ライフサイエンスコーパス: GTP

1 GTP hydrolysis by dynamin triggers disassembly of fully

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

3 GTP hydrolysis is a biologically crucial reaction, being

4 d, requiring dozens of protein factors and 2 GTP-regulated steps.

5 P into 3',8-cyclo-7,8-dihydro-GTP (3',8-cH(2)GTP) during the molybdenum cofactor (Moco) biosynthesis.

6 ne nucleotide exchange factor-induced Eu(3+)-GTP association to RAS, monitored at 615 nm, and subsequ

7 , monitored at 615 nm, and subsequent Eu(3+)-GTP-loaded RAS interaction with RAF-RBD-Alexa680 monitor

8 milled at 23 nm/s, hydrolyzed GTP at 3.6-3.7 GTP min(-1) FtsZ(-1), and had an average length of 30-40

9 uires cap recognition by eIF3d, a new 5'-m(7)GTP recognizing protein.

10 , PaFtsZ had a strong GTPase activity, ~ 7.8 GTP min(-1) FtsZ(-1) at pH 7.5, and assembled into mainl

11 crotubules are thought to be stabilized by a GTP cap at their ends.

12 ), synergistically split 100S ribosomes in a GTP-dependent but tRNA translocation-independent manner.

13 e found that Arl4A interacts with Robo1 in a GTP-dependent manner and that the Robo1 amino acid resid

14 ut not TbArl3C interacted with TbUnc119 in a GTP-dependent manner, suggesting functional specializati

15 st showed that Arl4D interacts with EB1 in a GTP-dependent manner.

16 Dynamin 2 (DNM2) is a GTP-binding protein that controls endocytic vesicle scis

17 We show that YcjX is a GTP-binding protein that shares at its core the canonica

18 that the growing MT ends are protected by a "GTP cap" that consists of GTP-bound tubulin dimers.

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

20 ires binding to membrane-anchored and active GTP-bound RAS.

21 molecular switch in a constitutively active GTP-bound form that drives, unchecked, oncogenic downstr

22 m its inactive GDP-bound state to its active GTP-bound state.

23 ate hydrolysis resulting in prolonged active GTP-bound RAC2.

24 membrane-anchored KRAS dimers in the active GTP- and inactive GDP-loaded states.

25 tion as switchable landmarks with the active GTP-bound form recruiting to the membrane a specific set

26 -sensitive antibody that detects the active (GTP-bound) Rac1 without interacting with the GDP-bound i

27 olecular switches that cycle between active, GTP-bound and inactive, GDP-bound states.

28 binding of c-Raf-RBD to KRas in its active, GTP-bound state (KRasGTP).

29 odon-anticodon interactions before and after GTP hydrolysis.

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

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

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

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

34 RET technique was also applied for G(i)alpha GTP-loading and pertussis toxin-catalyzed ADP-ribosylati

35 sence of other activators, membrane-anchored GTP-Rab5A provides strong, virtually binary on-off switc

36 3P production triggered by membrane-anchored GTP-Rab5A.

37 hermosuccinogenes that operates with ATP and GTP exhibits unusual kinetics toward F6P, as it appears

38 o GSH production was suppressed, and ATP and GTP levels were impaired.

39 model, we show that the proteins are ATP and GTP transporters located on the surface of parasites dur

40 lize with human cGAS and occupy the ATP- and GTP-binding active site.

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

42 cytes, including cytoskeletal components and GTP-binding proteins, which would be expected to compete

43 dly asymmetric, with unusually high dGTP and GTP levels compared with those in whole mouse embryos or

44 domain) can occur in the absence of EF-G and GTP, EF-G is essential for enforcing coupled movement of

45 impacting the cellular pools of GMP, GDP and GTP.

46 imarily regulated by the exchange of GDP and GTP.

47 e simulated these mutations in both GDP- and GTP-bound Cdc42.

48 ystem influences (p)ppGpp, c-di-GMP, GMP and GTP concentrations.

49 ymes downstream of Nrf2 and restored GSH and GTP.

50 atalytic domains of GDP-bound (inactive) and GTP-bound (active) Cdc42 in solution.

51 or Tu (EF-Tu), aminoacyl-tRNA (aa-tRNA), and GTP.

52 The RAS proteins are GTP-dependent switches that regulate signaling pathways

53 Septins are GTP-binding proteins involved in diverse cellular proces

54 Septins are GTP-binding proteins that self-assemble into higher orde

55 ivation-dependent membrane insertion of ARF1*GTP molecules required for coated membrane vesicle forma

56 Here, we demonstrate the proximity of ARF1*GTPs in vivo by fluorescence resonance energy transfer-f

57 (NULL), implying an enhanced ability of ARF6-GTP to drive distant spread.

58 T2-GFP probe that specifically binds to Arf6-GTP.

59 anges in BBSome conformation induced by ARL6(GTP) binding.

60 he BBSome by itself and in complex with ARL6(GTP), and we describe the changes in BBSome conformation

61 conformation changes gradually in the cap as GTP is hydrolyzed.

62 ependent activation requires the cognate ATP/GTP substrate pair, while negative-cooperativity suppres

63 de-binding states, only one of which (RagA/B*GTP-RagC/D*GDP) permits mTORC1 association.

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

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

66 ted cells they do not actively cycle between GTP- and GDP-bound states.

67 Remarkably, "cross"-dimerization between GTP- and GDP-bound KRAS molecules is unfavorable.

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

69 ogenesis, rRNA processing, ribosome binding, GTP binding, and hydrolase activity.

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

71 We find that Kif7 preferentially binds GTP-tubulin at microtubule ends over GDP-tubulin in the

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

73 ll as a short segment of a closed MT in both GTP- and GDP-bound states.

74 iochemical studies, we demonstrate that both GTP and dGTP bind to Rel, but only GTP (but not dGTP) ca

75 s (GAPs), activating the hydrolysis of bound GTP.

76 Gyp1-46 is not limited to Ypt7-tm with bound GTP, indicating that this GAP has an additional mode of

77 SOS1 exchanges GDP by GTP, activating Ras.

78 lting in the recruitment of coat proteins by GTP-bound ARFs.

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

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

81 Septins are conserved GTP-binding cytoskeletal proteins that polymerize into f

82 Two BjuGalpha proteins exhibit conserved GTP-binding and GTP-hydrolysis activities, and function

83 RAS GTPase is a highly conserved GTP-binding protein with crucial functions for cell grow

84 SAFB knockdown decreased GTP loading of RAS, abrogated alternative prenylation, a

85 d interacts directly with the zinc-dependent GTP cyclohydrolase IA, FolE (GCYH-IA).

86 at MPA rapidly inhibits Pol III by depleting GTP.

87 clization of GTP into 3',8-cyclo-7,8-dihydro-GTP (3',8-cH(2)GTP) during the molybdenum cofactor (Moco

88 Here we report a direct, GTP-dependent interaction between KRAS4A and hexokinase

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

90 e that the active site does not discriminate GTP from dGTP, for a substrate.

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

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

93 at recycles inactive eIF2*GDP to active eIF2*GTP.

94 itical for efficient recruitment of the eIF2*GTP*Met-tRNAiMet ternary complex to the ribosome and for

95 ailability of the eIF2 ternary complex (eIF2-GTP-tRNAi) by affecting the interaction of eIF2 with its

96 ex formation and decreases the level of eIF2-GTP-Met-tRNA(i)(Met) ternary complexes.

97 This allows continued formation of the eIF2-GTP-Met-tRNAi ternary complex and unabated global transl

98 5G-R57E accelerated dissociation of the eIF2.GTP.Met-tRNAi ternary complex (TC) from reconstituted PI

99 cGMP and that cancer cells possess elevated GTP levels, it is surprising that a detailed structural

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

101 lowing-down GTP hydrolysis leads to extended GTP caps.

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

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

104 n animals and fungi, the exchange of GDP for GTP on Galpha controls G protein activation and is cruci

105 1 (P-Rex1) catalyzes the exchange of GDP for GTP on Rac GTPases, thereby triggering changes in the ac

106 GEFs catalyze exchange of GDP for GTP; the GTP-bound, activated, Rab then recruits a diver

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

108 ch normally target proteins to membranes for GTP-loading.

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

110 Septins are filament-forming, GTP-binding proteins that assemble on positive, micromet

111 the synthesis of cyclic GMP-AMP (cGAMP) from GTP and ATP(3).

112 i-GMP and (p)ppGpp are both synthesized from GTP molecules, they play antagonistic roles in regulatin

113 nimolecular biosensors for endogenous Galpha-GTP and free Gbetagamma: the two active species of heter

114 lpha, for which we synthesized a novel gamma-GTP-Eu(3+) molecule.

115 clude that, in addition to the canonical GDP-GTP exchange-dependent mechanism, plant G proteins can f

116 -protein transducin (G(T)) by catalyzing GDP-GTP exchange on its alpha subunit (Galpha(T)).

117 s the enzyme to allosteric inhibition by GDP/GTP.

118 a variety of effectors depending on its GDP/GTP-bound state.

119 omains, these contribute to the same general GTP-recognition mechanism employed by all G proteins.

120 ate stimulation, highlights a heterotrimeric GTP-binding protein (G protein)-independent mechanism fo

121 e region, couple to different heterotrimeric GTP-binding proteins (G proteins) to transmit signals.

122 Here, we have used the slowly-hydrolyzable GTP analog, guanylyl-(alpha,beta)-methylene-diphosphonat

123 , how do these regulatory proteins hydrolyze GTP without an obvious general base in the active site t

124 ability of the small GTPase RAS to hydrolyze GTP, keeping this molecular switch in a constitutively a

125 ents that treadmilled at 23 nm/s, hydrolyzed GTP at 3.6-3.7 GTP min(-1) FtsZ(-1), and had an average

126 After successful decoding, EF-Tu hydrolyzes GTP, which triggers a conformational change that ultimat

127 tions that increase GTP hydrolysis or impair GTP-binding activity provide neuroprotection although vi

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

129 static PhuZ filaments that are defective in GTP hydrolysis.

130 Rap1 was in GTP-associated active state in both types of lEVs, and R

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

132 particularly GTP-RagC, leading to increased GTP loading of RagA.

133 Inhibiting GTP synthesis radiosensitizes GBM cells and patient-deri

134 enhancing both the affinity of the inhibitor GTP binding and inhibition of GDH catalytic activity. We

135 e focused on nucleotide exchange inhibitors, GTP-RAS interaction inhibitors, and activators increasin

136 pathway in which an on-pathway intermediate, GTP C-3' radical, abstracts H-4' atom from (4'R)-5'-deox

137 gnal inputs are transmitted by intracellular GTP-binding (G) proteins.

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

139 iating with distinct polarity factors in its GTP- and GDP-bound states.

140 GTPase MglA stimulates T4P formation in its GTP-bound state by direct interaction with the tetratric

141 y affecting the interaction of eIF2 with its GTP-GDP exchange factor eIF2B.

142 Dimerization of KRAS-GTP, stabilized by electrostatic interactions between R1

143 se to the availability of key nutrients like GTP and branched-chain amino acids.

144 structural basis for neurofibromin-mediated GTP hydrolysis.

145 of T4P formation at the leading pole by MglA-GTP and SgmX and indirect inhibition of T4P formation at

146 s pole by stimulating the conversion of MglA-GTP to MglA-GDP.

147 Furthermore, excess NADPH, GTP and ADP greatly diminish N-malonylation near their n

148 ed to stall with eIF5B and a nonhydrolyzable GTP analog.

149 quires 40S ubiquitination by ZNF598, but not GTP-dependent factors, including the Pelo-Hbs1L ribosome

150 ssion of the rate-limiting enzyme of de novo GTP synthesis is associated with shorter survival in GBM

151 NA synthesis, stabilization of the nucleolar GTP-binding protein nucleostemin, and enlarged, malforme

152 logs (GpppA and GpppG) and single-nucleotide GTP but not ATP, CTP, or UTP.

153 s in K-Ras are specific to bound nucleotide (GTP or GDP), and we provide a structural basis for this.

154 xpected to compete for decreasing amounts of GTP at early time points.

155 The binding of GTP or GDP constitutes a selective switch for Ypt7, but

156 ctivity. We further show that the binding of GTP to the NADH-bound GDH activates a triangular alloste

157 re protected by a "GTP cap" that consists of GTP-bound tubulin dimers.

158 The first step, the conversion of GTP to cyclic pyranopterin monophosphate (cPMP), require

159 drolase I (GCH1) catalyzes the conversion of GTP to dihydroneopterin triphosphate (H2NTP), the initia

160 talyzes an unprecedented 3',8-cyclization of GTP into 3',8-cyclo-7,8-dihydro-GTP (3',8-cH(2)GTP) duri

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

162 he tubulin dimer following the hydrolysis of GTP have been suggested to generate stress and drive dep

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

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

165 An FDA-approved inhibitor of GTP synthesis potentiates the effects of radiation in fl

166 TP-binding pocket and alters the kinetics of GTP exchange.

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

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

169 ecule approach to elucidate the mechanism of GTP-Rab5A-associated VPS34CII kinase activation in a rec

170 he first time we explore a role for 2'-OH of GTP and show how it is important in generating the nucle

171 dy elucidating a catalytic role for 2'-OH of GTP in (p)ppGpp synthesis allows us to propose different

172 phosphate from ATP to the oxygen of 3'-OH of GTP/GDP.

173 F5B, located close to the gamma-phosphate of GTP and centered around the universally conserved tyrosi

174 22 nM) and its tightening in the presence of GTP (3.69 +/- 0.65 nM), at a dissociation rate >10(-2) s

175 ly in terms of the biochemical properties of GTP- and GDP-bound alphabeta-tubulin predict the concent

176 ight light, living mice increase the rate of GTP and ATP synthesis in their retinas; concomitant with

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

178 se Yck3 renders fusion strictly dependent on GTP-activated Ypt7, whether bound to membranes by prenyl

179 that both GTP and dGTP bind to Rel, but only GTP (but not dGTP) can form the product.

180 suppresses Mn2+ utilization by either ATP or GTP alone.

181 cing the possible passage of incoming UTP or GTP through the RdRp-specific entry tunnel, we found two

182 cell migration, whereas expression of WT or GTP-bound Rab5 (Rab5/Q79L), but not Rab5/S34N, promoted

183 revealed that, similar to 8-oxo-dGTP, r8-oxo-GTP adopts an anti conformation opposite a templating cy

184 a diminished catalytic efficiency for r8-oxo-GTP compared with canonical deoxyribonucleotides but tha

185 However, unlike 8-oxo-dGTP, r8-oxo-GTP did not form a planar base pair with either templati

186 ase beta (pol beta) and characterized r8-oxo-GTP insertion with DNA substrates containing either a te

187 These results suggest that r8-oxo-GTP is a potential mutagenic substrate for DNA polymeras

188 nonical deoxyribonucleotides but that r8-oxo-GTP is inserted mutagenically at a rate similar to those

189 provide structural insights into how r8-oxo-GTP is processed by DNA polymerases.

190 nformational changes of pol beta with r8-oxo-GTP, we demonstrate impaired pol beta closure that corre

191 cleotides are analogously oxidized to r8-oxo-GTP, which can constitute up to 5% of the rGTP pool.

192 2 interacts with inactive Rags, particularly GTP-RagC, leading to increased GTP loading of RagA.

193 sphorylates cytoplasmic PI(3,4,5)P3-positive GTP-Rab10, before EEA1 and Rab5 recruitment to early mac

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

195 to one Rag locks the heterodimer to prevent GTP binding to the other.

196 t the alarmones are necessary for protecting GTP homeostasis against excess environmental xanthine in

197 t defined by the mean size of the protective GTP-tubulin cap.

198 associates with Rab35, where it promotes Rab GTP exchange.

199 ith an in vitro pulldown assay with GST-Rab5(GTP) Of the 35 p110beta helical domain mutants assayed,

200 he cell surface and exhibited increased Rab5-GTP levels, consistent with endocytosis.

201 adhesion-induced FAK activity increased Rab5-GTP levels.

202 (Tyr(397))-dependent manner, preventing Rab5-GTP loading, as shown by knockdown and transfection reco

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

204 lizes distinct domains to interact with Rab7-GTP and the ER transmembrane protein Protrudin and toget

205 ltiple approaches, we show that VPS35-RABG3f-GTP interaction is necessary to trigger downstream event

206 exhibit more effective downregulation of Rac GTP loading following HGF stimulation and enhanced inhib

207 still show a high signal with the anti-Rac1-GTP antibody, which is lost upon silencing of vimentin e

208 p-regulation of vimentin and high basal Rac1-GTP levels when measured biochemically.

209 er cell models known to have high basal Rac1-GTP levels, here we have established that this antibody

210 multiple PNs, also exhibited increased RAC1-GTP and phospho-ERK levels compared with Nf1(flox/flox);

211 multiple PNs, also exhibited increased RAC1-GTP and phospho-ERK levels compared with Nf1(flox/flox);

212 apse marker, through decreasing a novel Rac1-GTP/p-Pak1-T423/p-P38-T180/p-MK2-T334/p-Limk1-S323/p-Cof

213 otic cytokine, TGF-beta1 promoted rapid Rac1-GTP loading in human kidney 2 (HK-2) human renal epithel

214 nit of mTORC1 and explains why only the RagA(GTP)/RagC(GDP) nucleotide state binds mTORC1.

215 tingly, NopA triggers an accumulation of Ran-GTP, which accumulates at nucleoli of transfected or inf

216 In addition, RAP1(GTP)-mediated adhesion is only facilitated through alpha

217 d dissociation rates from RAS-GTP and by RAS-GTP concentration.

218 association and dissociation rates from RAS-GTP and by RAS-GTP concentration.

219 s tested, the NF1-LRD fails to hydrolyze Ras-GTP to Ras-GDP, suggesting that its suppressive function

220 or JAK-signaling, prevented TSLP-induced RAS-GTP boost.

221 of SOS1 that can increase the amount of RAS-GTP in cells.

222 rafenib, which increases the affinity of Ras-GTP:RAF1 interactions.

223 lation by assembling a supercomplex with Ras-GTP and mTORC2.

224 PS34CII kinase activation in a reconstituted GTP-Rab5A-VPS34CII-PI3P-PX signaling pathway on a target

225 EFs, indicating that the drastically reduced GTP turnover restricts oligomer disassembly from the mit

226 n CLASP repairs lattice damage by regulating GTP-tubulin incorporation into the break site.

227 Loss of Ras-related GTP binding protein C homolog 1 RAGC-1, the ortholog for

228 TP) turnover, guanosine diphosphate release, GTP binding, and G protein dissociation studies revealed

229 d by either means, but only Ypt7-pr requires GTP for activation and is inactive either with bound GDP

230 evels of the canonical formin activator Rho1-GTP.

231 s than normal and have higher levels of Rho1-GTP at the division site than wild-type cells.

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

233 cAMP inhibition, 31% E(max); mA(3)AR, [(35)S]GTP-gamma-S binding, 16% E(max)) and in vivo and also an

234 ved that one cluster is adjacent to the SAR1 GTP-binding pocket and alters the kinetics of GTP exchan

235 progression to elongation during the second GTP-regulated step.

236 ate (dGTP), but not inhibitor binding, since GTP locks dGTPase in its apo- form.

237 over, ROC(N1437H) was found to have a slower GTP dissociation rate, indicating that N1437H might inte

238 Small GTP-binding proteins represent a highly conserved signal

239 We identified the Rho family small GTP-binding protein Ras-related C3 botulinum toxin subst

240 , the roles of the plant complement of small GTP-binding proteins in these cellular processes are des

241 e activity of Rho GTPases, a family of small GTP-binding proteins that regulate actin cytoskeleton as

242 s have been shown to recognize a stabilizing GTP/GDP-Pi cap at the tip of growing MTs, but informatio

243 P-tagged Drp1 constitutes aberrantly stable, GTP-resistant supramolecular assemblies both in vitro an

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

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

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

247 re of the contacts between the two Galpha(T).GTP subunits and PDE6 that supports an alternating-site

248 The structure reveals two Galpha(T).GTP subunits engaging the PDE6 hetero-tetramer at both t

249 TP-bound transducin alpha subunit (Galpha(T).GTP) and the cyclic GMP (cGMP) phosphodiesterase 6 (PDE6

250 crotubule dynamic instability, implying that GTP acts elsewhere to exert its stabilizing influence on

251 Previous kinetic studies suggested that GTP binding to one Rag locks the heterodimer to prevent

252 The GTP hydrolysis driven cycling between a closed, farnesyl

253 The GTP-dependent signaling of these proteins is controlled

254 The GTP-specific AAA + protein McrB powers translocation alo

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

256 formational changes in both the GDP- and the GTP-bound systems, but in the GTP-bound Cdc42, the switc

257 itching, i.e., what is different between the GTP- and GDP-tubulin states that enables microtubule gro

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

259 GEFs catalyze exchange of GDP for GTP; the GTP-bound, activated, Rab then recruits a diverse local

260 e GDP- and the GTP-bound systems, but in the GTP-bound Cdc42, the switch I interactions with GTP are

261 exibility in the GDP-bound Cdc42 than in the GTP-bound Cdc42.

262 ream signaling and helps maintain RAS in the GTP-bound form.

263 In the GTP-bound state, RhoJ interacts with the cytoplasmic dom

264 protein-effector complex is composed of the GTP-bound transducin alpha subunit (Galpha(T).GTP) and t

265 the Ric8A C-terminal tail helps organize the GTP-binding site of Galpha.

266 d our evidence suggests that NMT prefers the GTP-bound while SIRT2 prefers the GDP-bound ARF6.

267 Furthermore, the N1437H mutation reduced the GTP binding affinity by ~2.5-fold when compared with oth

268 microtubule stability and establish that the GTP cap coincides with the EB-binding region.

269 er the EB binding region is identical to the GTP cap is unclear.

270 rate that EBs bind with high affinity to the GTP conformation of microtubules.

271 ter than dimer recruitment, the loss of this GTP cap will lead the MT to undergo rapid disassembly.

272 pic stabilization of GDP binding compared to GTP binding originates in the backbone hydrogen bonding

273 Here we show that MglA complexed to GTP recruits a newly characterized Tfp regulator, termed

274 copy (cryoEM) structure of PDE6 complexed to GTP-bound Galpha(T).

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

276 e signaling pathways: the exchange of GDP to GTP by linked G-proteins and the recruitment of beta-arr

277 inactive states, and this cycle is linked to GTP binding and hydrolysis.

278 the first group were more closely related to GTP-binding protein 1 (GTPBP1), whereas trGTPases in the

279 KIF1A binds more weakly to GTP-tubulin than GDP-tubulin and competes with end-bindi

280 mation of the ribosome complex that triggers GTP hydrolysis.

281 ) are filamentous guanosine-5'-triphosphate (GTP)-binding proteins, which affect microtubule (MT)-dep

282 Guanosine triphosphate (GTP) cyclohydrolase I (GCH1) catalyzes the conversion of

283 hat depends on a Ran-guanosine triphosphate (GTP) signal [12], which is sufficient to drive continuou

284 Guanosine triphosphate (GTP) turnover, guanosine diphosphate release, GTP bindin

285 ed for assembly by a guanosine triphosphate (GTP)-driven reaction cycle, and the emerging microtubule

286 fter the delivery of aminoacyl-tRNA by EF-Tu*GTP.

287 fter EF-Tu release can be reengaged by EF-Tu.GTP from solution, coupled to GTP hydrolysis.

288 IMPDH1 in vivo, important for understanding GTP homeostasis in the retina and the pathogenesis of ad

289 small GTPase that is part of COPII and, upon GTP binding, recruits the other COPII proteins to the en

290 to the endoplasmic reticulum, where it uses GTP as a phosphate donor to phosphorylate INSIG1 at Ser2

291 Reactions performed using GTP analogs substituted with different chemical moieties

292 reduces preferential binding to GDP- versus GTP-rich microtubules disrupts SVP delivery and reduces

293 oofreading step it is necessary to visualize GTP-catalysed elongation, which has remained a challenge

294 We also find that the CTL weakens GTP binding while enhancing the catalytic rate, whereas

295 hboring PFs tends to be larger compared with GTP ones.

296 esolution-as apoenzyme and in complexes with GTP*Mg2+, IDP*PO4, and dGDP*PO4-that highlight conformat

297 AGAP2 (Arf GAP with GTP-binding protein-like domain, Ankyrin repeat and PH d

298 able the Ric8A-bound Galpha to interact with GTP.

299 -bound Cdc42, the switch I interactions with GTP are retained.

300 endosomes/lysosomes, where it interacts with GTP-Rab7.