ライフサイエンスコーパス: open state

1 alpha in yeast by accelerating return to the open state.

2 s sufficient to stabilize this complex in an open state.

3 competes with PIP2 to stabilize the channel open state.

4 und P450cam to change from the closed to the open state.

5 nels by prolonging the residence time in the open state.

6 dulate the activation gate and stabilize its open state.

7 to the change in conformation from closed to open state.

8 xpected to have closed clefts in the channel-open state.

9 n with the conformation similar to the fully open state.

10 hen it enters the central pore cavity in the open state.

11 Binding to the GPCR stabilizes the open state.

12 ive to the Gate domains may access an inward-open state.

13 ation, the HBC gate can be stabilized in the open state.

14 t states: an inward-open state and a lateral-open state.

15 ger loop (TL), allowing visualization of its open state.

16 opts a potentially desensitized or partially open state.

17 bind when the trimer transiently samples an open state.

18 ates a non-fouling, liquid-lined pore in the open state.

19 reas the McjD-based model could represent an open state.

20 YE, which was determined to be in a "primed" open state.

21 NKCC1 captured in a partially loaded, inward-open state.

22 are found to prefigure the transition to the open state.

23 eines in TMs 1 and 12 stabilized the channel open state.

24 utward-open state to the Na(+)-bound, inward-open state.

25 that fourfold pore symmetry persists in the open state.

26 e indicative of changing from a closed to an open state.

27 nsition state decreases the stability of the open state.

28 ating, in particular on the stability of the open state.

29 ck, whereas the fast mode blocks RyR2 in the open state.

30 y be exchanged if the channel resides in the open state.

31 pore gate closure, trapping channels in the open state.

32 whereas incorrect dNTPs are delivered to the open state.

33 rgy barrier between them is located near the open state.

34 n the closed state, but not in the ATP-bound open state.

35 onal changes and approaching or reaching the open state.

36 a conductor with a prolonged lifetime in the open state.

37 125 and Arg104 biases the hemichannel to the open state.

38 ethiosulfonate, but only when applied in the open state.

39 s of S6 (S6(T)) to stabilize the gate in the open state.

40 ve, consistent with S4-S5(L) stabilizing the open state.

41 , nanogatekeeper switches from the closed to open state.

42 by a stabilization of the ANO1 Ca(2+)-bound open state.

43 tidaredoxin (Pdx), shifts P450cam toward the open state.

44 al Hv1 blocker on a model of human Hv1 in an open state.

45 in the absence of a structure in the matrix-open state.

46 the channels into long sojourns in the fully open state.

47 ts from a closed ground state to a CD4-bound open state.

48 (L267N/L270N) stabilized channels in a fully open state.

49 ensor that are associated with the channel's open state.

50 f the N terminus and transition to an inward-open state.

51 cyclic guanosine monophosphate (cGMP)-bound open state.

52 49-A agonist-bound structure at pH 6.0 in an open state.

53 n outward-open, outward-occluded, and inward-open states.

54 ndent dynamic equilibrium between closed and open states.

55 the other TM segments both in the closed and open states.

56 repeatedly between whole hexamer closed and open states.

57 ana, MSL1, presumably in both the closed and open states.

58 cycling between cytoplasmic-open and matrix-open states.

59 conformational states termed the closed and open states.

60 n state, intermediate between the closed and open states.

61 ribute to gating and selectivity in discrete open states.

62 g solvent exposure of Y671 in the closed and open states.

63 tions that lead to a significant fraction of open states.

64 conformational transition toward the inward-open state, a role that is likely to be shared across th

65 bsence of ligand and that it remains in this open state after binding AMPPCP, as we had observed for

66 ausing NMDA receptors to dwell longer in pre-open states along the activation pathway.

67 (AM(C)), MYO1C(16) populated the actomyosin open state (AM(O)) and AM(C) equally, and MYO1C(35) favo

68 (AMD(C)) 5-fold more than the actomyosin.ADP open state (AMD(O)) and to a greater degree than MYO1C(C

69 AM complex in two distinct states: an inward-open state and a lateral-open state.

70 ely uniform distribution of cellulose in the open state and a more fibrillar pattern in the closed st

71 drastic structural change between an active open state and an inactive closed conformation.

72 HpNikR adopts an equilibrium between an open state and DNA-binding competent states regardless o

73 the 1B domain of PRRSV nsp10 adopts a novel open state and has a unique C-terminal domain structure,

74 In the MitTx-bound open state and in the previously determined low-pH desen

75 CALHM2 channel in the Ca(2+)-free active or open state and in the ruthenium red (RUR)-bound inhibite

76 revents the transition of the receptor to an open state and increases its dwell time in an intrinsica

77 that these domain interactions stabilize the open state and limit the rate of charge return.

78 g ranolazine does not selectively affect the open state and may also interact with inactivated states

79 structure of LmrP in a ligand-bound outward-open state and observed an embedded lipid in the binding

80 orms were crystallized, one in an apparently open state and one in an occluded state, indicating that

81 ermectin and related molecules stabilize the open state and potentiate neurotransmitter binding.

82 fit mechanism, i.e., the ligand binds to the open state and subsequently triggers a rapid closing of

83 , whereas the fast gate operates between the open state and the closed state and exhibits a residual

84 e of WT-CFTR by stabilizing a posthydrolytic open state and thereby fosters decoupling between the ga

85 PRE complex equilibrium toward the classical/open state and toward states that favor EF-G dissociatio

86 uT, including a substrate-free state, inward-open state, and competitive and non-competitive inhibito

87 article only blocks sodium channels from the open state, and mutagenesis studies demonstrate that thi

88 e IVM binding between subunits stabilizes an open state, and that the relaxed nonIVM conformations mi

89 a previously uncharacterized 'outward-facing open' state, and highlight the relevance of global struc

90 we show that homocellular GJs in a passively open state are crucial for electrical uniformity within

91 e dimensional changes between the closed and open state are unaffected by the mutations.

92 Energetically, the lesioned open states are similar in energy to those of the corres

93 These open states are stably maintained in highly condensed mi

94 er likely to be representative of the inward-open state associated with substrate release.

95 l microstates, stabilizing a substrate-bound open state at the expense of a substrate-bound closed st

96 aVAb mutants that capture tightly closed and open states at a resolution of 2.8-3.2 A.

97 We report both closed- and open-state atomic cryo-EM structures of a full-length Ca

98 in the x-ray atomic structures of closed and open state bacterial pLGICs, we propyose that the model

99 or Ub E1s, but none has been reported in the open state before pyrophosphate release or in the closed

100 One of these conformational states, the open state, binds to the GPCR; the second conformation,

101 Thus, our data support a model in which open state block of this channel occurs not via binding

102 X-ray structures of the open state bound to a nonhydrolyzable ATP analog (AMPPCP

103 po resting/closed state, in an activated/pre-open state bound with partial agonists and a positive al

104 in constructs locked in either the closed or open state by chemical cross-linking or deletion mutagen

105 tations mainly impaired stabilization of the open state by propofol, i.e., reduced gating efficacy.

106 ependent voltage sensors directly coupled to open states can simulate experimental changes in I (Ks)

107 ts, both mutations markedly destabilized the open state, causing a dramatic decrease in channel volta

108 tes and increased the energy barriers toward open states, causing NMDA receptors to dwell longer in p

109 rug access to a side pocket generated in the open-state channel configuration and lined by S6 and S4-

110 In the open-state channel model, F351 lines a pocket that also

111 rted cryogenic electron microscopy (cryo-EM) open-state channel structure, multiple microseconds-long

112 ding sites must be saturated to stabilize an open state conducive to peptide recognition, yet the pEF

113 dergoes spontaneous deviations away from the open-state configuration.

114 However, the open state conformation exhibited varying degrees of hyd

115 se c-di-GMP-binding motifs also stabilize an open state conformation in apo MrkH via contacts from th

116 inding to SUR1 biases K(ATP) channels toward open states, consistent with SUR1 variants with lower K(

117 rts the idea that this substrate-independent open state correlates with an intermediate outward facin

118 An "open"-state crystal structure of lysine 5,6-aminomutase

119 ount that the variable equilibria of the two open states depend on light intensity, voltage, and the

120 e activation of ELK channels involves a slow open-state dependent rearrangement of the direct interac

121 ons; functionally, they all yielded a stable open state despite varying potencies.

122 Binding of ranolazine to either preopen or open states did not affect the excitability of the simul

123 state structure is a symmetric pentamer, the open state displayed unexpected asymmetric architectures

124 Relief of auto-inhibition to an active, open state, due to a conformational change of the ELMO1

125 ifferences in the energies of the closed and open states, due to different interactions between the v

126 te structures, an intermediate state, and an open state, each embedded in a phosphatidylcholine bilay

127 stepwise sojourns through multiple discrete open states, each with unique channel gating and conduct

128 ort requires cycling from outward- to inward-open states, efficient proton transport still occurs in

129 a closed state (engaged with duplex DNA), an open state (engaged with a transcription bubble), and an

130 e nexus transforms Orai1 into a persistently open state exactly mimicking the action of STIM1.

131 his prompts the ATP binding site to adopt an open state, favoring ATP release and reducing the veloci

132 d configuration for the gap junction but the open state for the hemichannel.

133 closed state" steric barrier compared to an "open state" for the re-face.

134 OsSWEET2b in an apparent inward (cytosolic) open state forming homomeric trimers.

135 esized that the Pdx-induced shift toward the open state frees the essential Asp251 from salt bridges

136 orted, and structural models for the channel open state have been proposed, but a complete characteri

137 d but homology models of the CFTR closed and open states have been produced based on the crystal stru

138 a spontaneous closing transition to the half-open state in response to the gamma rotation in the synt

139 NS2B is remote from NS3pro and exists in an open state in the absence of an inhibitor; however, in t

140 ions increase the contribution of the active open state in the absence of Ca(2+) (M(-)).

141 conditions of antibiotic challenge and in an open state in the presence of AcrB inhibitor.

142 The transitions from the closed to the open state in the two VSDs are known to occur cooperativ

143 Among our key findings is the existence of open states in all SNase mutants containing "buried" res

144 ts have less stable closed states than their open states, in marked contrast to the wild-type enzyme,

145 E, A1632T failed to slow current decay (i.e. open-state inactivation) and did not increase resurgent

146 It is both an open state inhibitor and a resting state inhibitor.

147 ansition to this conformation from the fully open state is accompanied by well-defined changes in the

148 Its negative charge in the open state is decisive for proton selectivity.

149 unlesioned pol-beta anti(G:C) system, whose open state is energetically higher than the closed state

150 However, an open state is enhanced in full-length membrane reconstit

151 ccluded state and deprotonated in the inward-open state is further confirmed via the use of absolute

152 The structure of the cytoplasmic-open state is known, but it has proved difficult to unde

153 activates TRPV2_Quad but the ligand-induced open state is relatively unstable, whereas binding of ca

154 The open state is short-lived and has weak or nonexistent in

155 ations are resolved and more ordered, 2) the open state is the major component, and 3) Ca(2+) stabili

156 Shifting to the open state is thought to be important in the formation o

157 lf-saturated configuration suggests that the open state is unstable and reverts toward a closed state

158 tion, elevated retinal affinity, an extended open-state lifetime, and photocurrent amplitudes greatly

159 ercolates" 10 times slower than Na(+) in the open state, likely due to a conformational and orientati

160 ere, we describe the structure of the matrix-open state locked by bongkrekic acid bound in the ADP/AT

161 CAD binding supports a role in open state maintenance and reveals a second phase of CAD

162 We conclude that open-state MalE stabilizes MalFGK2 in the outward-facing

163 of ATP is rate-limiting, (ii) the binding of open-state MalE to the transporter induces ATP cleavage

164 looser substrate-protein interactions in the open state may not be compatible with the observed regio

165 uctural differences between their closed and open states may help in designing improved drugs that bi

166 The results support our proposed open state model and shed light on the preferred tautome

167 In combination with docking to closed and open state models of TRPA1, photoaffinity labeling sugge

168 C paralog transitions from the closed to the open state more readily than the ssTnC paralog, an unfav

169 ional switch between inward-open and outward-open states necessary for drug efflux.

170 s O(1)', O(2)', and O(3)', between the fully open states O(1), O(2), and O(3), were polarity selectiv

171 model activator binds to the closed (C3) and open states (O).

172 ure, ChR2 transitions from a high-conducting open state (O1) to a low-conducting open state (O2) with

173 Under steady-state light conditions, the two open states, O1 and O2, mediate the photocurrents with d

174 nducting open state (O1) to a low-conducting open state (O2) with differing ion selectivity.

175 gate in an open conformation, revealing the open state of a BacNav with intact voltage sensors.

176 ed insights into the structure of a possibly open state of a eukaryotic Cys-loop receptor, the basis

177 ium-selective ion channels, and captures the open state of an ASIC.

178 coral snake, to define the structure of the open state of ASIC1a.

179 We propose that Pds5 stabilizes a transient, open state of cohesin to promote its release from chromo

180 ort a mechanism by which POPG stabilizes the open state of ELIC relative to the desensitized state by

181 nds bind in the central cavity of the inward-open state of hGLUT1, and all binding sites overlap the

182 and impairs working memory by increasing the open state of hyperpolarization-activated cyclic nucleot

183 ound MBP promotes the transition to the semi-open state of MalK when the transporter is in the membra

184 nnels, and the generation of Ip requires the open state of Orai1, not STIM1 itself.

185 /S45A) at biotin-binding sites stabilize the open state of SA L3,4 loop, thereby further reducing bio

186 1 can contribute to the stabilization of the open state of syntaxin-1 during its transition from "clo

187 The results provide new understanding on the open state of the channel and how STIM proteins may exer

188 with the plasma membrane and stabilizes the open state of the channel.

189 n four K(+) channel subunits, inducing a pre-open state of the channel.

190 nalogues could trigger the transition to the open state of the enzyme.

191 2+) binds very weakly (K(d) <= 37 mM) to the open state of the enzyme.

192 the 'cytoplasmic cap', which stabilizes the open state of the ion channel pore and creates lateral,

193 hat the cognate nucleotides are bound to the open state of the polymerase.

194 reduction in the time spent in a long-lived open state of the receptor.

195 They preferably bind to the open state of the sodium channel by interacting with two

196 a parallel coiled coil state, mimicking the open state of the stator.

197 work also applies to the previously reported open state of the wild-type apo-SA.

198 a homology model of human P2X4, based on the open state of zfP2X4, yielded evidence of a putative gin

199 osamide targets the intermediate preopen and open states of hNav1.5 Na(+) channels.

200 We constructed models of both the closed and open states of Hv1 channels that are consistent with the

201 DM stabilized channel open states of RyR1, RyR2, and cortical preparations exp

202 ever, the molecular nature of the closed and open states of syntaxin is not well defined.

203 models are representative of the closed and open states of the Hv1 channel.

204 open, outward-partially occluded, and inward-open states of the transport cycle.

205 e turret and reveal fully open and partially open states of TRPV2, both with unoccupied vanilloid poc

206 facilitated by the formation of short-lived "open" states of the pores upon linker dissociation.

207 The widespread toxin-antitoxin loci and 'open' state of the pangenome provided evidence of plasti

208 elow K(d), CorA adopts a dynamic (putatively open) state of multiple conformations that imply structu

209 ed state (in the free hormone) and an active open state (on receptor binding).

210 sely contacts the FAD domain, whereas in the open state, one of the FMN domains rotates away from its

211 an alternative flap orientation of a curled open state or an asymmetric configuration when interacti

212 allowing substrate entry or product release (open state), or catalysis (closed state).

213 Thus, increased temperature stabilized the open state over the closed state of Kv11.1a/1b channels

214 ockade of a Shaker Kv channel that undergoes open-state P/C-type inactivation exhibits fast onset and

215 op equilibrium position from a predominantly open state (P185A) to 50:50 (F182A), 35:65 (P188A), and

216 ling a strong temperature dependence of both open-state population and exchange rate.

217 iles for Na(+) and for Cl(-) ions within the open state pore revealed more rugged energy landscapes u

218 This stabilizes the open-state position of the GluN1 M3 helices.

219 otentiates NMDAR function by stabilizing the open-state position of the GluN1 M3 helices.

220 Here, by measuring the closed- and open-state reactivity of MTSET to substituted cysteines

221 ws Hsp104 to relax back to its lowest energy open state ready to restart the cycle.

222 l guest molecule, while the other, the fully open state, recognizes a cationic guest molecule.

223 nd to the V23T-MscL sub-conductive and fully open states recorded in native bacterial membranes or li

224 mediate anesthetic binding and stabilize an open state regulated by pore residue Leu-122.

225 s in the intermediate-open and the activated-open states, resulting in changes of open pore propertie

226 ons with a structure of Band 3 in an outward-open state reveal that the Core domains of Bor1 have rot

227 csA channel determined at low K(+) or in the open state revealed a constricted conformation of the se

228 The general features of the 'open state' SA among different SA variants may facilitat

229 predicted to introduce steric strain in the open state show markedly reduced CD4 interactions.

230 pyran (a ring-close) and merocyanine (a ring-open) states, simple exposure of the hydrogels to white

231 HF2 accelerates the rate of closed-state and open-state sodium channel inactivation, which synergizes

232 t leucine substitution, results in increased open state stability and hence significantly reduced ATP

233 However, as a consequence of the increased open state stability, both Kir6.1(V65M) and Kir6.2(V64M)

234 Consequently, it was proposed that an open-state stabilization of the PD imposes a mechanical

235 nd the molecular basis of Ca(2+) binding and open-state stabilization, we performed 100 ns molecular

236 free from crystal packing and remain in an 'open state', stabilized by a consistent H-bonding networ

237 mics simulations to predict an AMPA receptor open state structure and rationalize the results of muta

238 The open state structure harbours an intracellular motif we

239 the anion-selective alpha1 glycine receptor open-state structure-instead of the five native alanines

240 onformation has previously been observed in "open" state structures formed after CD4 receptor binding

241 fts measured, it can be interpreted that the open-state structures are transient at physiological pH,

242 The 'early' open states substantially contribute to IK,L activation

243 repertoire of parameters that may gate their opening state, such as voltage-sensitivity, modulation b

244 SC is flexible and exists in both closed and open states, suggesting that the mammalian SC D2 domain

245 e 5,000-fold higher affinity of the extended-open state than the bent-closed and extended-closed stat

246 ons confirm designation of NaVAb/1-226 as an open state that allows permeation of hydrated Na(+), and

247 -spots and suggest a facile transition to an open state that can accommodate ligand binding.

248 We propose a model for the structure of the open state that has stabilizing intersubunit interaction

249 e channel stochastically switches between an open state that permits ion conductance and a closed sta

250 ormation of a labeled UvrD monomer to a more open state that shows no helicase activity.

251 een proposed to cycle between an "unfolded"/"open" state that allows an NTP substrate to enter the ac

252 nct structural states, a closed state and an open state, that are adopted by the C-terminal arm of Cc

253 ot pass through the side channel, but in the open state, the leading strand surprisingly interacts wi

254 In the ligand-free open state, the loop is exposed to solvent, where it can

255 The open state then triggers the sequential activation of co

256 It reduces time in the open state, thereby decreasing substrate protein loss.

257 mol energy difference between the closed and open states, thus oversensitizing the receptor.

258 In contrast, TL switches from an inactive open state to a closed active state to facilitate nucleo

259 of dynein from the autoinhibited state to an open state to facilitate dynein activation.

260 ese negatively charged compounds bind in the open state to positively charged arginines and lysines b

261 he antiporter from the proton-bound, outward-open state to the Na(+)-bound, inward-open state.

262 otion that alternates between the closed and open states to shuttle electrons from the CTD via the NT

263 s switch helps mediate a transition from an 'open' state to a 'closed' state that tightly binds nucle

264 g closed states while facilitating closed-to-open state transitions.

265 to identify residues that contribute to the open-state transitions and the discrete ion selectivity

266 51 heterodimer) from a closed to a partially open state upon addition of a nonnucleoside inhibitor.

267 e and undergo a conformational change to the open state upon binding.

268 bulk rearrangement of DraNramp to the inward-open state upon metal binding and facilitate return of t

269 eturn of the empty transporter to an outward-open state upon metal release.

270 ite dynamic and exchanges between closed and open states upon interaction with FHA.

271 at these sites could be latched into a full open state using the bifunctional cross-linker 1,2-ethan

272 and Asn-258), the transition between the two open states (Val-86), open channel stability, and the hy

273 at agonist-bound receptors transition to the open state via two conformations, an "unconstrained pre-

274 The outward-open state was obtained by electron crystallography with

275 The inward-open state was obtained by x-ray crystallography in the

276 Here, utilizing K(V)7.1's unique two open states, we report a two-stage E-M coupling mechanis

277 nformational transition of M2 from closed to open state when the AH domain is included in the M2 cons

278 amics of the spike motion between closed and open states when CD4 is bound.

279 sted that F56Bpa interacts with KCNQ1 in the open state, whereas F57Bpa interacts predominantly in re

280 ity by increasing intrinsic stability of the open state, whereas the cluster of Y981S/G985E/M1056I su

281 de bond (E235C/K393C) sets the channel in an open state, whereas the other (E235C/Y389C) switches the

282 namics model of the channel structure in the open state which confirms our direct observations.

283 med ChR2-XXL (extra high expression and long open state), which displays increased expression, improv

284 t the double mutant is trapped in the inward-open state, which binds the drug, but cannot couple to t

285 and its analogue-dependent transition to the open state, which is one step that was proposed to compl

286 hannel formed by domains 1A and 1B adopts an open state, which may create enough space to accommodate

287 ured in the crystal structure to a much more open state, which we consider likely to be representativ

288 These open states, which are distinct from the swinging door s

289 nditions represent the channel in closed and open states, which uncovered substantial tertiary and qu

290 ate, the SBP has been proposed to rest in an open-state, which is not recognised by the transporter.

291 s and formation of new hydrogen bonds in the open state, while the mutant pore residue reshaped the p

292 the enzyme preferentially adopts a globally open state with accessible binding sites.

293 /cofactor pair is spatially separated in the open state with inhibited enzyme function, whereas in th

294 le and reversible transitions of MscL to the open state with measured parameters of lateral expansion

295 of F233 mutated to alanine indicate that the open state with the fourth arginine in S4 above the hydr

296 e protein N gate is present in an 'arms-wide-open' state with the undimerized N-terminal ParE ATPase

297 and the linker, that becomes flexible in the open state, with 627 and NLS dislocating into a highly d

298 of the total energy, toward stabilizing the open state, with a smaller contribution from VSD I ( app

299 that the RNA binding pore adopts closed and open states, with the latter able to accommodate RNA.

300 non-inactivating channels and structures of open states without a pore plug, indicating that this pr