ライフサイエンスコーパス: rebinding

1 pyrophosphate release (or fast pyrophosphate rebinding).

2 lso necessary for proper GTP binding (or GDP rebinding).

3 and force-induced cross-linker unbinding and rebinding.

4 ith receptor equilibration limited by ligand rebinding.

5 se of SpoIID from the complex and subsequent rebinding.

6 , consistent with membrane retention via SH2 rebinding.

7 resents a negligible enthalpic barrier to NO rebinding.

8 The results are compared with NO rebinding.

9 ure the rates of cross-bridge detachment and rebinding.

10 increased to a t(1/2) of 1.6 h by preventing rebinding.

11 after agonist exposures too brief to permit rebinding.

12 ncy and the innermost barrier controlling CO rebinding.

13 id phase (25-30% amplitude) of O(2) geminate rebinding.

14 are increased, with less consequence for CO rebinding.

15 iation processes under conditions minimizing rebinding.

16 structure that allows nucleotide release and rebinding.

17 responds to the slower geminate phase for O2 rebinding.

18 g site that prevents released phosphate from rebinding.

19 mational alterations that enhance subsequent rebinding.

20 protonation as well as a reduction before OH rebinding.

21 " mechanism of concerted SEC11 debinding and rebinding.

22 ction accounting for the effects of TCR-pMHC rebinding.

23 discard" short dsRNA rapidly and to suppress rebinding.

24 n or slowly evolving on the time scale of CO rebinding.

25 he subsequent geminate rebinding reaction (t(rebinding) = 31.6 ps) by monitoring infrared bleach reco

26 ation occur, contrary to sGC, followed by NO rebinding (7 ps) and back-reduction (230 ps and 2 ns).

27 ation between MIP chemical structure and its rebinding ability.

28 with the non-Arrhenius slow down of geminate rebinding above approximately 180 K.

29 receptor sites with significantly increased rebinding affinity for the template.

30 uscule vesicle volume that facilitates rapid rebinding after dissociation.

31 HbA lead to markedly biphasic bimolecular CO rebinding after laser photolysis.

32 ral processes, including geminate rebinding, rebinding after ligand escape to the solvent, and interc

33 e in the crowded cellular environment, since rebinding after the first phosphorylation is enhanced by

34 Kinetics of geminate rebinding also suggest that quaternary enhancement may b

35 om recent studies on the physics of geminate rebinding and conformational changes in myoglobin.

36 e the large amplitude picosecond CO geminate rebinding and find that it is correlated with the absenc

37 nd Changeux (MWC) to include geminate ligand rebinding and nonexponential tertiary relaxation within

38 ne proteins that were biotinylated following rebinding and photoactivation of labeled GAPDH, aldolase

39 s in the free energy barriers throughout the rebinding and release pathway upon increase of the pH ar

40 a local effect: a cluster promotes the rapid rebinding and second activation of singly activated subs

41 lytical estimate of the probability of rapid rebinding and show that well-mixed ordinary differential

42 nts, higher glycerol concentrations increase rebinding (and decrease the fluorescence recovery rate)

43 Higher Fab concentrations reduce rebinding (and increase the fluorescence recovery rate)

44 performance was evaluated using equilibrium rebinding assays.

45 work, a general analytical theory for ligand rebinding at cell surfaces was developed for a reversibl

46 ial site was followed by RT dissociation and rebinding at the -7 cleavage site, and the dissociation

47 ons which follow from the general theory for rebinding at the membrane surface.

48 turns over Exo1, multiple cycles of nuclease rebinding at the same DNA site can still support limited

49 a two exponential fit to time courses for CO rebinding at varying CO concentrations yields rate const

50 mperature measurements of the enthalpic MbCO rebinding barrier (18 +/- 2 kJ/mol).

51 midazole ligand reveals the magnitude of the rebinding barrier associated with proximal histidine lig

52 approximately 180 K), the average enthalpic rebinding barrier for H(2)O-PPIX-CO was found to be appr

53 pletely rebinds by 35 K, indicating that the rebinding barrier for NO is lower than MbCO, consistent

54 sessed and it is found that the enthalpic CO rebinding barrier is increased significantly when imidaz

55 The electronic coupling, rebinding barrier, and Landau-Zener force terms can be o

56 d the enthalpic contribution to the proximal rebinding barrier, H(p), to be 11 +/- 2 kJ/mol.

57 titatively using a distribution of enthalpic rebinding barriers associated with heterogeneity in the

58 lumination, discrete populations with higher rebinding barriers were observed.

59 We have characterized the ligand-rebinding behavior of single crystal native sperm whale

60 species was necessary to model the enhanced rebinding below 30 K, which likely appears because of qu

61 Rebinding between 200 and 300 K displays several process

62 rating the very fast dynamics and remarkable rebinding capabilities of the intramolecular donor-accep

63 ong with a decrease in the fraction of hemes rebinding CO with the slow rate constant characteristic

64 ATP rebinding could then cause reversal of this structural t

65 nerate the geminate and solvent phase ligand rebinding curves for photodissociated COHbY.

66 Finally, we show that rapid rebindings drastically alter the reaction's Michaelis-Me

67 find that the displaced SBF is blocked from rebinding due to incorporation of its recognition sites

68 as well as slow rather than fast dynamic LH rebinding (due to DNA stem destabilization), and low com

69 ase can be correlated to varying the release-rebinding equilibrium of IMC, through simulation.

70 tomated docking by AutoDock, and spontaneous rebinding events in unbiased molecular dynamics simulati

71 inside the microtubule bundle is hindered by rebinding events when open sites are within approximatel

72 ng properties, the MIP was analyzed by batch rebinding experiments and subsequently used as SPE sorbe

73 The results obtained from batch rebinding experiments showed the presence of two associa

74 is presented that explains a variety of MbNO rebinding experiments, including the dependence of the k

75 derivatives following rapid mixing and of CO rebinding following flash photolysis have been examined

76 mponent is determined by competition between rebinding from a position closer to the iron atom and es

77 ft the proximal heme pocket and requiring NO rebinding from solution to proceed via the distal heme f

78 seconds that can be directly associated with rebinding from specific hydrophobic cavities.

79 A, can be assigned, respectively, to ligand rebinding from the following: (i) the distal heme pocket

80 cular phase representing second-order ligand rebinding from the solvent.

81 Rebinding from these positions corresponds to the slower

82 As a result of water release/rebinding from/to the coproduct formation site the Compo

83 Such impulsive bond breaking and late rebinding generate proteinquakes and strongly perturb th

84 nhomogeneous on the time scale of the ligand rebinding giving rise to KHB.

85 ve the capacity to recycle to chromatin upon rebinding hormone.

86 These three phases are ascribed to rebinding: (i) from the distal heme pocket, (ii) from th

87 absorption recovery, analogous to methionine rebinding in photolyzed ferrous cytochrome c.

88 importin alpha5 but rather to prevent cargo rebinding in preparation for recycling.

89 g to one subunit decreases the rate of Pro-2 rebinding in the second, leading to a net increase in af

90 study the ultrafast dynamics of geminate CO rebinding in two CooA homologues, Rhodospirillum rubrum

91 CYP3A4 and the amplitude of the geminate CO rebinding increased significantly as a result of binding

92 city for one substrate over another drops as rebinding increases and pseudo-processive behavior becom

93 ach indicates that the probability of ligand rebinding increases exponentially with the number of sit

94 ed signaling pathway exhibits high levels of rebinding-induced pseudo-processivity, unlike other prop

95 ated tRNA and shows that trans editing after rebinding is a competent kinetic pathway.

96 Moreover, induced rebinding is able to reproduce the striking, and hithert

97 CO rebinding is expected to compete with protein folding an

98 ver, this loss of specificity with increased rebinding is typically also observed if two distinct enz

99 ion from inhomogeneous to homogeneous ligand rebinding kinetic.

100 A was also investigated, and although the CO rebinding kinetics are significantly perturbed, there ar

101 The nonexponential CO rebinding kinetics at both pH 5 and pH 7 are accounted f

102 While CO rebinding kinetics depend strongly on the nature of the

103 Below approximately 60 K the rebinding kinetics do not follow these predictions unles

104 O for both trHbs, time-dependent biphasic CO rebinding kinetics for P-trHb at low CO partial pressure

105 work compares the geminate and solvent phase rebinding kinetics from two trHbs, one from the ciliated

106 the ligand access channel as indicated by CO rebinding kinetics in flash photolysis experiments.

107 e), we observe significant effects on the CO rebinding kinetics in the 10 ns to 10 ms time window.

108 The CO rebinding kinetics in these CooA complexes take place on

109 e distal pocket is mutated (e.g., V68W), the rebinding kinetics lack the slow phase.

110 brational coherence spectra and nitric oxide rebinding kinetics of Caldariomyces fumago chloroperoxid

111 The rebinding kinetics of CO to protoheme (FePPIX) in the pr

112 We also report CO rebinding kinetics of MP in the 150 fs to 140 ps time wi

113 Comparison of the temperature-dependent NO rebinding kinetics of native Mb with that of the bare he

114 In this work, the rebinding kinetics of NO and CO to NP4 are investigated

115 The rebinding kinetics of NO to the heme iron of myoglobin (

116 Comparison of the CO rebinding kinetics of RrCooA, truncated RrCooA, and DNA-

117 We show that the removal and rebinding kinetics of the template and various potential

118 Careful analysis of the CO rebinding kinetics reveals that in NP4 and, to a larger

119 sual because most other heme systems have CO rebinding kinetics that are too slow to make the measure

120 The response of the rebinding kinetics to temperature, ligand concentration,

121 ntrol, an analogous increase in the geminate rebinding kinetics was not observed.

122 8-ns photodissociation quantum yield and the rebinding kinetics, point to a pivotal functional role f

123 udy proximal and distal influences on ligand rebinding kinetics.

124 e influence of the proximal ligand on the CO rebinding kinetics.

125 ulation-specific differences in the observed rebinding kinetics.

126 experiments showed overall fast biphasic CO rebinding kinetics.

127 DM-catalyzed dissociation of each isomer and rebinding, leading to a final isomer composition determi

128 s is followed by dissociation and subsequent rebinding, leading ultimately to a preponderance of the

129 However, when the two CO rebinding lifetimes are extended into milliseconds by re

130 Thus, occlusion of complex rebinding may play a significant role in a variety of bi

131 vidently occurred by an affinity release and rebinding mechanism that did not require motor activity

132 Our data are well explained by the sliding-rebinding model for catch-slip bonds extended to incorpo

133 EPS are robustly predicted by a rebinding model that considers the microenvironment of p

134 We also found that, consistent with the rebinding model, the effective diffusion constant is neg

135 Both allosteric and sliding-rebinding models have emerged to explain catch bonds.

136 The dinucleotide rebinding observed as inhibition under these conditions

137 tation of nitrosylated sGC, only NO geminate rebinding occurs in 7.5 ps.

138 Rebinding occurs when the TCR-pMHC on-rate outcompetes T

139 The data presented here show that weak rebinding of a single PsbO subunit to PsbO-depleted PSII

140 o the kinetic model to account for potential rebinding of accumulated solution NO.

141 Also, rebinding of ACPs dampens full relaxation of stress.

142 of P2X3 by nanomolar [agonist] occurs by the rebinding of agonist to desensitized channels before rec

143 for its acetylation sites, due to the rapid rebinding of alphaTAT1 onto highly concentrated alpha-tu

144 fected by the buried water molecules and the rebinding of an external K(+) ion.

145 straction of a hydrogen atom followed by the rebinding of an OH group.

146 Functionality is probed through the geminate rebinding of both CO and O2.

147 ion of Aurora B kinase activity prevents the rebinding of BubR1 to metaphase kinetochores after a red

148 ity is chelator-insensitive, indicating that rebinding of Ca(2+) restores the structural integrity of

149 bsequent restoration of dark [Ca2+]i and the rebinding of Ca2+ to its release site, but after brighte

150 vation or a slow conformational change after rebinding of Ca2+ to SR regulatory proteins.

151 ot produce conformational changes that block rebinding of cation.

152 Rebinding of CO and of Cys-52 following CO photodissocia

153 Measurements of the geminate rebinding of CO establish a kinetic difference between t

154 ing of CO to C-trHb, very fast solvent phase rebinding of CO for both trHbs, time-dependent biphasic

155 dications of ultrafast (picosecond) geminate rebinding of CO to C-trHb, very fast solvent phase rebin

156 Thus, in human erythrocytes, rebinding of DADMe-ImmH is 50-fold more likely than diff

157 inhibits replication by promoting continual rebinding of DnaC to DnaB and consequent prevention of h

158 (2) The rate of binding and rebinding of dNTP to captured complexes affects dwell ti

159 hotobleaching also revealed dissociation and rebinding of EB1 to the microtubule wall with a similar

160 ) state upon substrate hydroxylation (k(2)), rebinding of excess substrates (k(3)), and indicated tha

161 Rebinding of FMN at these conditions is nominal, and the

162 in the presence of a protein trap to prevent rebinding of free protein to the DNA using the methods d

163 rphine-MOR complex for beta-arrestin and the rebinding of Galphai2 after GTP hydrolysis retained the

164 Rebinding of hyperphosphorylated cyclin E--Cdk2 to inter

165 e supported by our data involves binding and rebinding of InlB to multiple binding sites on heparin i

166 These changes are partially reversed upon rebinding of M(O2CR)2 at room temperature ( approximatel

167 es the low-temperature stretched exponential rebinding of MbCO to a quenched distribution of heme geo

168 At high Mg2+, rebinding of Mg2+ to E.ADP forces release of ADP from th

169 nges of actin are caused by dissociation and rebinding of myosin cross-bridges, and that during contr

170 e cofactor, consistent with some release and rebinding of NAD+ during catalytic cycles.

171 T pathway which involves loss of NADP(+) and rebinding of NADPH to precede loss of the product H4F (n

172 cooperative process, which favours immediate rebinding of newly dissociated pb10 to the 120 hexamers

173 7 ps kinetic phase that we attribute to the rebinding of NO directly from the distal pocket.

174 In both cases, the rebinding of NO induces the cleavage of the Fe-His bond

175 icates that one or more barriers that impede rebinding of oxygen from docking sites in the heme pocke

176 ed by the mutations, the picosecond geminate rebinding of oxygen is at most minimally affected.

177 here that the extent of nanosecond geminate rebinding of oxygen to the variant and its isolated beta

178 were generated for the nanosecond and slower rebinding of photodissociated CO to trHbN in solution an

179 otubules when dephosphorylation of CENP-E or rebinding of PP1 to CENP-E is blocked.

180 f N-propargyliminoglycine and the subsequent rebinding of propynal to the enzyme make the latter mech

181 oscopy (EIS) was used to evaluate subsequent rebinding of PSA to the apta-MIP surface.

182 crease of [Kglutamate] beyond 1 M results in rebinding of salt-displaced polymerase to DNA.

183 ot be explained by differential retention or rebinding of sigma70 during elongation, or by differenti

184 ions (near-geminate combination of NO versus rebinding of solution NO) on catalytic behavior of each

185 dinucleotide synthesis is proposed in which rebinding of the dinucleotide to the enzyme-DNA complex

186 enes xylosoxidans (AXCP) in which picosecond rebinding of the endogenous His ligand following heme-NO

187 ide-free Ran in a conformation that prevents rebinding of the guanine nucleotide.

188 ysis and product release steps promote tight rebinding of the helicase to the nucleic acid.

189 For this protein, dissociation and rebinding of the hexacoordinating amino acid side chain,

190 However, if dissociation and rebinding of the machines occurs at a finite rate (finit

191 tein to the other, as opposed to release and rebinding of the metalloid.

192 ock circumvention involves the unbinding and rebinding of the motors.

193 (k(NO) = 1.4 x 10(11) s(-1)) and shown that rebinding of the proximal histidine to the 4-coordinate

194 eaper-induced apoptosis, most likely through rebinding of the released factors.

195 ation leads to partner exchange, rather than rebinding of the same CD2-CD58 pairs.

196 Selective rebinding of the target analyte was observed as a freque

197 The rebinding of the target analytes to their fragments' cav

198 ted bimolecular complexes by occluding rapid rebinding of the two binding partners.

199 ficant desensitization occurs in response to rebinding of transmitter to the AMPA receptors.

200 u = 225 and 880 micros, are attributed to CO rebinding on the basis of mixed-gas experiments.

201 The dependency of the apparent rate of CO rebinding on the intensity of the probe beam in single-w

202 (E11) mutation causes drastic differences in rebinding on the nanosecond time scale, whereas the effe

203 proximal NO by precluding direct proximal NO rebinding once it has left the proximal heme pocket and

204 he spectral changes, they clearly involve CO rebinding or changes in the environment of an already bo

205 ggest an alternative to the hydroxyl radical rebinding paradigm.

206 a time and probed the stochastic rupture and rebinding paths.

207 the appearance and disappearance of internal rebinding phases in the absence of steric and polar inte

208 relaxation properties of HbY on the geminate rebinding process forms the basis of a model that accoun

209 that the fast (enthalpically barrierless) NO rebinding process observed below 200 K is independent of

210 ter laser photolysis to enhance the geminate rebinding process within the photoproduct.

211 imately 1 and 190 mus, prior to the 20 ms CO rebinding process.

212 pe, and functionality during selective 2,4-D rebinding processes confirming the results obtained duri

213 changes, internal electron transfer, and CO rebinding processes in cytochrome c oxidase from Rhodoba

214 ass transition (Tg approximately 180 K), the rebinding progress slows as temperature increases, and t

215 allowed isolation of polymers with very good rebinding properties and sensitivities.

216 The rebinding property of the MIP film was studied by using

217 The rebinding rate constants for alpha and beta chains are o

218 We also observe that the bimolecular NO rebinding rate is enhanced by 3 orders of magnitude both

219 Further comparison of the CO rebinding rate of the imidazole bound protoheme with the

220 plitude geminate phase with a fundamental CO rebinding rate that is approximately 45 times faster tha

221 RecA filament on the DNA was observed with a rebinding rate two orders of magnitude greater than in t

222 state marker bands demonstrate the change of rebinding rate with pressure.

223 The Cys-52 rebinding rate, 4000 s(-1), is essentially unchanged bet

224 The rebinding rates for the native and mutant species are si

225 provide a complete description that explains rebinding rates that range from femtoseconds to millisec

226 tting observation of the subsequent geminate rebinding reaction (t(rebinding) = 31.6 ps) by monitorin

227 rophores Cy3 and Cy5 to quantify the melting/rebinding reaction by fluorescence resonance energy tran

228 Further insight into the rebinding reaction was obtained by mapping the full pote

229 splays several processes, including geminate rebinding, rebinding after ligand escape to the solvent,

230 The photoproduct undergoes subsequent rebinding/recovery with a time constant of approximately

231 Importantly, rebinding requires that connections be added to the well

232 olecule called the 'template' and capable of rebinding selectively to this target molecule.

233 printed nanomaterials exhibited satisfactory rebinding selectivity, kinetics and reusability.

234 actor (NADP(+)) release and cofactor (NADPH) rebinding, show different temperature dependences for PO

235 s induced by GnRH were most likely caused by rebinding since over 70% of the original response was ab

236 g and approximately 60 K, the nonexponential rebinding slows down as the temperature is lowered and t

237 ve enzymes can act processively due to rapid rebindings (so-called quasi-processivity).

238 Geminate-rebinding studies on these mutants indicate that disrupt

239 Biochemical fractionation and rebinding studies support a model in which Oda7 particip

240 T-like structure persists well after ligand rebinding, suggesting a slow T-to-R transition.

241 Bimolecular rebinding takes place at a statistically averaged rate,

242 s in time constants associated with geminate rebinding, tertiary relaxation, and quaternary relaxatio

243 In batch rebinding tests, the imprinted nanocomposites reached sa

244 reatly higher imprinting factor and specific rebinding than obtained with the same recipe but by solu

245 sink method was used to prevent analyte from rebinding the ligand-coated Octet tips and enabled us to

246 Upon rebinding, the TNV-polythiophene complex changes the flu

247 Thus, one method by which the rebinding theory can be tested is to use TIR-FPR.

248 oss its interface with L-selectin to promote rebinding, thereby providing a mechanism for catch bonds

249 cribed as a single-exponential process, with rebinding time constants of 29.4 +/- 1 and 9.3 +/- 1 ps,

250 large nonexponential geminate amplitude with rebinding time scales of approximately 10(-11)-10(-9) s

251 f mutagenesis on geminate and bimolecular O2 rebinding to 90 mutants at 27 different positions were u

252 We assign the fast phase of NO rebinding to a conformation of the ferric protein with a

253 d by reversible gyrase dissociation from and rebinding to a DNA segment, changing the supercoiling le

254 ansient diffusion through solution and rapid rebinding to a nearby, membrane-associated target lipid.

255 M(-1) s(-1) in beta subunits, whereas ligand rebinding to alphaTrp(E7) subunits after photolysis is m

256 Rapid bimolecular rebinding to an open alpha subunit conformation occurs i

257 reglucosylated rapidly and became capable of rebinding to calnexin.

258 The ultrafast kinetics of CO rebinding to carbon monoxide oxidation activator protein

259 anical work produced during the breaking and rebinding to determine a free-energy difference, DeltaG,

260 a DNA scaffold increased the probability of rebinding to F-actin and enabled processive steps along

261 efined by the rate constants for release and rebinding to GroEL relative to the rate constant for the

262 ay of the transient Cu(B)(1+)-CO complex and rebinding to heme a(3) rates, suggesting that no structu

263 Femtosecond to nanosecond dynamics of O(2) rebinding to human WT myoglobin and its mutants, V68F an

264 d excess of FK506 (to prevent rapamycin from rebinding to its cytosolic receptor FKBP-12).

265 We report kinetics of CO rebinding to microperoxidase (MP) and 2-methylimidazole

266 After photodissociation, ligand rebinding to myoglobin exhibits complex kinetic patterns

267 Geminate oxygen rebinding to myoglobin was followed from a few nanosecon

268 dies of CO photodissociation and bimolecular rebinding to neuroglobin focusing on the ligand migratio

269 elease of the ADP-helicase from mRNA and its rebinding to Nup214.

270 phasic, resulting from inhibitor release and rebinding to PNP catalytic sites.

271 By comparing the rate of CO rebinding to protoheme in glycerol solution with and wit

272 is characterized by a single kinetic phase, rebinding to RmFixL* is characterized by two kinetic pha

273 Whereas CO rebinding to RmFixLN is characterized by a single kineti

274 Subsequent adenylylation of enzyme prevents rebinding to the adenylylated DNA intermediate comprisin

275 lucosylation of glycoproteins supports their rebinding to the carbohydrate-binding ER molecular chape

276 Enthalpic barriers for O2 rebinding to the copper(I) center ( approximately 10 kJ

277 xin undergoes frequent dissociation from and rebinding to the DNA.

278 ereby inhibiting its protonation and slowing rebinding to the Fe.

279 h heme domain) show similar rates for ligand rebinding to the five-coordinate heme domain and the abs

280 In full-length sGC, CO geminate rebinding to the heme does not occur.

281 rate of microtubule association that drives rebinding to the microtubule after force-dependent motor

282 ted from the microtubule by ATP, followed by rebinding to the microtubule by the ADP-containing head.

283 igen-stimulated oscillatory dissociation and rebinding to the plasma membrane with a time course that

284 there is a significant probability of ligand rebinding to the same or neighboring subunits within a t

285 sults, we propose a model in which rapid TCR rebinding to the same pMHC after chemical dissociation i

286 We show that inclusion of induced rebinding to the same pMHC in kinetic proofreading model

287 r "foot stomps," with one hand detaching and rebinding to the same site, and back-steps under suffici

288 aments and would be followed by cross-bridge rebinding to thin filaments.

289 originally thought to be associated with CO rebinding to two different partially folded states of cy

290 erized carbon monoxide photodissociation and rebinding to two forms of the heme domain of Bradyrhizob

291 d then cooled to 25 degreesC were capable of rebinding to, and of reactivating, the O2-evolution acti

292 pose a role for the on rate through multiple rebindings to the same TCR.

293 Mb rebinding was detected by direct electrocatalytic reduct

294 Mb rebinding was examined in Mb-free diluted human serum sp

295 y slow so that at each cycle of dissociation rebinding was favored over folding and a kinetically sta

296 e -7 cleavage site, and the dissociation and rebinding were enhanced when the M184V mutation was pres

297 ck" in the distal pocket, promoting internal rebinding, whereas the out conformation inhibits geminat

298 nsic reduction in selectivity with increased rebinding, which benefits inefficient reactions, rather

299 2+) from aqueous solution was studied during rebinding with the leached IIP particles as a function o

300 ethering and rolling, probably by increasing rebinding within a bond cluster.