable domain, is sufficient to mediate GTP hydrolysis-dependent membrane constriction.

166 tor G (EF-G) in a guanosine 5'-triphosphate (GTP)-hydrolysis-dependent manner.

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

168 are able to propose a detailed model for how GTP hydrolysis destabilizes the microtubule and thus pow

169 nd biochemical assays for atlastin-catalyzed GTP hydrolysis, dimer formation, and membrane fusion.

170 ed to how GTP-tubulin forms polymers and why GTP hydrolysis disrupts them.

171 FtsZ is a GTPase, but the free energy of GTP hydrolysis does not appear to be used for generation

172 tails, including the catalytic mechanism and GTP hydrolysis-driven conformational changes, are yet to

173 It was thought that GTP hydrolysis drives the recycling of SRP and SR, but i

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

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

176 complex, which promotes rapid IF2-dependent GTP hydrolysis, either dissociates reversibly into 30 S

177 GTP hydrolysis exhibited a delay that included a lag pha

178 FtsZ GTP hydrolysis facilitates monomer turnover during the c

179 How does dynamin use the energy of GTP hydrolysis for membrane remodeling?

180 SDS as a ribosomopathy caused by uncoupling GTP hydrolysis from eIF6 release.

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

182 deactivation is achieved by G alpha-mediated GTP hydrolysis (GTPase activity) which is enhanced by th

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

184 r that PDV1 and PDV2 inhibits DRP5B-mediated GTP hydrolysis in a ratio dependent manner.

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

186 n the presence of GTP, suggesting a role for GTP hydrolysis in the depolymerization of the filaments.

187 l change that normally occurs in response to GTP hydrolysis in the lattice, without detectably changi

188 This behavior is driven by GTP hydrolysis in the microtubule lattice and is inhibit

189 SRP RNA also accelerates GTP hydrolysis in the SRP.SR complex once formed.

190 To understand how the ribosome triggers GTP hydrolysis in translational GTPases, we have determi

191 scission, pointing to a fundamental role for GTP hydrolysis in vesicle release rather than in coat as

192 ion factor thermo unstable (EF-Tu)-dependent GTP hydrolysis in vitro.

193 We analyzed GTP hydrolysis in water, Ras, and Ras.Ras-GTPase-activat

194 GTP hydrolysis increases the probability that scanning r

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

196 tant Rab7 is counterbalanced by unregulated, GTP hydrolysis-independent membrane cycling.

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

198 Fusion depends on a GTP hydrolysis-induced conformational change in the cyto

199 Thus GTP hydrolysis initiates stable head-domain contact in t

200 ale movement of EF-G's domain IV, induced by GTP hydrolysis, into the domain rotation of RRF that eve

201 Elongation factor-catalyzed GTP hydrolysis is a key reaction during the ribosomal el

202 chinery and explains how assembly-stimulated GTP hydrolysis is achieved through G domain dimerization

203 one, forming a ternary complex in which Arl2 GTP hydrolysis is activated to alter alphabeta-tubulin c

204 presence of thiostrepton, ribosome-dependent GTP hydrolysis is inhibited for both EF-G and EF4, with

205 erface and that the relation of curvature to GTP hydrolysis is more complicated than previously thoug

206 ith different constructs of AtNOA1 show that GTP hydrolysis is necessary but not sufficient for the p

207 re consistent with the model suggesting that GTP hydrolysis is not directly coupled to mRNA/tRNA tran

208 dY binding to target DNA, demonstrating that GTP hydrolysis is not necessary for CodY-dependent regul

209 Thus, although GTP hydrolysis is not required, the molecular rearrangem

210 ases, the rate of such movement is slowed if GTP hydrolysis is prevented.

211 GTP hydrolysis is required for +TIP tracking, because en

212 ctive cofactor forms, the chemical energy of GTP hydrolysis is required for gating cofactor transfer.

213 in ribosome biogenesis and that one role of GTP hydrolysis is to stimulate dissociation of RbgA from

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

215 it's intrinsic activation timer (the rate of GTP hydrolysis) is regulated spatially and temporally by

216 rogen atoms playing an important role in the GTP hydrolysis mechanism.

217 n occur by canonical nucleotide exchange and GTP hydrolysis mechanisms.

218 y demonstrates that the regulation of AtGPA1 GTP hydrolysis mediates sugar signal transduction during

219 t agents targeted toward regulation of LRRK2 GTP hydrolysis might be therapeutic agents for the treat

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

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

222 A to the distal end of this RNA, where rapid GTP hydrolysis occurs.

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

224 nificantly lengthened and more variable when GTP hydrolysis of the exocytic Rab is delayed.

225 ASAP1 mediates GTP hydrolysis on Arf4 and functions as an Arf4 effector

226 In an attempt to understand ribosome-induced GTP hydrolysis on eEF2, we determined a 12.6-A cryo-elec

227 re, we show that the SRL is not critical for GTP hydrolysis on EF-Tu and EF-G.

228 Our data suggest that GTP hydrolysis on EF-Tu is controlled through a hydropho

229 nd then, again, in a proofreading step after GTP hydrolysis on EF-Tu.

230 cate that the SRL is critical for triggering GTP hydrolysis on elongation factor Tu (EF-Tu) and elong

231 traces also point to a mechanistic model for GTP hydrolysis on elongation factor Tu mediated by aa-tR

232 receptor (GPCR) pathways by accelerating the GTP hydrolysis on G protein alpha subunits thereby promo

233 ation factor Tu (EF-Tu) that is required for GTP hydrolysis on interaction with the ribosome.

234 lity of R9AP . RGS9-1 . Gbeta5 to accelerate GTP hydrolysis on transducin is independent of its means

235 Gyp7-stimulated GTP hydrolysis on Ypt7 therefore appears to trigger both

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

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

238 conformational change in EF-Tu that follows GTP hydrolysis, or irreversible dissociation after or co

239 0 S ribosomal subunit, enabling irreversible GTP hydrolysis (Pi release) by the eIF2.GTP.Met-tRNAi te

240 s of parallel rapid kinetics measurements of GTP hydrolysis, Pi release, light-scattering, and change

241 Ras-catalyzed guanosine 5' triphosphate (GTP) hydrolysis proceeds through a loose transition stat

242 bosylated eEF2 (ADPR-eEF2), before and after GTP hydrolysis, providing a structural basis for analyzi

243 d in a significant increase in the intrinsic GTP hydrolysis rate and a loss of ribosome-stimulated GT

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

245 via their ability to increase the intrinsic GTP hydrolysis rate of Galpha subunits (known as GTPase-

246 RIT1 exhibits an intrinsic GTP hydrolysis rate similar to that of H-RAS, but its in

247 it turnover rate that are independent of the GTP hydrolysis rate.

248 ction, the mutations did not alter intrinsic GTP hydrolysis rates in vitro.

249 2_A66dup) proteins display reduced intrinsic GTP hydrolysis rates, accumulate in the GTP-bound confor

250 T assembly regulation, we need to understand GTP hydrolysis reaction kinetics and the GTP cap size.

251 al that the GAP(334) or NF1(333)-facilitated GTP hydrolysis reaction proceeds through a loose transit

252 ly rate-limiting in the NF1(333)-facilitated GTP hydrolysis reaction.

253 GTPase activation protein (GAP)-facilitated GTP hydrolysis reactions, we measured the (18)O KIEs in

254 The most common methods for monitoring GTP hydrolysis rely on luminescent GDP- or GTP-analogs.

255 ) in tTG(V1,2) altered GTP binding, enhanced GTP hydrolysis, rendered the variants insensitive to GTP

256 ubsequent binding of elongation factor G and GTP hydrolysis results in a clockwise rotation of the 30

257 arrestin and the rebinding of Galphai2 after GTP hydrolysis retained the complex within the lipid raf

258 pG blocks GTPase-activating-protein-assisted GTP hydrolysis, revealing a potent mechanism of GTPase s

259 of the known molecular functions for eEFSec: GTP hydrolysis, Sec-tRNA(Sec) binding, and SBP2/SECIS bi

260 nduces a rearrangement of EF-Tu that renders GTP hydrolysis sensitive to mutations of Asp21 and His84

261 the surface of microtubules, distal from the GTP-hydrolysis site and inter-subunit contacts, can alte

262 e fact that the mutations are not present in GTP hydrolysis sites.

263 lution, which corresponds to the initial pre-GTP hydrolysis stage of factor attachment and stop codon

264 e-TC), which corresponds to the initial, pre-GTP hydrolysis stage of factor attachment.

265 e initial binding of EF-G nor the subsequent GTP hydrolysis step.

266 pid binding correlates with liposome-induced GTP hydrolysis stimulation.

267 filament dynamics at steady state: rates of GTP hydrolysis, subunit exchange between protofilaments,

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

269 erminal is partly independent of dynamin and GTP hydrolysis, suggesting a new mechanism leading to ve

270 ng motif in cpFtsY result in higher rates of GTP hydrolysis, suggesting that negative regulation is p

271 eIF1 prevents the irreversible GTP hydrolysis that commits the ribosome to initiation a

272 tries based on structural changes induced by GTP hydrolysis that decreases the spacing between adjace

273 tional motion relative to the ribosome after GTP hydrolysis that exerts a force to unlock the ribosom

274 re we show that OPA1 has a low basal rate of GTP hydrolysis that is dramatically enhanced by associat

275 Dynamin exhibits a high basal rate of GTP hydrolysis that is enhanced by self-assembly on a li

276 via inhibition of oligomerization-stimulated GTP hydrolysis that promotes membrane constriction.

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

278 did not decrease the rate of single-turnover GTP hydrolysis, the >20-fold increase in K(1/2) conferre

279 GTP hydrolysis then uncouples the mRNA-tRNA complex from

280 hich facilitates GATOR1 recruitment and RagA(GTP) hydrolysis, thereby providing a negative feedback l

281 tutions perturbed their ability to stimulate GTP hydrolysis, they did not reverse selectivity.

282 A GAP domain in ArhGAP44 triggers local Rac-GTP hydrolysis, thus reducing actin polymerization requi

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

284 sive to signal peptide recruitment, coupling GTP hydrolysis to productive protein targeting.

285 pleted cells suggests that CLASPs facilitate GTP hydrolysis to reduce EB lattice binding.

286 energy of irreversible peptidyl transfer and GTP hydrolysis to surmount activation barriers to large-

287 pathway, dynamin uses mechanical energy from GTP hydrolysis to this effect, assisted by the BIN/amphi

288 ocation-competent conformation of EF-G while GTP hydrolysis triggers EF-G release from the ribosome.

289 Further GTP hydrolysis triggers local outer membrane fusion at t

290 ovide evidence for a novel link between Fzo1 GTP hydrolysis, ubiquitylation, and mitochondrial fusion

291 The signaling pathway that leads to GTP hydrolysis upon codon recognition is critical to acc

292 ctive mutant KRas displays a reduced rate of GTP hydrolysis via both intrinsic and GTPase-activating

293 rate of intrinsic nucleotide exchange, while GTP hydrolysis was unchanged.

294 tramolecular arginine finger that stimulates GTP hydrolysis when correctly oriented through rearrange

295 mation, bundling, and depolymerization after GTP hydrolysis, which involves a relatively small number

296 nding is elevated, ultimately culminating in GTP hydrolysis, which may destabilize the bilayer suffic

297 GTP binding, which causes activation, and of GTP hydrolysis, which terminates activation.

298 ,G62S cells; however suppressor M18V impairs GTP hydrolysis with little effect on PIC conformation.

299 Activation of the water molecule involved in GTP hydrolysis within the HRas.RasGAP system is analyzed

300 Without GTP hydrolysis, Z rings could still assemble and generat