ライフサイエンスコーパス: GTP hydrolysis

1 fore GTP hydrolysis) and proofreading (after GTP hydrolysis).

2 odon-anticodon interactions before and after GTP hydrolysis.

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

4 789/Q61 organization, impairing GAP-mediated GTP hydrolysis.

5 facilitate spontaneous membrane fission upon GTP hydrolysis.

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

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

8 ird, dynamin catalyzes membrane fission upon GTP hydrolysis.

9 gaged by EF-Tu.GTP from solution, coupled to GTP hydrolysis.

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

11 st be retained for uncompromised activity in GTP hydrolysis.

12 Galpha subunits are turned off by GTP hydrolysis.

13 is critically involved in the activation of GTP hydrolysis.

14 oting an intermediate state generated during GTP hydrolysis.

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

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

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

18 dal directional cue therefore requires Cdc42 GTP hydrolysis.

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

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

21 h is a noncanonical interface that regulates GTP hydrolysis.

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

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

24 tivation of Ras family proteins by impairing GTP hydrolysis.

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

26 3 in Rap into the active site for catalyzing GTP hydrolysis.

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

28 nslocon in a multistep process controlled by GTP hydrolysis.

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

30 from EF-Tu and EF-Tu from the ribosome after GTP hydrolysis.

31 nal rigidity and relaxation before and after GTP hydrolysis.

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

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

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

35 agnesium ion contributes to the catalysis of GTP hydrolysis.

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

37 became rigidly stabilized in the absence of GTP hydrolysis.

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

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

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

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

42 structural basis for neurofibromin-mediated GTP hydrolysis.

43 mation of the ribosome complex that triggers GTP hydrolysis.

44 static PhuZ filaments that are defective in GTP hydrolysis.

45 vated G-protein alpha-subunits, accelerating GTP hydrolysis.

46 sosome contacts, which are modulated by RAB7 GTP hydrolysis.

47 e-dependent oligomerisation of McrB precedes GTP hydrolysis.

48 ee by GDP, which is suggestive of sequential GTP hydrolysis.

49 elity of protein synthesis at the expense of GTP hydrolysis.

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

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

52 ified 70S ribosomes in vitro, independent of GTP hydrolysis.

53 a helical domain during different stages of GTP hydrolysis.

54 face as seen for mammalian microtubules upon GTP hydrolysis.

55 average distances between turns reduce with GTP hydrolysis.

56 itochondria via combined oligomerization and GTP hydrolysis.

57 ction associated with EB protein binding and GTP hydrolysis.

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

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

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

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

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

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

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

65 The GTP hydrolysis activities of Rho GTPases are stimulated

66 a proteins exhibit conserved GTP-binding and GTP-hydrolysis activities, and function in maintaining o

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

86 functional zones of MFN2, lead to changes in GTP hydrolysis and homo/hetero-association ability.

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

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

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

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

91 This ER-shaping activity is independent of GTP hydrolysis and located in a highly conserved peptide

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

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

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

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

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

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

98 Our results suggest that after GTP hydrolysis and P(i) release, the loss of interaction

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

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

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

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

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

104 re thought to prevent GAP protein-stimulated GTP hydrolysis and render KRAS-mutated colorectal cancer

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

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

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

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

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

110 e tRNA both during initial selection (before GTP hydrolysis) and proofreading (after GTP hydrolysis).

111 ted by mitochondrial proteins promoting Rab7 GTP hydrolysis, and allows for the bidirectional crossta

112 spectroscopy to monitor nucleotide exchange, GTP hydrolysis, and effector interactions of multiple sm

113 ical behavior, including nucleotide binding, GTP hydrolysis, and interaction with effectors.

114 The derived model supports a mechanism of GTP hydrolysis, and it shows that upon interaction of Rb

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

116 alpha subunits in G-proteins, accelerate the GTP hydrolysis, and thereby rapidly dampen GPCR signalin

117 esidues play in regulating ribosome binding, GTP hydrolysis, and translation initiation both in vitro

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

119 the necessary catalytic machinery for basal GTP hydrolysis, are intrinsically asymmetric.

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

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

122 Here, using site-directed mutagenesis, GTP hydrolysis assays, coimmunoprecipitation experiments

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

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

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

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

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

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

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

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

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

132 ivate ADAP1's enzymatic activity to catalyze GTP hydrolysis by ARF6.

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

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

135 GTP hydrolysis by dynamin triggers disassembly of fully

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

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

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

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

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

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

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

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

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

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

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

147 he fundamental mechanism of enzyme-catalyzed GTP hydrolysis by GTPases remains highly controversial.

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

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

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

151 Rapid GTP hydrolysis by monomeric Cdc10 drives assembly of the

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

153 etermination, and a GAP mode that stimulates GTP hydrolysis by RagA but remains structurally elusive.

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

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

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

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

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

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

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

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

162 valence bond simulations of GTPase-catalyzed GTP hydrolysis, comparing solvent- and substrate-assiste

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

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

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

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

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

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

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

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

171 ng, suggesting a coordinated and directional GTP-hydrolysis cycle.

172 are unique in employing the AAA+ domain for GTP hydrolysis-dependent activation of DNA cleavage.

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

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

175 wall remodeling enzymes through the Z-ring's GTP hydrolysis-dependent treadmilling dynamics.

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

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

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

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

180 The GTP hydrolysis driven cycling between a closed, farnesyl

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

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

183 by atomic force microscopy reveals that, on GTP hydrolysis, dynamin oligomers undergo a dynamic remo

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

185 GTP hydrolysis enables the GTPase domain of EF-Tu to ext

186 GTP hydrolysis exhibited a delay that included a lag pha

187 FtsZ GTP hydrolysis facilitates monomer turnover during the c

188 d in RAS GTPases, we assessed GAP-stimulated GTP hydrolysis for KRAS and observed a similar impairmen

189 e the critical importance of the kinetics of GTP hydrolysis for microtubule stability and establish t

190 n rather than by a smaller rate constant for GTP hydrolysis for near- and non-cognate TCs.

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

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

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

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

195 monstrated that RAC2[E62K] retains intrinsic GTP hydrolysis; however, GTPase-activating protein faile

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

197 abipA strain, indicating a critical role for GTP hydrolysis in BipA function.

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

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

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

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

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

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

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

205 GTP hydrolysis increases the probability that scanning r

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

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

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

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

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

211 GTP hydrolysis is a biologically crucial reaction, being

212 active site, as the preferred mechanism for GTP hydrolysis is a conserved solvent-assisted pathway.

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

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

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

216 When the speed of GTP hydrolysis is faster than dimer recruitment, the los

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

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

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

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

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

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

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

224 Slowing-down GTP hydrolysis leads to extended GTP caps.

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

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

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

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

229 cal insight into the enzymatic regulation of GTP hydrolysis not only resolves a decades-old mechanist

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

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

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

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

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

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

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

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

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

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

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

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

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

243 s hypothesis-testing mutations that increase GTP hydrolysis or impair GTP-binding activity provide ne

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

245 explained simply by a stochastic first-order GTP hydrolysis/phosphate release.

246 0 S ribosomal subunit, enabling irreversible GTP hydrolysis (Pi release) by the eIF2.GTP.Met-tRNAi te

247 activated Galpha and decreases the K(m) for GTP hydrolysis, potentially by altering the binding mech

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

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

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

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

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

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

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

255 2_A66dup) proteins display reduced intrinsic GTP hydrolysis rates, accumulate in the GTP-bound confor

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

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

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

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

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

261 , whose effects are partially rescued by the GTP hydrolysis-resistant RanQ69L mutant.

262 ing are further regulated by Mfn1/2 and Drp1 GTP hydrolysis, respectively.

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

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

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

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

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

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

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

270 plasmic tail of SLC38A9 in the pre- and post-GTP hydrolysis state of RagC, which explain how SLC38A9

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

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

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

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

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

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

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

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

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

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

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

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

287 Further GTP hydrolysis triggers local outer membrane fusion at t

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

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

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

291 MFN1, MFN2 forms sustained dimers even after GTP hydrolysis via the GTPase domain (G) interface, whic

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

293 Using mutated human tubulin with blocked GTP hydrolysis, we demonstrate that EBs bind with high a

294 To elucidate the mechanism of GTP hydrolysis, we determined crystal structures of YcjX

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

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

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

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