ライフサイエンスコーパス: substrate binding

1 ht into dynamic loop movements that occur on substrate binding.

2 dimer that adopts a closed conformation upon substrate binding.

3 on for ENZ, PRO substantially contributes to substrate binding.

4 from the 2Fe-2S cluster plays a key role in substrate binding.

5 EH crystal structure was used to rationalize substrate binding.

6 ate of alternating access but did not impair substrate binding.

7 groups vicinal to the epimerization site for substrate binding.

8 "opening" a tyrosine gate allowing enhanced substrate binding.

9 evant for both the ZIP2-H(+) interaction and substrate binding.

10 tify the critical residues for catalysis and substrate binding.

11 nges of the oxygenase and TPR domains during substrate binding.

12 WW domain interresidue contacts involved in substrate binding.

13 tructural network communication, and impairs substrate binding.

14 xposed and accessible for donor and acceptor substrate binding.

15 he catalytic pocket and could participate in substrate binding.

16 p2, alleviating autoinhibition and promoting substrate binding.

17 cleft state, explaining the initial mode of substrate binding.

18 the Fe(II)-aquo bond is minimally altered by substrate binding.

19 ronic and structural changes that occur upon substrate binding.

20 ed at amino acid residues inferred to impact substrate binding.

21 y affect residue 132, which helps coordinate substrate binding.

22 e site and provides additional restraints on substrate binding.

23 ents describing the steady-state kinetics or substrate binding.

24 mutagenesis to identify residues involved in substrate binding.

25 plementary roles in catalyst aggregation and substrate binding.

26 auses a change in the DeltaH associated with substrate binding.

27 data establish a new bipartite mode of USP7 substrate binding.

28 rotein, to identify key residues involved in substrate binding.

29 de bonds and reductively eliminate H(2) upon substrate binding.

30 ency improvement is based on higher affinity substrate binding.

31 le, while also providing insight into native substrate binding.

32 H-site motif is the primary determinant for substrate binding.

33 outward-facing transporter conformation upon substrate binding, a conformation possibly underlying an

34 tants and found that they retain appreciable substrate-binding ability despite being defective in Lip

35 tion states of the ionizable residues in the substrate-binding active-site cavity are; resolving this

36 bility to bind glutathione without a loss of substrate binding activity.

37 ts into a general principle that confers the substrate binding adaptability and specificity to OGA in

38 The temperature dependence of p38alpha:substrate binding affinity, as measured by surface plasm

39 ng for metabolic flux control by fine-tuning substrate-binding affinity for the key enzymes in the co

40 ted SNPs located around the pY pocket weaken substrate-binding affinity in biophysical assays.

41 Reversible initial substrate binding allows ClpXP to check potential substr

42 mbine, in an enzyme-like fashion, a site for substrate binding and a catalytically active site.

43 formations: a more open form that allows for substrate binding and a closed form, which we predicted

44 ively studied, especially its mechanisms for substrate binding and a fidelity-related conformational

45 These structures provide clear insights into substrate binding and catalysis and clearly elucidate wh

46 provide insights into key features linked to substrate binding and catalysis and may aid the structur

47 sidues in BaeAB's BaeA subunit important for substrate binding and catalysis, including an asparagine

48 changes in RAG-1, allosterically stimulating substrate binding and catalysis.

49 nion hole and primary specificity pocket for substrate binding and catalysis.

50 n differences in mobile elements involved in substrate binding and catalysis.

51 , and Arg(245) to interrogate their roles in substrate binding and catalytic activity.

52 al domain (NTD) that plays critical roles in substrate binding and catalytic complex assembly.

53 y a lack of structural information regarding substrate binding and cleavage.

54 n of the target deoxycytidine is favored for substrate binding and deamination.

55 s structural disorder tends to be located in substrate binding and domain linking regions.

56 The E1099K mutation altered enzyme/substrate binding and enhanced the rate of H3K36 methyla

57 40 domain of FBXW7, which is responsible for substrate binding and frequently mutated in human cancer

58 d residue His-257, to understand its role in substrate binding and in the catalytic mechanism of this

59 hiff base linkage at Lys-255 is critical for substrate binding and isomerization.

60 s of evidence show that ClpS's inhibition of substrate binding and its ATPase repression are separabl

61 The putative substrate binding and processing site is located on the

62 Here, we probe the interaction between substrate binding and protein conformation by monitoring

63 that a specific allosteric coupling between substrate binding and protonation is a key step to initi

64 terium smegmatis EmbB, providing insights on substrate binding and reaction mechanism.

65 molecular understanding of the mechanisms of substrate binding and recognition in the GH26 family and

66 induced allosteric regulation of polypeptide substrate binding and release.

67 ed the role of those residues in determining substrate binding and specificity of CYP2J2.

68 ism that achieves error correction by having substrate binding and subsequent product formation occur

69 omplex with our analogs affords insight into substrate binding and the catalytic mechanism.

70 ide optimal three-dimensional structures for substrate binding and the subsequent accelerated reactio

71 ors-small molecules that competitively block substrate binding and thereby prolong neurotransmitter a

72 tates nucleotide exchange and a new round of substrate binding and translocation.

73 biochemical analyses, our studies reveal the substrate binding and transport mechanism of MCTs, eluci

74 ral roles of key loop regions in influencing substrate binding and turnover.

75 uggesting that these residues participate in substrate binding and/or catalysis.

76 Interestingly, the DeltascfC substrate-binding and DeltascfD permease mutants, but no

77 crosstalk, thermodynamic activation profile, substrate binding, and interaction with other similarly

78 the conformational dynamics of inhibitor and substrate binding, and show that a specific allosteric c

79 (cat) and K (0.5) for catalysis, K (0.5) for substrate binding, and the Hill coefficients describing

80 n the nitroTyr aaRS active site for improved substrate binding, and then constructed of a small libra

81 ting points for the development of tankyrase substrate binding antagonists.

82 scribed to the flexible loops that cover the substrate-binding areas.

83 tris(thiolate) trigonal planar complex upon substrate binding as furthermore supported by density fu

84 large conformational changes associated with substrate binding as the enzyme transitions from a binar

85 roles for this essential cysteine residue in substrate binding, as a general acid to advance the Cys-

86 terminants for galactosamine specificity and substrate binding at the -2 to +1 binding subsites.

87 modulates membrane interactions facilitating substrate binding at the active site (km) and the other,

88 terization of a mutated PNPOx form, in which substrate binding at the active site is heavily hampered

89 nal changes in the stalk domain-triggered by substrate binding at the distal end of EccC3 and subsequ

90 This dimeric ERdj3 shows impaired substrate binding both in the ER and extracellular envir

91 Substrate binding breaks the six-fold symmetry of the co

92 leration of a catalytic step occurring after substrate binding but before NAD(+) cleavage.

93 tic activity is not a result of hindrance of substrate binding, but rather a consequence of accelerat

94 We examined substrate binding by docking chlorothalonil (2,4,5,6-tet

95 l of CYP2J2, and explored its sensitivity to substrate binding by molecular dynamics simulations of t

96 structures gives insights into large protein substrate binding by PDI and suggests that the previous

97 Results shows that M120 favors the substrate binding by selectively enhancing the affinity

98 city and underpin the notion that productive substrate binding by these enzymes is complex, depending

99 atalytic N-terminal DHH domain linked to the substrate binding C-terminal DHHA1 domain via an extende

100 ground mutants display significantly reduced substrate binding, catalytic efficiency, and inhibitor b

101 he Fsq structure also uncovered no potential substrate-binding cavities, as the FAD is fully enclosed

102 Natural enzymes catalyze reactions in their substrate-binding cavities, exhibiting high specificity

103 single bulky side chain forms the end of the substrate binding cavity predisposes them to single amin

104 ces that alter the orientation of a putative substrate binding cavity.

105 al a homo-heptamer and show a large putative substrate-binding cavity accessible to the matrix space.

106 TP-driven movements of LptB and those of the substrate-binding cavity in LptFG are bi-directionally c

107 esult in a partially collapsed inward-facing substrate-binding cavity.

108 glutathione-binding site and the associated substrate-binding cavity.

109 gaged" conformation that aligns the PFD-TRiC substrate binding chambers.

110 ibitor molecules bind end-to-end in the long substrate binding channel.

111 to decipher significant differences of beta2 substrate-binding channels and to complete the set of su

112 ta5i subunits exploit the differences in the substrate-binding channels identified by X-ray crystallo

113 to the PCF11 substrate uncovered a conserved substrate binding cleft (SBC) in MAGEs.

114 leavage is defined by interactions along the substrate binding cleft as well as selective stabilizati

115 e residues position a flexible loop over the substrate-binding cleft and modulate the second coordina

116 The structure of Agd3 includes an elongated substrate-binding cleft formed by a carbohydrate binding

117 conformations of the activation loop and the substrate-binding cleft in GAC are allosterically couple

118 Our analyses revealed that the substrate-binding cleft of PPEP-1 is shaped complementar

119 the ancillary domain as an extension of the substrate-binding cleft, contributing to galactomannan p

120 coupling between the activation loop and the substrate-binding cleft, separated by ~16 angstrom.

121 1alpha mutations exclusively localize to the substrate-binding cleft.

122 However, differences in the substrate-binding clefts result in distinct enzyme-subst

123 conformational change associated with donor substrate binding, common strategies employed by fucosyl

124 We also find that RNA editing substrate binding complex (RESC) mediates the interactio

125 We present evidence that RNA editing substrate binding complex bridges the 5' end-bound PPsom

126 Substrate binding components of ECF-transporters are mem

127 tions suggest that subtle differences in the substrate binding configuration can have significant con

128 p40 containing not only the J and C-terminal substrate binding (CTD) domains but also the functionall

129 olecular dynamics (MD) showed nucleotide and substrate binding determinants formed coupled nodes in l

130 Hsp70 binds Hsf1 via its canonical substrate binding domain and Hsp70 regulates Hsf1 DNA-bi

131 ansition of the ankyrin repeat motifs in the substrate binding domain of cpSRP43 drives its activatio

132 ains an N-terminal J domain and a C-terminal substrate binding domain, similar to type II cellular J

133 utations (78%) that mostly affected the WD40 substrate binding domain; 10% of mutations occurred in t

134 and release of polypeptide substrates at the substrate-binding domain (SBD) of Hsp70s.

135 are not degraded but can bind and block the substrate-binding domain (SBD) of Siah1/2 to prevent the

136 g of its nucleotide-binding domain (NBD) and substrate-binding domain (SBD).

137 demonstrate that Ssa1 contacts Hsf1 via its substrate-binding domain and that abolishing either regu

138 When BiP is in the ATP conformation its substrate-binding domain blocks Grp94; in contrast, Grp9

139 Phosphorylation of Hsp70s at T495 in the substrate-binding domain disrupted Hsp70's ATPase activi

140 as Esp1) contains four domains (I-IV), and a substrate-binding domain immediately precedes the cataly

141 determined the crystal structure of the CAR substrate-binding domain in complex with AMP and succina

142 (2020) discover that the C-terminal substrate-binding domain of FBXL5 contains a redox-sensi

143 Here, we show that the C-terminal substrate-binding domain of FBXL5 harbors a [2Fe2S] clus

144 s cluster at the surface of the loops of the substrate-binding domain of FBXW11, and the variants are

145 Intriguingly, variations in the substrate-binding domain of these HSP70s did not play a

146 position characterized by a lack of specific substrate binding domains, but contains in its helical d

147 as predicted, simultaneously occupying both substrate binding domains.

148 ily reveals a modular fold with cofactor and substrate-binding domains allowing for diversity of reco

149 r the common docking and glutamate:aspartate substrate-binding domains at the known binding site for

150 unication between the nucleotide-binding and substrate-binding domains of Hsp70.

151 domain, with respect to C-terminal, specific substrate-binding domains.

152 quirement that a large fraction of the total substrate-binding energy be utilized to drive conformati

153 This reduces the substrate-binding energy expressed at the Michaelis comp

154 ntification of cooperativity between the two substrate binding events.

155 l in a manner expected to interfere with NTP substrate binding, explaining the partial competitive me

156 ur model systems and analyzed structural and substrate-binding features of wild-type CS and its ~13 m

157 equiring a luciferase enzyme, a luciferin, a substrate binding fraction (SBF) that releases luciferin

158 A substrate-binding groove was formed between the EF domai

159 extensive loop structures that surround the substrate-binding groove, generating a negative surface

160 nd LAVP, which block substrate access to the substrate-binding groove.

161 is composed of a GSH binding "G site" and a substrate binding "H site".

162 Substrate binding has been mainly achieved by a V-shaped

163 actor binding and reaction with O(2) precede substrate binding) have been proposed.

164 gid protein matrix provides a frame for fast substrate binding in multiple conformations, accompanied

165 We propose that high-affinity substrate binding increases the specificity and efficien

166 Substrate binding induces a conformational change of the

167 rpheein model of enzyme hysteresis, in which substrate binding induces conformational changes that pr

168 How substrate binding influences the conformational state of

169 The catalyst-substrate binding interactions have been probed by inela

170 y succinate-sensitive position suggests that substrate binding is a low-affinity, ordered process.

171 Given that substrate binding is often weak in order to enhance over

172 of native Cu nitrite reductase involve both substrate binding ( K(M)) and catalysis ( k(cat)).

173 ing, but rather a consequence of accelerated substrate binding kinetics as shown by saturation transf

174 observation likely indicative of suboptimal substrate binding leading to autocatalytic oxidative dam

175 nd whose activity is repressed by a flanking substrate-binding leucine-rich repeat (LRR) domain when

176 Certain substrate-binding lipoproteins of these transporters, su

177 SRM is organized into three substrate-binding lobes poised to bind their respective

178 ifferences in amino-acid sequence within the substrate-binding loop regions lead to different preferr

179 lytically important loops-the WPD, Q, E, and substrate-binding loops-work in dynamic unity throughout

180 revealed that roseltide rT7 uses a canonical substrate-binding mechanism for proteasomal inhibition e

181 ding, suggesting a unique "squeeze and lock" substrate-binding mechanism.

182 sordered (D/E-rich) region, and a C-terminal substrate-binding MIDAS domain.

183 The flipped substrate-binding mode indicates that two-electron reduc

184 Substrate binding modes vary widely, from simple 1:1 com

185 h and without evidence of donor and acceptor substrate binding obtained using a crystal engineering a

186 Importantly, while substrate binding occurs on the S = 3/2 surface, oxidati

187 pproach to elucidate the role of dynamics in substrate binding of a functionally necessary alpha-heli

188 base excision, while the other only requires substrate binding of OGG1--both resulting in conformatio

189 s study investigates structural features and substrate binding of YpenMan26A, a non-CBM carrying endo

190 ucture reveals how concurrent nucleotide and substrate binding organizes the conserved spastin pore l

191 of these enzymes suggested the presence of a substrate-binding platform encompassed by the NTD and th

192 his mechanism, residues F259 and I359 in the substrate binding pocket couple the binding of substrate

193 ubstitutions within the unwound GMG loop and substrate binding pocket that mimick the binding sites o

194 functions by alternating access of a central substrate binding pocket to either side of the membrane.

195 ane binding cap, membrane access channel and substrate binding pocket.

196 wever, Ec-dGTPase residues at the end of the substrate-binding pocket mimic Watson-Crick interactions

197 We found that SIZ1 docks in the substrate-binding pocket of COP1 via two valine-proline

198 data are consistent with the formation of a substrate-binding pocket providing access to the catalyt

199 e Spf1 revealed a large, membrane-accessible substrate-binding pocket that alternately faced the ER l

200 the mammalian enzyme, AtFAAH has a more open substrate-binding pocket that is partially lined with po

201 identify variable structural features of the substrate-binding pocket that underlie the divergent evo

202 putative DNA-binding surface and extends the substrate-binding pocket to a new pocket, pocket III.

203 functionality that enhances affinity to the substrate-binding pocket, and fine-tuning of the chemica

204 ing of preferred amino acid sequences to its substrate-binding pocket, caspase-7 also uses exosites t

205 with the observed structural features of the substrate-binding pocket, kinetic analysis showed that A

206 cture revealed significant changes in the S2 substrate-binding pocket, making it noticeably smaller,

207 MRK-740 binds in the substrate-binding pocket, with unusually extensive inter

208 oes not directly compete with peptide in the substrate-binding pocket.

209 in the activation domain stabilizing the S1 substrate-binding pocket.

210 this region likely confers plasticity to the substrate-binding pocket.

211 of AtLEGbeta revealed unrestricted nonprime substrate binding pockets, consistent with the broad sub

212 and PebS share a canonical fold with similar substrate-binding pockets, the structural determinants f

213 oth a concerted mechanism (both cofactor and substrate binding prior to reaction with O(2)) and a seq

214 The peptidoglycan-recycling substrate binding protein (SBP) MppA, which is responsib

215 ponent of TRAP transporters is a periplasmic substrate binding protein (SBP).

216 peptide-binding protein (OppA) serves as the substrate-binding protein (SBP) of the oligopeptide tran

217 nal changes of FliY, where the l- enantiomer-substrate-binding protein complex interacted more effici

218 Here, we demonstrate that the substrate-binding protein DppA of the inner membrane Dpp

219 The substrate-binding protein FeuA binds the ligand ferri-ba

220 We found that the substrate-binding protein FliY binds l-cystine, l-cystei

221 fic transmembrane domains that co-occur with substrate binding proteins possibly for uptake of sidero

222 Substrate-binding proteins (SBPs) are associated with AT

223 By disrupting the substrate-binding proteins from each import system (nikA

224 d by a cleft, a fold with strong homology to substrate-binding proteins in bacterial ABC transporters

225 h from an open to a closed conformation upon substrate binding, providing specificity for transport.

226 ior volume that contains the active-site and substrate-binding region; this "membrane-interior reacti

227 trate by adopting a helical configuration of substrate-binding residues that extends through the cent

228 We also determine how residues in the substrate binding site affect the opening and closing of

229 The sequences of Thal and RebH lining the substrate binding site differ in only few residues.

230 Mutation of key residues in the substrate binding site expand the selectivity to include

231 Mechanistic studies mapped SN binding to the substrate binding site in the catalytic region of CaMKII

232 ly discovered that mutations proximal to the substrate binding site of glycosyltransferase 8 domain c

233 high selectivity when targeting the peptide substrate binding site of NTMT1/2.

234 with each metal playing a distinct role as a substrate binding site or redox mediator.

235 ion of an initial complex, presumably in the substrate binding site, followed by a slower change to t

236 ecreased OGT stability and disruption of the substrate binding site, resulting in loss of catalytic a

237 IR domains, respectively, reveal a conserved substrate binding site.

238 th a 5-C atom linker only interacts with the substrate-binding site and functions as a substrate.

239 They all have a single substrate-binding site and two gates, which are present

240 changes in the loops at the entrance of the substrate-binding site are stabilized by direct interact

241 se changes that occur upon occupation of the substrate-binding site by an active site-directed inhibi

242 ed that, because DapF (Ct) utilizes a shared substrate-binding site for both racemase and epimerase a

243 uggest the presence of a putative allosteric substrate-binding site in a hydrophobic pocket on the en

244 available structures have revealed a single substrate-binding site in the SBD that binds a single se

245 GGT with the cysteinylglycine region of the substrate-binding site occupied.

246 xetine and its analogues bind to the central substrate-binding site of SERT, stabilize the outward-op

247 consistent with an extracellular allosteric substrate-binding site that modulates the rate-limiting

248 ubstitution of Phe-269, located close to the substrate-binding site, also affected substrate selectiv

249 ZIP2-mediated metal transport, identify the substrate-binding site, and suggest a structure-based tr

250 Although buried near the substrate-binding site, S267X substitutions were easily

251 uous transport pathway extends from the MlaE substrate-binding site, through the channel of MlaD, and

252 tional state, involving rearrangement of the substrate-binding site-associated re-entrant hairpin loo

253 n through structural alteration of the NAA10 substrate-binding site.

254 s an important role in defining the acceptor substrate-binding site.

255 PK through structural alteration of the NatE substrate-binding site.

256 that is larger than expected for a localized substrate-binding site.

257 hree domains about a fulcrum provided by the substrate-binding site.

258 involving a large rigid body movement of the substrate-binding site.

259 ng effects allosterically couple the ion and substrate binding sites and modify the kinetics of state

260 nal rearrangements, resulting in exposure of substrate-binding sites and sHsp activation.

261 each monomer partially occupies the ATP- and substrate-binding sites of the partner monomer.

262 nizes effectors, and highlights the multiple substrate-binding specificities of its adaptor subunit.

263 mutagenesis and functional studies inform on substrate binding, specificity, and modulation of the Ag

264 catalytic cavity allowed us to identify five substrate-binding subsites (-1, +1, +2, +3, and +4).

265 tly indicated that the B2 loop, covering the substrate-binding subsites -3 and -4 in TrCel7A, was a k

266 of the regulatory C-terminal tail expose the substrate-binding surface and RDEL motif, ensuring clien

267 The TSS motif phosphorylations alter the substrate-binding surface consistent with a mechanism of

268 Moreover, the substrate-binding surface exhibited a dominant and exten

269 tiple substitutions at five positions on the substrate-binding surface that we identified by sequence

270 Only six substitutions occur at the substrate-binding surface, and the others change domain-

271 a dimeric RagA(2)B(2) complex, with the RagB substrate-binding surface-anchored lipoprotein forming a

272 on a multitude of amino acids located on the substrate-binding surface.

273 that these monocopper enzymes have extended substrate-binding surfaces for interacting with their fi

274 ions is the modulation of the hydricity with substrate binding that makes the reaction favorable.

275 This effect could be explained by productive substrate binding that protects LPMOs from oxidative sel

276 Upon substrate binding, these residues position a flexible lo

277 Upon substrate binding, they assemble from hexahelical TatC a

278 Introducing substrate binding through depletion catalyzes dimer chai

279 vious molecular dynamics simulations wherein substrate binding to an allosteric site remote from the

280 Alternatively, simultaneous alphaKG and substrate binding to Fe(II)-DAOCS produces five-coordina

281 Substrate binding to ProT(QQQ) caused allosteric tighten

282 ith the wild-type enzyme, demonstrating that substrate binding to the high-energy state is not occlud

283 eactions involve stepwise processes in which substrate binding to the main group metal acts as a prec

284 Substrate binding to the WW domain alters its transient

285 They further show that substrate binding to the WW domain simultaneously alters

286 al characterization, and to directly monitor substrate binding to UNC-45.

287 ion of two domain movements that include the substrate-binding transport domain and the scaffold doma

288 strate-enclosing loops on either side of the substrate-binding tunnel, which constitutes a CBH that c

289 in the 2nd SIA-binding site, indicating that substrate binding via this site enhances NA catalytic ac

290 ons in the heme-binding (R374W and R448C) or substrate-binding (W116C) site of 11beta-hydroxylase, or

291 Reverse-oriented substrate bindings were observed in the substrate-comple

292 s-including three expected to participate in substrate binding-were mutated individually and characte

293 eir cognate activators tightly to outcompete substrate binding while blocking their own ubiquitylatio

294 es a basis for understanding the coupling of substrate binding with O(2) activation in chitin-active

295 formational changes between these states and substrate binding with or without LptC.

296 aptamers with analyte to trigger TiO(2)@AgNP substrates binding with Raman tag-labeled gold nanoparti

297 thiOppA domains differentially contribute to substrate binding, with one domain playing a dominant ro

298 Here, we investigate the nature of substrate binding within Lactococcus lactis LmrP, a prot

299 ed us to probe the molecular determinants of substrate binding within two AA9 LPMO subclusters.

300 The substrate binding yields characteristic Cotton effects t