ライフサイエンスコーパス: binding interface

1 surface of the beta-region in A2 as the MurA-binding interface.

2 merous symmetry and distortion at a receptor-binding interface.

3 site and lie close to the clamp loader-clamp-binding interface.

4 ve motion of water molecules to create a dry binding interface.

5 ional changes and formation of the G-protein-binding interface.

6 of the PLC-beta PH domain as the Gbetagamma binding interface.

7 to a conformational switch distant from the binding interface.

8 ially overlaps the well-characterized EB1:MT binding interface.

9 ctions by stabilizing the PECAM-1 homophilic binding interface.

10 rinsic heterogeneity at its BH3-only protein binding interface.

11 bility to sterically occlude the M-CSF.c-FMS binding interface.

12 substitutions at the DNase-Immunity protein binding interface.

13 ces flanking the platelet GPIbalpha receptor binding interface.

14 mer with a flat and extensive cationic lipid binding interface.

15 rypsin cleavage sites, are excluded from the binding interface.

16 -helix that sterically blocks its ETS domain binding interface.

17 these residues line a potential nucleic acid-binding interface.

18 racterize because they are hidden inside the binding interface.

19 ment, yielding a high-resolution plot of the binding interface.

20 membrane surfaces through a protein-protein binding interface.

21 osine in order to disrupt the most important binding interface.

22 e and Arg2320 is poised at the center of the binding interface.

23 inhibitor and is located along the substrate-binding interface.

24 ed carboxy-terminal tail and burying its PER-binding interface.

25 bilayers through a positively charged lipid-binding interface.

26 -terminal extension, altering the Psb27-CP43 binding interface.

27 protein known to form part of the substrate-binding interface.

28 Their assembly required a cadherin cis-binding interface.

29 m which we define accurately the CAP-Gly/EB1 binding interface.

30 that both the P- and D-loop form part of the binding interface.

31 hromoshadow domain does not provide a direct binding interface.

32 (5F)W was substituted for residues near the binding interface.

33 g energy of noncovalent contacts at the FcRn binding interface.

34 les for two groups of amino acids at the RNA binding interface.

35 energy barrier from the dimer with a native binding interface.

36 am responses through the canonical G-protein-binding interface.

37 ng and creating the capsid auxiliary protein binding interface.

38 nteractions with the MHCII and the DM-pMHCII binding interface.

39 second glycosylation site on the same virus-binding interface.

40 domain that are located distal to the Galpha-binding interface.

41 s a result of only two mutations outside the binding interface.

42 parameters were used to map the cytb 5-cyt c binding interface.

43 s than ribose 2'-OH in both the RIalpha-cAMP binding interfaces.

44 s rolling, typically to alternate and weaker binding interfaces.

45 rization and the availability of alternative binding interfaces.

46 ow these plant viruses maximize their use of binding interfaces.

47 set of secondary-structure-based packing at binding interfaces.

48 xisting methods for mapping kinase-substrate binding interfaces.

49 (L249-S252 and Y254) that can act as direct binding interfaces.

50 ed one binding site delineated by 3 putative binding interfaces.

51 bridge linking the primary and complementary binding interfaces.

52 combination of both in stabilizing specific binding interfaces.

53 tant sequences, suggesting plasticity in the binding interfaces.

54 Each PC4 dimer comprises two DNA-binding interfaces.

55 dent to versatile and context-dependent TALE binding interfaces.

56 storted variations) found at protein-protein binding interfaces.

57 via pseudosymmetric patterning of orthogonal binding interfaces.

58 to either co-conservation or covariation of binding interfaces.

59 arranged to the residues found in known drug binding interfaces.

60 tease dimers that reveal a putative collagen-binding interface aided by glycosaminoglycans.

61 multiple, productive conformations at the AT binding interface, allowing the complex to sustain high

62 n, along with the multipartite nature of the binding interface, allows calmodulin transiently to stri

63 here a myosin structure possessing an actin-binding interface and a tunnel (back door) that creates

64 ing regions of myosin assures a proper actin-binding interface and active site have formed before pro

65 tated all histidine residues in the collagen binding interface and additionally all of those that wer

66 Cys(820) thiolate within the low dielectric binding interface and Arg(506) functions to orient Glu(5

67 ctrometry validated the identified substrate-binding interface and demonstrate that TRiC contacts ful

68 M variants with mutations both in the direct binding interface and distant from the binding site.

69 specificity were far from the proteins' DNA-binding interface and interacted epistatically to change

70 x complexes formed in the MOM, including the binding interface and membrane topology, using site-spec

71 ication between the active site, microtubule-binding interface and neck-linker via loop7 and loop13.

72 ry may challenge our view of the protein-RNA binding interface and provide a unique solution for futu

73 Both the predicted binding interface and regions with direct contacts agree

74 f G29, a residue at the edge of the receptor binding interface and the center of the structural turn

75 des the communication link between the actin-binding interface and the nucleotide pocket.

76 two functional sites of the betaSBD-the NBD binding interface and the substrate-binding site-confers

77 ), and molecular docking to characterize the binding interface and to predict the three-dimensional q

78 f MeCP2-DNA for mutations around the MBD-DNA binding interface, and defective chromatin clustering fo

79 enuation and a more specific protein-protein binding interface are observed in bicelles as compared w

80 ternary complexes where unnatural symmetric binding interfaces are favored over canonical antibody i

81 However, binding interfaces are frequently affected by amino acid

82 phylogenetic differences in the sequences of binding interfaces are not the result of adaptive fine t

83 rive Ras into orientations in which effector-binding interfaces are occluded by the cell membrane.

84 and that the overall domain arrangements and binding interfaces are preserved on passing from the cry

85 Met257 and Met433 were located near the FcRn binding interface as indicated by HDX MS and structural

86 KMN) network acts as the primary microtubule-binding interface at kinetochores [3] and provides a pla

87 tatistical analysis localizes the TRIM5alpha binding interface at or near the CypA binding loop of CA

88 hich we challenged our students to study the binding interface between 2 important biosynthetic prote

89 , replacing CENP-A S68 with E68 disrupts the binding interface between CENP-A and HJURP in all-atom M

90 structural modelling that identifies an AMP-binding interface between CFAP45 and AK8.

91 nd a high affinity of the hexapeptide to the binding interface between CoV-2 RBD and ACE2, which we i

92 ions involving eIF5B and eIF1A: (i) a second binding interface between eIF5B and eIF1A; (ii) a dynami

93 semen, suggesting that interfering with the binding interface between fibronectin and the amyloids c

94 n interacting region (PPIR), which forms the binding interface between interacting polypeptide chains

95 ving key residues in the active site and the binding interface between kinesin and microtubule.

96 lexed with ssDNA reveals a divergence in the binding interface between prokaryotic and eukaryotic PC4

97 P gamma-phosphate is found at the nucleotide-binding interface between RAD51 subunits of the NPF know

98 that synthetic peptides corresponding to the binding interface between Rbm38 and eIF4E, including an

99 We show a binding interface between the GFI1 linker and the SP-RIN

100 We show that the circular binding interface between the pore lumen and the folded

101 ted the first atomic structural model of the binding interface between the tropomyosin-binding site o

102 50 amino acids) that can naturally mimic the binding interfaces between proteins and thus, influence

103 Exchanging the receptor-binding interfaces between TcsL and TcdB switches their

104 ificant reduction in loop flexibility at the binding interface, but in a number of cases it can also

105 e ligand and received by the receptor at the binding interface; but their transmission over space and

106 Mapping of the binding interface by hydrogen-deuterium exchange coupled

107 thout the need to disrupt the strand-swapped binding interface by mutagenesis.

108 erefore we targeted specific residues in the binding interface by rational design generating improved

109 o an allosteric creation of a more favorable binding interface by the first ligand.

110 core mutations in MarA (distant from the DNA-binding interface) change the relative affinities of its

111 , revealing that the overall interaction and binding interface closely resemble the structures of cel

112 e Sgf73 ZnF, binds to nucleosomal DNA with a binding interface composed of arginine residues located

113 The binding interface comprises a central tryptophan within

114 ss-Tipin interaction is based on a composite binding interface comprising different domains of Timele

115 4C revealed an untwisted, flat, carbohydrate-binding interface comprising the side chains of four try

116 N-glycan termini, which are distal from the binding interface, contribute to the affinity.

117 king and consequent allosteric modulation of binding interfaces could be used to engineer proteins wi

118 f BAP1, which generate a composite ubiquitin-binding interface (CUBI).

119 The remarkable results of binding-interface determination and quaternary structure

120 nd that A3A binds ssRNA, but the RNA and DNA binding interfaces differ and no deamination of ssRNA is

121 Mutations at the binding interface disrupt the Vps33A-Vps16 interaction b

122 Mutations in the TDP2 UBA-Ub binding interface do not affect nuclear import of TDP2,

123 markable analytical platform for bioaffinity binding interface due to its favorable combination of ex

124 tation of either the dimerisation or the DNA binding interface eliminates ParB-GFP foci formation in

125 gy Transfer (FLIM-FRET) we show that the two binding interfaces enable Bim to double-bolt lock Bcl-XL

126 We show how the physical simplicity of this binding interface enabled the evolution of a new protein

127 This discrete binding interface enables the PAR glycohydrolase (PARG)

128 Examination of a set of protein binding interfaces establishes good agreement between re

129 The nucleosome-binding interface exclusively occupies the strong double

130 This is the first binding interface experiment to successfully demonstrate

131 Although the binding interfaces feature clusters of hydrophobic resid

132 3, and Thr345) could act as membrane anchor, binding interface for a second rhodopsin, or rearrange c

133 emphasizing the importance of the NCAM/EphA3 binding interface for cluster formation.

134 by occupying the activation function (AF)-2 binding interface for coactivators and N-terminal AR AF-

135 To identify "hot spot" residues in the ETON binding interface for STIM1 interaction, numerous Orai1

136 ycles, we mapped the energy landscape of the binding interface for two interacting disordered domains

137 ffold in infected cells and creates distinct binding interfaces for different cellular target protein

138 of short linear motifs (SLiMs) that serve as binding interfaces for modular protein domains.

139 inding site at helices 1 and 2 of UBXD1-N as binding interfaces for p97.

140 emergence of inserts constituting conserved binding interfaces for proteins or nucleic acids and the

141 ing, we present a description of a potential binding interface formed between the E2 protein and CD81

142 The binding interfaces from the two solution structures prov

143 While the STIM1 and Orai1 binding interfaces have been mapped, signaling mechanism

144 nments of protein-ligand and protein-protein binding interfaces, identifying individual amino acids t

145 Mutations in the CI:MOR binding interface impair complex formation in vitro, and

146 Both mutations fall at the dyskerin-NOP10 binding interface in a region distinct from those implic

147 The CaM-binding interface in Akt(PHD) was mapped to two loops ad

148 43 that are crucial for the formation of the binding interface in Arabidopsis.

149 The structures revealed a conserved ligand-binding interface in D2 and a unique mechanism for VEGFR

150 Complementarily, a 106-A-long substrate-binding interface in Hsp90 enables many low-affinity con

151 We previously characterized the TRN-SR2 binding interface in IN and introduced mutations at thes

152 Although the SH2 domain is a less common binding interface in Shc proteins, we demonstrate that i

153 mpeting small molecule interact at the known binding interface in solution.

154 egulatory mechanism of GCAPs including their binding interface in the target is unresolved.

155 chnique allows differentiation of nucleosome-binding interfaces in distinct states.

156 How the three unique potential receptor-binding interfaces in LTalpha1beta2 trigger signaling vi

157 The binding interface involves multiple domains of CaMKII.

158 Our results suggest that the MtrC/E binding interface is an important modulator of MtrE func

159 at a prevalence of high loop rigidity at the binding interface is an indicator of increased binding s

160 The binding interface is centered on the C-terminal domain o

161 A critical loop in the PA binding interface is displaced for about 4 angstrom, lea

162 The significance of this membrane-binding interface is established through SOD1 activity a

163 Each binding interface is highly electrostatic, with positive

164 The binding interface is organized to arrange contacts betwe

165 ue that is positioned distal to the TCR-pMHC binding interface is shown to contribute to the peptide

166 bstitutions at residues in the predicted RNA-binding interface (K42C/C71V, R46C/C71V, V95C/C71V) were

167 nisms, including disruption of the G protein-binding interface, loss of protein stability, or alloste

168 The extensive capsid-binding interface maps on the structurally divergent fac

169 show that membrane-localized RBD has its RAS-binding interface mostly inaccessible because of its pro

170 s of transient dwell times and determine via binding-interface mutants that they are distinguished by

171 he results support that the BH3-only protein binding interface of Bcl-xL is much more dynamic compare

172 identify six amino acid residues in the DNA-binding interface of DNMT3B (N652, N656, N658, K777, N77

173 e use a chemical biology approach to map the binding interface of ERK and Cic.

174 cation and characterization of the chemokine-binding interface of evasins could thus inspire the deve

175 Here, we identified the MAD2-binding interface of FAT10 to be located on its first ub

176 se it links centromeres with the microtubule-binding interface of kinetochores.

177 The same binding interface of LvgA also interacts with the C-term

178 at CTD is a part of an extensive kinetochore-binding interface of Mad1, and rationalize graded kineto

179 ments provide evidence that the observed DNA-binding interface of MHF is important for cellular resis

180 ion of a single glycine within the GPIbalpha binding interface of normal VWF enhances the probability

181 binding partners, the UAA approach maps the binding interface of the bait protein used for crosslink

182 hibition by synergistically blocking the DNA-binding interface of the ETS domain and stabilizing an a

183 ed hydrogen-deuterium exchange MS to map the binding interface of the evasin P672 that physically int

184 By targeting the binding interface of the gammac and cytokines, we succes

185 and other data suggest that the microtubule-binding interface of the human kinetochore behaves like

186 We propose an RNA binding interface of the MthRnl based on the mutational

187 ation, and water molecules structured in the binding interface of the nSH3:PRM complex.

188 on, NMR experiments are used to identify the binding interface of the P450-cytb5 complex in the nanod

189 stitution disrupted the high-affinity ligand-binding interface of the prolactin receptor, resulting i

190 PCNA-binding interface of the Rev1-BRCT domain comprises cons

191 lso show that MEKK1 mutations at the tubulin-binding interface of the TOG domain recur in patient-der

192 4A and G1324S) within the platelet GPIbalpha binding interface of the VWF A1 domain impair the hemost

193 present a 2.4 angstrom resolution map of the binding interface of this antibody on HLA-A*11:01 and co

194 The binding interface of ubiquitin with liposomes is mapped

195 upon filament formation monitor the specific binding interfaces of ASC-PYD association.

196 two mechanisms, which target distinct APC/C binding interfaces of Cdc20, enables cyclin B accumulati

197 Mutating the binding interfaces of CENP-H for either CENP-K or CENP-I

198 chemical shift perturbation to identify the binding interfaces of IscX and IscU in their complex.

199 ng based on sub-structural similarity to the binding interfaces of known drug binding sites.

200 ludes both the N- and C-terminal Gtbetagamma binding interfaces of phosphorylated Pdc, thus providing

201 ve mass spectrometry to separately study the binding interfaces of RNA/protein complexes of different

202 The DNA-binding interfaces of the androgen (AR) and glucocortico

203 t collection, effectively target the dynamic binding interfaces of the GACKIX domain of the coactivat

204 tutions in these proteins, we found that the binding interfaces of uPA:plasminogen and uPA:PAI-1 may

205 nd structure-based prediction to analyze the binding interfaces of urokinase (uPA):plasminogen activa

206 NMR was used to map the binding interfaces of XPA DBD and RPA70AB.

207 ognate receptor(s) have revealed a conserved binding interface on hIL-18.

208 spectroscopy experiments validated the ACPS binding interface on holo-ACPP using chemical shift pert

209 tational analyses confirmed an extended VipD-binding interface on Rab5, explaining why this L. pneumo

210 We conclude that the main RetGC-binding interface on RD3 required for the negative regul

211 igher affinity than sigma(S) to RssB and its binding interface on RssB overlaps with that for sigma(S

212 truction we describe a previously overlooked binding interface on the actin filament targeted by PfAD

213 The binding interface on the large ribosomal subunit is buri

214 lar weight complexes, we are able to map the binding interfaces on beta(2)m for collagen I and detect

215 s state-of-the-art performance at predicting binding interfaces on both antibodies and antigens, and

216 ied deep learning-based framework to predict binding interfaces on both antibodies and antigens.

217 ational changes, including changes away from binding interface, on electrostatics are mimicked with a

218 We observe 2 binding interfaces, on the LukG and the LukH protomers,

219 Moreover, our data show that the C-terminal binding interface only plays a subsidiary role in trigge

220 dependencies between nucleotides within the binding interface or multiple modes of binding.

221 ctions-were identified within host and viral binding interfaces predicted by our models.

222 tware produced by scoring those models using binding interfaces predicted by the interface predictor,

223 f EF/LF to the protective antigen C-terminal binding interface, preventing toxin entry into the cell.

224 4 angstrom, leading to the weakening of the binding interface prior to translocation.

225 The binding interface profiling approach should find useful

226 We identify the phosphoubiquitin-binding interface, provide a model for the phosphoubiqui

227 differences between the ligand- and receptor-binding interfaces, providing an explanation for the abs

228 tive state are those which define the native binding interface, reminiscent of the role played by nat

229 at this motif is one element of a tripartite binding interface required to form a high-affinity Bim1-

230 nus of PilM, and binding PilN abrogates this binding interface, resulting in PilM monomerization.

231 exit site, analysis of the cpSRP54/ribosome binding interface revealed a direct interaction of cpSRP

232 h mutational analysis, we validated the RPN2-binding interface revealed by our structures and quantif

233 hermore, structure-guided mutagenesis of the binding interface revealed that novel binding interactio

234 Analysis of the binding interface reveals a mechanism of C5 inhibition,

235 rsity and raises new ideas about the VP1-VP2 binding interface(s) that is important for viral replica

236 Mutational analysis of amino acids in the binding interface showed that residues contributing to I

237 h is located at a site remote from the PBD46 binding interface, shows a significant dynamic response

238 akin mutations have been discovered to alter binding interfaces, structures, and stabilities of folde

239 n-25) is located within the trans homophilic-binding interface, suggesting a role for an Asn-25-assoc

240 Analysis of the AMPAR-STZ binding interfaces suggests that electrostatic interacti

241 al enzymes generally present two similar Coh-binding interfaces supporting a dual-binding mode, which

242 r to disrupt that protomer's TPR-U-box tight binding interface, swiftly exposing and activating one o

243 its a 7 degrees rotation about the substrate-binding interface, termed the quaternary shift.

244 led a 1:1 stoichiometry and a more extensive binding interface than anticipated from the paradigmatic

245 In a more stringent test, an engineered binding interface that achieves wild-type-like charge co

246 lso defined a new host protein-viral protein binding interface that can potentially be targeted for t

247 f the 60S-Listerin complex that identifies a binding interface that clashes with the 40S ribosomal su

248 nd identify a new host protein-virus protein binding interface that could become a useful target in f

249 rrounding the previously defined eVP24-KPNA5 binding interface that decrease eVP24-KPNA affinity or b

250 vergent amino acid residues within the E1-E2 binding interface that define organism-specific enzyme i

251 affinity variant of Jagged1 (Jag1) reveals a binding interface that extends 120 angstroms along five

252 a unique, extensive, neurexophilin-neurexin binding interface that extends the jelly-roll beta-sandw

253 -shift NMR of P[19] VP8* identified a ligand binding interface that has shifted away from the known R

254 ped to one of the loops (L3) in the membrane binding interface that help anchor the toxin monomers to

255 ssays to investigate this important IFN-beta binding interface that is centered on IFNAR1 residues Ty

256 preserves the structure of the DENR's MCT-1-binding interface that is essential for the dimerization

257 Finally, our model predicts a novel binding interface that is well-populated in the Ca(2+)-b

258 e enzyme-substrate pair of GEF-RhoA at their binding interface that leads to enhanced efficacy and sp

259 rally, dockerins present two similar cohesin-binding interfaces that support a dual binding mode.

260 the topological neighborhood of the antigen binding interface, the Anap emission wavelength is blue-

261 c transcription factors create a new protein-binding interface through dimerization/oligomerization.

262 the metal binding residue, His97, to the DNA binding interface through the alphaR helix that is prese

263 In vitro reconstitutions map the key binding interface to a few acidic residues in the N-term

264 ts reveal that PARP3 employs a conserved DNA-binding interface to detect and stably bind DNA breaks a

265 ch critically contribute to the LRPPRC-SLIRP binding interface to enhance its stability.

266 dditional hIL-23p19 substitutions within its binding interface to hIL-23R and found that the combined

267 y, we systematically dissected the LMO2/LDB1-binding interface to investigate the role of this intera

268 results reveal how the FHA1 uses a canonical binding interface to recognize the Cdc7 phosphopeptide a

269 d activates new interactions at the TCR-pMHC binding interface to resist bond dissociation under forc

270 s RAS-binding domain (RBD) contains the main binding interface to the RAS G domain, its cysteine-rich

271 ng signal to the cargo factor, the number of binding interfaces to the cargo factor, and more.

272 Our study of histone binding interfaces uncovers a remarkably high number of

273 The crystallographically observed binding interface was confirmed by a comprehensive cell-

274 The binding interface was further refined through molecular

275 The binding interface was identified by small angle x-ray sc

276 The binding interface was probed with point mutations, none

277 eraction of unrelated probes recognizing the binding interface was utilized in a simple prediction al

278 and mutagenesis analyses of the heterodimer binding interface, we identified a peptide that mimics t

279 rientation of the PECAM-1-PECAM-1 homophilic-binding interface, we undertook studies aimed at determi

280 as fragment-centric topographical mapping of binding interfaces, we have clarified current controvers

281 Key regions that modulate the binding interface were verified by site-directed mutagen

282 In addition, two alternative binding interfaces were discovered, which are essential

283 changes demonstrate plasticity in the PA-PB1 binding interface which may be exploited in the developm

284 iopoietin P domain, adjacent to the receptor-binding interface, which confers the specific agonist/an

285 31L mutant exhibits a disordering of the RIF binding interface, which effectively reduces the RMP aff

286 oss the beta2-beta3 hairpin in the GPIbalpha binding interface, which restrains the conformational de

287 t cell surface dockerins contain two cohesin-binding interfaces, which can present different or ident

288 bNAbs cause only localized effects at their binding interface, while the binding of less potent anti

289 ture and augmenting our understanding of the binding interface with atomic-level detail.

290 ce quenching of a tryptophan on the membrane-binding interface with brominated lipids along with muta

291 g identified residues of FBD involved in the binding interface with cyt c, most of which are located

292 Its predicted binding interface with FKBP consists primarily of electr

293 Metazoan eIF4Gs share this extended binding interface with m4E-BPs, with significant implica

294 affinity maturation techniques targeting its binding interface with SIRPalpha.

295 proteins with an enrichment of mutations at binding interfaces with a protein, nucleic acid, or smal

296 mutations in NRF2 localize to one of its two binding interfaces with KEAP1, an E3 ubiquitin ligase th

297 tly in the formation of the trans homophilic-binding interface, with a total buried interface area of

298 n egg white lysozyme revealed an extended VH binding interface, with complementarity-determining regi

299 These mutants defined the Rab5-binding interface within p110beta as consisting of two p

300 interacts with this domain through the large binding interface without inducing any dramatic conforma