ライフサイエンスコーパス: allostery

1 stability (e.g. in relation to catalysis or allostery).

2 basis and underlying functional landscape of allostery.

3 idity, dynamics at different timescales, and allostery.

4 clusion of the catalytic site rather than by allostery.

5 to identify key residues in dynamics-driven allostery.

6 e in signaling, utilizing a process known as allostery.

7 n ideal platform for modulating activity via allostery.

8 the classical Monod-Wyman-Changeux model of allostery.

9 vior of loops upon protein binding including allostery.

10 teractions and intersubunit communication in allostery.

11 ations in this region compromise interdomain allostery.

12 rting the population-shift theory of protein allostery.

13 re ideally suited for the study of enzymatic allostery.

14 to understand the decentralized character of allostery.

15 arrangements responsible for this remarkable allostery.

16 owing for efficient long-range signaling and allostery.

17 e determination of the mechanistic basis for allostery.

18 the active site, implying its importance in allostery.

19 vides a novel tool for interrogating protein allostery.

20 g data reveal the molecular mechanism of the allostery.

21 can be important for biological function and allostery.

22 ernal motion to overall protein dynamics and allostery.

23 that affect inducer binding may also disrupt allostery.

24 ctional importance for the directionality of allostery.

25 ata to test statistical mechanical models of allostery.

26 for the analysis of such entropically driven allostery.

27 a hydrogen bond donor moiety for maintaining allostery.

28 ed ensemble as outlined in classic models of allostery.

29 re, an example for destabilizing interdomain allostery.

30 to advance our fundamental understanding of allostery.

31 the Monod-Wyman-Changeux two-state model of allostery.

32 ights into the molecular events that mediate allostery.

33 ays, but little is known about this presumed allostery.

34 riment, providing new opportunities to study allostery.

35 lecular recognition, catalytic function, and allostery.

36 ypothesis to protein structure databases and allostery.

37 ficant features of the mechanistic basis for allostery.

38 ouble-helical structure is the origin of DNA allostery.

39 ed millisecond-timescale dynamics underlying allostery.

40 uctures and for quantitative descriptions of allostery.

41 into the intimate link between catalysis and allostery.

42 uch, this mechanism is an example of dynamic allostery.

43 rol via an evolutionarily convergent form of allostery.

44 on of a transmembrane receptor in long-range allostery.

45 and offers a good platform for the study of allostery.

46 o identify residues that mediate FBP-induced allostery.

47 identify the structural determinants of this allostery.

48 or cooperative protein binding solely by DNA allostery.

49 en subunits, providing information about PAH allostery.

50 urther probe scenarios dealing with thrombin allostery.

51 exhibits classic signatures of transmembrane allostery.

52 ivation gate and is subject to transmembrane allostery.

53 lso shedding new insights into mechanisms of allostery, although the complexities of candidate allost

54 The simulations reveal that allostery amounts to the propagation of structural and d

55 Using long-simulations dynamic allostery analysis, this study describes an exploration

56 ive insight into the underlying mechanism of allostery and allow us to propose that the hinge twistin

57 low can enrich structure-activity studies of allostery and bias, and have also led to the discovery o

58 ce of protein dynamics in connecting protein allostery and catalysis to control catalytic activity of

59 sms including dual-binding modes, mechanical allostery and catch bonds.

60 w 2 widely recognized regulatory mechanisms, allostery and compartmentalization, which exemplify this

61 s are not mere connectors, and their role in allostery and conformational changes has been emerging i

62 le of intrinsically disordered segments, and allostery and cooperativity between subunits in biologic

63 sed on the classic biochemical principles of allostery and cooperativity.

64 nt conclusions toward the control of protein allostery and design of unique allosteric sites for pote

65 for example, to investigate membrane protein allostery and drug binding in a more natural and deterge

66 e conformational ensemble, the mechanisms of allostery and drug resistance, and the free energy of li

67 These results support the ensemble model of allostery and embody a strategy for the design of protei

68 Here, we clarify the concept of allostery and how it controls physiological activities.

69 Our work expands the perspective on allostery and implicates functional importance for the d

70 identify position 101 as a mediator of both allostery and photocycle catalysis that can impact organ

71 its SBD does not disturb Hsp70 inter-domain allostery and preserves BiP structure.

72 on of W571 as a conformational switch in Env allostery and receptor-mediated viral entry and provide

73 broad implications for our understanding of allostery and suggests that the general concept of the n

74 ng either problem reverses their inferences: Allostery and the amino acids that confer it were not ga

75 btained, we propose the mechanism of CYP46A1 allostery and the pathway for the signal transmission fr

76 light the current available methods to study allostery and their applications in studies of conformat

77 inhibitors as neuroprobes to study 5-HT(2C)R allostery and therapeutics for 5-HT(2C)R-mediated disord

78 Clamp allostery and translocation are more optimal for LF pept

79 insights on poorly understood yet important allostery and underpin an approach applicable for explor

80 We then compare different models of allostery, and discuss the significance of the concept o

81 TCR-CD3 complex, for dynamically-driven TCR allostery, and for pMHC-induced structural changes in th

82 ein-coupled receptors (GPCRs) signal through allostery, and it is increasingly clear that chemically

83 addition or parallel to other mechanisms of allostery, and may explain some current observations on

84 loop 2's roles in regulating RR specificity, allostery, and oligomerization.

85 protein functions, including ligand binding, allostery, and signaling.

86 Although existing models of allostery are firmly rooted in the current structure-fun

87 physical and evolutionary origin of protein allostery, as well as its importance to protein regulati

88 In order to elucidate allostery at atomic resoluion on the ligand-binding WW d

89 , steric, and conformational determinants of allostery at the atomic level were examined in molecular

90 t formally equivalent, there is little-to-no allostery at the level of DeltaG degrees bind.

91 we extend an earlier mechanical model of DNA allostery based on constrained minimization of effective

92 These studies provide a unique dynamic allostery-based perspective to kinase:peptide complexes

93 damentally different from textbook models of allostery because GCK is monomeric and contains only one

94 nd-bound conformation, providing support for allostery between the loop and pocket.

95 the active sites of HslV that facilitate the allostery between these distal sites.

96 This negative, entropically driven allostery between two functional sites of the betaSBD-th

97 is growing evidence that mechanosensing and allostery both play a role.

98 l models and pharmacological applications of allostery, but also by progress in the experimental appr

99 ntally validating transformative theories of allostery, but also in tapping the full translational po

100 udy was designed to examine the mechanism of allostery by comparing the degree to which opioid ligand

101 hain rotamer promotes the functional dynamic allostery by inducing coordinated motions that spread ac

102 with the Bohr effect (1904) to the birth of allostery by Monod and Jacob (1961).

103 r we treat in detail the case of fluctuation-allostery by which amplitude modulation of the thermal f

104 al and theoretical evidence demonstrate that allostery can be communicated through altered slow relax

105 experimental observations demonstrating that allostery can be facilitated by dynamic and intrinsicall

106 Allostery can be manifested as a combination of repressi

107 We argue that allostery can be rationalized in terms of pathways of re

108 We focus on the challenging questions of how allostery can both cause disease and contribute to devel

109 We describe the evolution of the allostery concept, from a conformational change in a two

110 lular regulatory concepts, such as (pathway) allostery, conformational spread, induced folding/unfold

111 solvation model (dichloromethane), show that allostery contributes approximately 30% to overall posit

112 via coevolving residues, whereas interdomain allostery, critical to chaperoning, is robustly enabled

113 Allostery enables tight regulation of protein function i

114 ssfully formulated, and are able to describe allostery even in the absence of a detailed structural m

115 ent to show that hemoglobin, the paradigm of allostery, exhibits two ligand binding phases with the s

116 Allostery exploits the conformational dynamics of enzyme

117 indings provide a foundation to map ribosome allostery, explore ribosome biogenesis, and engineer rib

118 ural model of the ligase revealed long-range allostery extending from the substrate through CUL5.

119 Allostery extensively regulates the activities of key en

120 , we investigate structural determinants for allostery, focusing on modifications to three moieties w

121 ears to be a general mechanism for providing allostery for this enzyme.

122 to quantify ion-pair binding and to separate allostery from electrostatics to understand their relati

123 To better understand the path of allostery from the RAG-2 PHD finger to RAG-1, here we em

124 We generalize the concept of allostery from the traditional non-active-site control o

125 ditorial, we briefly overview the history of allostery, from the pre-allostery nomenclature era start

126 Allostery has been observed and characterized in many pr

127 The concept of allostery has evolved in the past century.

128 erstanding of the molecular underpinnings of allostery has hindered the development of designer molec

129 ed, and the role of Glu-88 in force-assisted allostery has not been examined.

130 To understand the molecular details of this allostery, here, we introduce Env mutations aimed to pre

131 foundations of small molecule antagonism and allostery, highlight the inherent physicochemical challe

132 starting from one of the simplest models of allostery (i.e., the four-state thermodynamic cycle) and

133 The allostery identified in the components of the HPV is non

134 Whereas lipid allostery impacts the phosphotransferase function of the

135 e quantitative site-specific measurements of allostery in a bilayer environment, and highlight the po

136 ructural features responsible for generating allostery in a monomeric enzyme and suggests a general s

137 the energetic basis of the observed dynamic allostery in a PDZ3 domain protein using molecular dynam

138 details of how a single tryptophan mediates allostery in Btk.

139 Negative allostery in CAP occurs between identical cAMP binding s

140 Although the critical role of allostery in controlling enzymatic processes is well app

141 ell-known yet still underappreciated role of allostery in conveying explicit signals across large mul

142 We investigated allostery in core complexes assembled with two chemorece

143 Understanding the nature of allostery in DNA-nuclear receptor (NR) complexes is of f

144 This allostery in EnvZ is independent of membrane composition

145 roles of protein conformational dynamics and allostery in function are well-known.

146 Our study demonstrates temporal allostery in GPCRs, with implications for the modulation

147 scarinic receptor is the prototypic model of allostery in GPCRs, yet the molecular and the supramolec

148 These findings point to antagonistic allostery in ISRIB action on eIF2B, culminating in inhib

149 Monod, Wyman, and Changeux (MWC) explained allostery in multisubunit proteins with a widely applied

150 te mechanisms underlying the established NTD allostery in NMDA-type iGluRs, as well as the fold-relat

151 Together, these results support a model for allostery in PheH in which phenylalanine stabilizes the

152 s between structure, function, dynamics, and allostery in protein kinases, we carried out multiple mi

153 These findings introduce the concept that allostery in proteins could have its origins not in prot

154 e to retain slow relaxation dynamics-induced allostery in proteins in which evolution of the ligand-b

155 Allostery in proteins influences various biological proc

156 A new mechanism of allostery in proteins, based on charge rather than struc

157 t2M/t4M binding site enables programming of allostery in RNAs, recoding oligo-U domains as potential

158 atory target recognition, and ligand-induced allostery in RRNPP regulators and its impact on gene reg

159 been used to reveal the structural basis for allostery in several proteins and protein complexes of b

160 sults reveal a likely role for inter-residue allostery in specificity and an evolutionary decoupling

161 Historically, allostery in structured proteins has been interpreted in

162 finding offers a novel mechanistic basis for allostery in the absence of canonical structural change.

163 function paradigm, the mechanistic basis for allostery in the absence of structural change remains un

164 Remarkably, movement in allostery in the betaI domain of specificity determining

165 We present the evidence for the role of allostery in the context of a quantitative formalism tha

166 in a two-state model (1965, 1966) to dynamic allostery in the ensemble model (1999); from multi-subun

167 Much of the focus on GPCR allostery in the new millennium, however, has been on mo

168 Moreover, Q282A eliminated cis-allostery in the oligomerization variant.

169 Here, we investigate allostery in the peroxisome proliferator-activated/retin

170 In this study, allostery in the second PDZ domain (PDZ2) in the human P

171 suggest a common role of specific models of allostery in their functions.

172 tional selection as the general mechanism of allostery in this canonical signalling domain.

173 Allostery, in particular, relies on ligand-modulated shi

174 ing is most evident in the case of classical allostery, in which a binding event in one protomer is s

175 into nanoclusters might allow for homotropic allostery, in which individual TCRs could positively coo

176 he key pharmacologic characteristics of GPCR allostery include improved selectivity due to either gre

177 tivity between EF-4, EF-3 and EF-2, EF-1 and allostery involving the four EF-hands.

178 The fact that allostery is a common means for regulation in biological

179 Protein allostery is a frequent cause of nonadditivity, but the

180 Allostery is a fundamental mechanism of biological regul

181 Allostery is a fundamental principle of protein regulati

182 Allostery is a fundamental process by which ligand bindi

183 Allostery is a fundamental regulatory mechanism of prote

184 Protein allostery is a phenomenon involving the long range coupl

185 Allostery is a ubiquitous biological regulatory process

186 Allostery is a ubiquitous mechanism to control biologica

187 Allostery is an intrinsic property of many globular prot

188 Allostery is at play in all processes in the living cell

189 Allostery is conformation regulation by propagating a si

190 substrates cooperatively and find that PafA allostery is controlled by the binding of target protein

191 Thus, elucidating the forces that drive allostery is critical to understanding the complex trans

192 Understanding the mechanism of interdomain allostery is essential to rational design of Hsp70 modul

193 Understanding protein allostery is essential to understanding protein function

194 The importance of loop dynamics and allostery is highlighted by a case study of an antibody-

195 ernating access transporters in which 1) cis-allostery is mediated by intrasubunit interactions and 2

196 the long-range communication that underlies allostery is not well understood.

197 While allostery is of paramount importance for protein regulat

198 ng hugely important in biological processes, allostery is poorly understood and no universal mechanis

199 Our current knowledge of allostery is principally shaped by a structure-centric v

200 ence of the membrane-spanning regions, lipid allostery is propagated entirely through peripheral inte

201 We provide a physical explanation for why allostery is related to dihedral complexes: it allows fo

202 Allostery is relayed to the alphaI domain by an internal

203 r results reveal that highly complex dynamic allostery is surprisingly vulnerable and provide further

204 It has been hypothesized that transmembrane allostery is the basis for inactivation of the potassium

205 Allostery is the process by which biological macromolecu

206 way to evaluate the effects of a mutation on allostery is to monitor the allosteric coupling constant

207 stablished link between protein dynamics and allostery led us to propose that differential permissibi

208 This allostery mainly regulates the kinetic on-rate, not off-

209 tion in the role of H+ from flux coupling to allostery may confer regulation by trafficking to and fr

210 We propose that such allostery may regulate DNA's flexibility and the assembl

211 in SHP2 with in vivo activity, suggests that allostery might provide a way forward for PTP inhibitor

212 rview the history of allostery, from the pre-allostery nomenclature era starting with the Bohr effect

213 Its kinase domain functions in allostery not catalysis, and the classical ATP-analog cl

214 Together, we demonstrate how the intrinsic allostery of cGAS efficiently yet precisely tunes its ac

215 lity of receptors and leverages the inherent allostery of GPCR-effector coupling.

216 sed that structurally and dynamically driven allostery, often discussed as limiting scenarios of allo

217 suggesting a selection pressure to fine tune allostery on changes to the CAP ligand-binding pocket wi

218 rough post-translational mechanisms, such as allostery or allokairy.

219 Genetic perturbations targeting allostery or key regulatory nodes in the glycolytic path

220 end on multimerization, such as intersubunit allostery or the capacity to do mechanical work(2).

221 ng transient but specific binding, promoting allostery, or allowing efficient posttranslational modif

222 n, which we call chemical shift detection of allostery participants (CAP).

223 This strategy for identifying allostery participants is likely to have applications fo

224 depend on both proton and potassium binding (allostery participants).

225 In this process, we also identify allostery participants, groups that respond to both bind

226 cis-Allostery persisted, but trans-allostery was lost in an

227 Allostery pervades macromolecular function and drives co

228 Ligand-induced protein allostery plays a central role in modulating cellular si

229 Allostery plays a crucial role in the mechanism of neuro

230 Further, the Ohm allostery prediction for the protein CheY correlates wel

231 This allostery produces a local conformational rearrangement

232 units are formed, suggesting that long-range allostery produces conformational changes that extend fr

233 same proteins in large complexes, studies of allostery, protein quality control during cryo-EM constr

234 d computation, the mechanism of this form of allostery proved difficult to identify at the molecular

235 cts of mutations on biophysical function and allostery reflect a complex mixture of multiple characte

236 echanisms by which the disorder functions in allostery remain to be elucidated.

237 understanding the molecular determinants of allostery remains an elusive goal.

238 Allostery represents a fundamental mechanism of biologic

239 ed by intrasubunit interactions and 2) trans-allostery requires intersubunit interactions.

240 Here, we outline a simple allostery scheme to clarify how an extracellular (ligand

241 2-deoxy-d-glucose uptake and eliminated cis-allostery (stimulation of sugar uptake by subsaturating

242 In contrast, the allostery-suppressing ligand decouples the side-chain ar

243 puzzle in our search for an understanding of allostery that allows us to make predictions on the resp

244 ings reveal residues involved in FBP-induced allostery that enable the integration of allosteric inpu

245 istances at the molecular scale in a form of allostery that is essential for the physiological functi

246 increase their activities by disrupting the allostery that normally serves to downregulate transposi

247 This triggers further allostery that opens the lectin/EGF domain hinge.

248 engage Ca(2+) and mannose without triggering allostery that opens the lectin/EGF domain hinge.

249 difications within an expanded framework for allostery that provides significant insights into how di

250 n which Glu-88 must engage ligand to trigger allostery that stabilizes the high affinity state under

251 deeper insights into the factors that govern allostery, the crystal structure of TylP was solved to a

252 ite consensus about the conceptual basis for allostery, the idiosyncratic nature of allosteric mechan

253 ansition in a widely studied model system of allostery, the PDZ2 domain, is investigated by transient

254 In addition to their role in allostery, the signals control the initiation of catalys

255 and popular method for the study of protein allostery, the widespread phenomenon in which a stimulus

256 demonstrate how the bidirectional nature of allostery-the fact that the two sites involved influence

257 A myriad of cellular events are regulated by allostery; therefore, evolution of this process is of fu

258 losis, which shows extremely complex dynamic allostery: three distinct aromatic amino acids jointly c

259 of virus conversion to A-particles involves allostery through conformation selection.

260 Allostery through DNA is increasingly recognized as an i

261 these pathways adopt different strategies of allostery to allow the tuning of their activities in res

262 tes, allowing the positions most crucial for allostery to be identified.

263 r strategies that couple the peptide-induced allostery to gene regulation.

264 ral structurally distinct PARPi drive PARP-1 allostery to promote release from a DNA break.

265 w that PTP1B uses conformational and dynamic allostery to regulate its activity.

266 M EGFR-selective TKIs alter JM structure via allostery to restore the conformation found when WT EGFR

267 Other inhibitors drive allostery to retain PARP-1 on a DNA break.

268 n its own is sufficient to confer functional allostery to the unregulated enzyme.

269 Allostery, topology, and building block stoichiometry al

270 namics simulations to study the mechanism of allostery underlying negative cooperativity between the

271 hus reveals rigorous mechanistic elements of allostery underlying the dynamics of biomolecular system

272 e at the agonist-binding domain mediates the allostery underlying the negative cooperativity.

273 urating extracellular maltose) but not trans-allostery (uptake stimulation by subsaturating cytochala

274 be their importance for protein dynamics and allostery using as examples key proteins in cellular bio

275 o have investigated the mechanisms of CYP3A4 allostery using biophysical and advanced spectroscopic t

276 introduction to the investigation of protein allostery using molecular dynamics simulation.

277 This allostery was accompanied by a striking conformational c

278 cis-Allostery persisted, but trans-allostery was lost in an oligomerization-deficient GLUT1

279 nd keeping in mind the equilibrium nature of allostery, we consider alternative possibilities for wha

280 s in the mouse PHD and testing for rescue of allostery, we demonstrate that H3K4me3 binding and trans

281 Using a network-based formalism of allostery, we introduced a community-hopping model of al

282 onformational and dynamic changes that drive allostery, we performed time-resolved electrospray ioniz

283 understand the role of this region in Hsp70 allostery, we used molecular dynamics simulations to exp

284 Key residues of PDZ2 allostery were identified with good agreement with NMR s

285 idual residues to whole-protein dynamics and allostery were systematically assessed via rigid body si

286 We review recent data on heterotropic allostery where peptide-MHC and membrane cholesterol ser

287 binding events and an effect consistent with allostery, where hybridization at certain sites on an SN

288 Allostery, where remote ligand binding alters protein fu

289 this new knowledge to offer a perspective of allostery which is consistent with chemical views of mol

290 d on the Monod-Wyman-Changeux (MWC) model of allostery, which posits that chromatin fluctuates betwee

291 observation points to charge-reorganization allostery, which should be operative in addition or para

292 We expect this frustration-based model of allostery will prove to be generally important in explai

293 PDK1 reveal multiple hotspots of synergistic allostery with cumulative effects greater than the sum o

294 teristics, initiate a propensity for dynamic allostery with possible functional implications in bispe

295 s in the NMR methods tailored to investigate allostery with the goal of offering an overview of which

296 des insight into conformational dynamics and allostery within CFTR.

297 ledge of biased signaling and small molecule allostery within class B GPCRs is discussed, highlightin

298 PDZ domains are classic examples of dynamic allostery without conformational changes, where distal s

299 Here, we describe how allostery works from three different standpoints: thermo

300 The question of how allostery works was posed almost 50 years ago.