ライフサイエンスコーパス: dimer interface

1 quely in RECQ1) is buttressed by the protein dimer interface.

2 rk of hydrogen bonds and salt bridges at the dimer interface.

3 ATPase, positions of the main domains, and a dimer interface.

4 ent of conserved proline residues across the dimer interface.

5 kp1-Rnl-Hen1 heterotrimer fused at the Pnkp1 dimer interface.

6 a number of sites near the crystallographic dimer interface.

7 PP2A/RACK1 binding site is buried within its dimer interface.

8 f the dimer, we mutated five residues on the dimer interface.

9 id the design of inhibitors that bind at the dimer interface.

10 etrical dimer with a large deep cleft at the dimer interface.

11 h recapitulating the role of Phe(B24) at the dimer interface.

12 ) in the predicted, tightly packed TM domain dimer interface.

13 f transmembrane helix IV, is observed at the dimer interface.

14 t this site restricts its involvement at the dimer interface.

15 r part of, or allosterically coupled to, the dimer interface.

16 lly coupled, conveying inhibition across the dimer interface.

17 which forms part of the mariner transposase dimer interface.

18 g of protomers through two histidines at the dimer interface.

19 on of binding kinetics by mutations at the X-dimer interface.

20 cooperativity due to steric hindrance at the dimer interface.

21 nt, with two nucleotides "sandwiched" at the dimer interface.

22 phate (Fru-6-P), binds along the other dimer-dimer interface.

23 on of the chemokine, which overlaps with the dimer interface.

24 ant role in maintaining structure across the dimer interface.

25 g the C-terminal residues that stabilize the dimer interface.

26 lectrostatic interactions that stabilize the dimer interface.

27 dimer by introducing a disulfide across the dimer interface.

28 iminished with disruption of the BRAF kinase dimer interface.

29 ut Trp/Arg side chains that stack across the dimer interface.

30 ons of the surface residues that mediate the dimer interface.

31 ing site on SLIP1 for SLBP lies close to the dimer interface.

32 hat both occurs through the crystallographic dimer interface.

33 hibitor binds in an allosteric manner at the dimer interface.

34 c coordination of Zn(2+) in trans across the dimer interface.

35 lpyruvate (PEP), which binds along one dimer-dimer interface.

36 d the positioning of the inhibitor at the IN dimer interface.

37 ch site (site 2) formed at the S100A8/S100A9 dimer interface.

38 (HSPG) receptor binding residues within the dimer interface.

39 by introducing a disulfide bridge across the dimer interface.

40 ked glycans onto the hydrophobic C(H)3-C(H)3 dimer interface.

41 eases the side chain of His23 from the dimer-dimer interface.

42 ngle disulfide bond with a large (1345 A(2)) dimer interface.

43 ubstrate-binding residues, and from the nsp5 dimer interface.

44 he unbound receptor are affected through the dimer interface.

45 ffers by an additional helix inserted in the dimer interface.

46 83), His(104), His(111), and Asp(109) at the dimer interface.

47 ral differences at the N-terminal domain and dimer interface.

48 nd neutralize charges in the vicinity of the dimer interface.

49 obic interactions stabilizing the entire BAR dimer interface.

50 n strategically located at the center of the dimer interface.

51 ransmembrane helices 2 and 6 in the putative dimer interface.

52 domain reveal the molecular nature of the CC dimer interface.

53 engaged in numerous interactions at the CTD dimer interface.

54 ith neonatal microcephaly, is located at the dimer interface.

55 es a central hydrogen bonding network at NS1 dimer interface.

56 tein motions, consistent with a destabilized dimer interface.

57 ing two modulator-binding sites at the GluK1 dimer interface.

58 hat it can be activated by disruption of the dimer interface.

59 immunity are conformational epitopes at the dimer interface.

60 ween specific charged amino acids across the dimer interface.

61 homodimer of ACT folds with Phe bound at the dimer interface.

62 nces in how the subunits are arranged at the dimer interface.

63 ent manner to form a ferroxidase center at a dimer interface.

64 ue quaternary epitope on the E protein dimer-dimer interface.

65 ium with the Cys(257) residue located on the dimer interface.

66 e protruding Jalpha helix and on the LOV-LOV dimer interface.

67 interactions observed at the N. clavipes NTD dimer interface.

68 r identifies subunits e and g at the lateral dimer interface.

69 d cooperatively recognize the antigen in the dimer interface.

70 Instead, TM2, TM6, and TM11 line the dimer interface.

71 ces in aromatic-aromatic interactions at the dimer interface.

72 value and is located within the hydrophobic dimer interface.

73 kinetics of receptor association at specific dimer interfaces.

74 dine (HAP) pocket between core protein dimer-dimer interfaces.

75 ry to confirm APJ homo-dimer and explore the dimer-interfaces.

76 an R-state conformation with a lysine at the dimer-interface acting as a peg in a hole, locking the a

77 Together, our data suggest that the Mre11 dimer interface adopts at least two different states dur

78 sts that binding stabilizes the weaker dimer-dimer interface against dissociation, the rate-limiting

79 a homologous BH4-binding site located in the dimer interface and a conserved tryptophan residue that

80 ng in the rearrangement of the kinase domain-dimer interface and a rotation of the RNase domains away

81 ALLINIs bind at the IN catalytic core domain dimer interface and bridge two interacting subunits.

82 re of apo-FAcD exhibits asymmetry around the dimer interface and cap domain, priming one protomer for

83 ent activation of IRF3 and thus excludes the dimer interface and CBP-binding site.

84 mutations of BRCA1 are found to disrupt the dimer interface and dimer formation.

85 ed stabilization of aromatic clusters at the dimer interface and enhancement of intersubunit hydrogen

86 ovine rhodopsin (Rho) to investigate the Rho dimer interface and functional consequences of its disru

87 a positively charged Arg residue at the beta-dimer interface and high NaCl concentrations destabilize

88 A positively charged cavity is formed on the dimer interface and involves several strictly conserved

89 nating in the epicenter further disrupts the dimer interface and leads to dimer dissociation.

90 ree conserved cysteine residues occur at the dimer interface and likely form the catalytic site.

91 rescence from a tryptophan positioned at the dimer interface and luminescence resonance energy transf

92 H1 indicates that the inhibitor binds at the dimer interface and makes direct contact with a residue

93 hat disrupts the BC-loop regions at the P450 dimer interface and results in a CYP126A1 monomeric crys

94 lly those residing at barttin binding sites, dimer interface and selectivity filter.

95 tion was identified from the analysis of the dimer interface and sequence alignments.

96 rs of thymidylate synthase (hTS) bind to the dimer interface and stabilize the inactive form of the p

97 nally to the interhelical axis and spans the dimer interface and that heparin binding enhances the st

98 lecules predicted to bind PF4 near the dimer-dimer interface and that interfere with PF4 tetramerizat

99 lex) confirm structural coupling between the dimer interface and the catalytic center.

100 The structure suggests that ATM/Tel1 dimer interface and the consecutive HEAT repeats inhibit

101 are non-native oligomers in which the native dimer interface and the electrostatic loop mediate the f

102 Our results show that residues at the dimer interface and the switch II region of Toc159G are

103 ion of single charge-reversal mutants at the dimer interface and use the resulting constructs to illu

104 f the E175 side chain that is located at the dimer interface and within hydrogen-bonding distance of

105 alcohol dehydrogenase (ht-ADH): Y25A (at the dimer interface) and V260A (at the cofactor-binding doma

106 5 was identified as being located in the A52 dimer interface, and consistent with that, A52-M65E was

107 dy binds to E proteins residues at the intra-dimer interface, and the virus quaternary structure-depe

108 onserved ATP-binding pocket that lies at the dimer interface, and we identify key residues in this bi

109 ingle position of the allosteric site of the dimer interface, and we show that the enzyme activity va

110 monstrate that the KAR M3-S2 linkers and LBD dimer interface are critical determinants for Neto2 modu

111 dues in the C-terminal CA subdomain (CA-CTD) dimer interface are needed for the stability of the firs

112 We also identify the D1 dimer interface as a novel site of Neto2 modulation and

113 f channel opening by F508del and support the dimer interface as a target for cystic fibrosis therapeu

114 d for Raf function, thus identifying the Raf dimer interface as a therapeutic target.

115 H 6.5, the major conformer exhibits the same dimer interface as full-length CA.

116 harmacophore, binds at the same GluN1/GluN2B dimer interface as ifenprodil but adopts a remarkably di

117 mission of conformational changes across the dimer interface as the most probable mechanism of altere

118 erivatives target a similar pocket at the IN dimer interface as the quinoline-based ALLINIs, the lead

119 c IN inhibitors (ALLINIs) that engage the IN dimer interface at the binding site for the host protein

120 ubunits form an extensive self-complementary dimer interface at the center of the complex, and the Er

121 e-binding pocket to the formation of a tight dimer interface at the N-gate by connecting regions from

122 ic acid derivatives that bind at the CCD-CCD dimer interface at the principal lens epithelium-derived

123 As expected, a peptide corresponding to the dimer interface became more solvent exposed over time at

124 tertiary structure and the integrity of the dimer interface because "I" represents an unstructured a

125 single Pro substitution at the middle of the dimer interface beta-strand is sufficient to generate a

126 kbone H-bonding interactions by substituting dimer interface beta-strand residues with proline (Pro)

127 three residues that form H-bonds across the dimer interface beta-strands.

128 ds to a novel allosteric site located at the dimer interface between the GluN1 and GluN2 agonist bind

129 he SelA catalytic site is close to the dimer-dimer interface, but the significance of the dimer penta

130 A combined binding site is formed at the dimer interface by equal contribution of each monomer.

131 of the mutants can facilitate access to the dimer interface by small molecules and thereby aid the d

132 In addition, mutations in the dimer interface can produce stable monomers that are sti

133 of the two chains separated by 110 A and the dimer interface comprising residues critical for IL-7 bi

134 import, the Toc159G dimer disengages and the dimer interface contacts translocating preproteins, whic

135 ablating a portion of the catalytic core and dimer-interface contacts of native TyrRS, each folded in

136 tent with binding of one molecule of 11m per dimer interface, contrary to most benzothiadiazine dioxi

137 ting that Leu29 and Leu36 are located at the dimer interface, contributing to the structure and stabi

138 y engineering rho-benzoylphenylalanine along dimer interfaces corresponding to the five different Sec

139 interface, suggesting that the cavity in the dimer interface could serve as an allosteric site of hTS

140 Structure-guided mutational analyses of RopB dimer interface demonstrated that single alanine substit

141 imeric in solution and in crystals, with the dimer interface displaying a surface groove that is line

142 of Nlh1 dramatically remodels the GAF domain dimer interface, disrupting the contacts with the ATPase

143 region at triosephosphate isomerase (TIM)'s dimer interface, distant from its catalytic site, is a t

144 eas a CatC mutant with a disrupted CRAF-CRAF dimer interface does not.

145 ction surface that lies perpendicular to the dimer interface, does not involve the chemokine N termin

146 ), which is also formed at the S100A8/S100A9 dimer interface, does not provide a high-affinity Mn(II)

147 nts--to the extracellular ligand binding and dimer interface domains of the EGFR can induce EGFR dime

148 ergoes dynamic motion that exposes the dimer-dimer interface during catalysis.

149 lts indicate that tryptophan residues at the dimer interface engage in photoinduced proton coupled el

150 that methylation of R198 and R200 within the dimer interface enhances growth factor ligand binding an

151 es of classical cadherins reveal an adhesive dimer interface featuring reciprocal exchange of N-termi

152 upies the UDG DNA-binding cleft, whereas the dimer interface forms a hydrophobic box to trap a mechan

153 hough CT263 lacks the active site-associated dimer interface found in prototypical MTANs, co-crystal

154 ivation also involves a reorientation of the dimer interface from a 'relaxed' to an 'active' state, b

155 A comparison of the Mre11 dimer interface from these structures suggests that the

156 zation reaction, the hydrophobic core of the dimer interface has few fully native interactions.

157 The dimer interface, however, is remarkably small and lacks

158 Substitutions at the dimer interface impaired IreB function and stability in

159 We demonstrate that a mutation at the GAPDH dimer interface impairs formation of the second RNA-GAPD

160 Mutating these dimer interfaces implicates one of them (dimer 1) in sol

161 A mutation at the dimer-dimer interface in a thermolabile psychrophilic homologu

162 (Val(19)-Cys(20)-Glu(21)) contribute to the dimer interface in solution.

163 sidues on the Escherichia coli SecA (ecSecA) dimer interface in the cytosol of intact cells.

164 be aided by lateral interactions outside the dimer interface in the icosahedral virion.

165 ciation, suggesting that stability of the D1 dimer interface in the ligand-binding domain (LBD) is an

166 nd C termini, subunit exchange, and variable dimer interfaces in ABC.

167 also reveal by crystallography two distinct dimer interfaces in the BTN3A1 full-length intracellular

168 t factors contribute to the stability of the dimer interfaces in the closed conformation and how clam

169 inhibitors stimulate formation of identical dimer interfaces in the EGFR transmembrane domain, as sh

170 resolution shows distinct asymmetry near the dimer interface, in the region harboring catalytically i

171 resolution shows distinct asymmetry near the dimer interface, in the region harboring catalytically i

172 The dimer interface includes hydrophobic and hydrophilic int

173 al-binding sites formed at the S100A8/S100A9 dimer interface, including a histidine-rich site compose

174 ific effects of oxidative "mutations" at the dimer interface, including lysine, arginine, proline and

175 ts are at a serotype-invariant site at the E-dimer interface, including the exposed main chain of the

176 -bridged, are established by the rotation of dimer interfaces, indicating cooperative Ca(2+) binding

177 for LEDGINs, the binding of tBPQAs to the IN dimer interface inhibits IN enzymatic activity in a LEDG

178 e residues (32, 91, and 96) clustered in the dimer interface, interacting differently in the two ligh

179 the TREX1 Arg-62 residues extend across the dimer interface into the active site of the opposing pro

180 The purified protein was a dimer whose dimer interface involves interactions between the coiled

181 Finally, mutations at a dimer interface, involving fusion domains associated in

182 e close proximity of charged residues at the dimer interface is a major determinant of the binding af

183 of the intermolecular disulfide, the Rgg2Sd dimer interface is destabilized and Rgg2Sd can adopt mul

184 P7B, does not disrupt dimerization, i.e. the dimer interface is formed by the domains that are conser

185 cotranslational interactions until the LuxB dimer interface is fully exposed.

186 here suggested that a properly aligned RopB dimer interface is important for GAS pathogenesis and hi

187 formation but activates RAF/MAPK only if the dimer interface is intact.

188 x-ray scattering analysis indicated that the dimer interface is located at the C terminus and provide

189 residues important for the stability of the dimer interface is maintained.

190 al studies demonstrate that the novel Norrin dimer interface is required for Fz4 activation.

191 The dimer interface is suited to resist hydrodynamic force a

192 ) motif (site 2) formed at the S100A8/S100A9 dimer interface is the site of high-affinity Mn(II) coor

193 important than specific amino acids and the dimer interface is unique from other A3 enzymes.

194 ollowing model: Gag dimerizes via the CA-CTD dimer interface just before or during membrane targeting

195 that destabilization of the PAS-B/tryptophan dimer interface leads to a faster mobility of mPER2 cont

196 N1/GluN2B N-terminal domain (NTD) upper lobe dimer interface leads to an irreversible allosteric inhi

197 dded in a pocket immediately adjacent to the dimer interface, linking the phosphorylation status of t

198 The X-dimer interface lowers the energy barrier associated wit

199 ackbone amide carbonyl positioned across the dimer interface may be responsible for the altered behav

200 he nonconserved amino acids distant from the dimer interface may control MERS-CoV 3CL(pro) dimerizati

201 Short B7-2 dimer interface mimetic peptides bind diverse superantig

202 An interactive site, at the HN dimer interface modulates HN fusion activation property,

203 dies indicated that Cys-20 is located at the dimer interface near the DNA-binding surface.

204 esidues 64 and 130, residues distal from the dimer interface occupied by H75, across the entire pH ra

205 e destabilization through mutagenesis of the dimer interface of a bacterial F(-)/H(+) antiporter, ClC

206 ate, but variation in B-cell epitopes at the dimer interface of DBP leads to induction of strain-limi

207 observation is that lithium ions bind to the dimer interface of GluK2/K5 heteromers and slow their de

208 ggering can be communicated across the dimer-dimer interface of H; and the physical integrity of the

209 We found that the dimer interface of HSPB5 is destabilized over physiologi

210 t BPTES binds to an allosteric pocket at the dimer interface of KGA, triggering a dramatic conformati

211 ents indicate that AXXXG motif is not on the dimer interface of p75-TM-WT, suggesting that the confor

212 ngle-residue variants in the active site and dimer interface of RsLOV alter photoadduct lifetimes and

213 d dimer interface (SEDI) antibody], that the dimer interface of SOD1 is abnormally exposed both in mu

214 d site-specific mutations into the BC domain dimer interface of Staphylococcus aureus PC (SaPC), equi

215 These results further characterize the dimer interface of the alpha-defensins, revealing a cruc

216 4I) directly weaken inhibitor binding at the dimer interface of the catalytic core domain but at the

217 NVR-010-001-E2 binds at the dimer-dimer interface of the core proteins, forms a new intera

218 The compound is bound at the dimer interface of the CT domain, at a site equivalent t

219 This alpha-hairpin is located in the dimer interface of the Ec-NhaA homodimer together with a

220 revealed a binding site at the GluN1-GluN2A dimer interface of the extracellular ligand-binding doma

221 CSP-NMR-guided HADDOCK modeling of the dimer-dimer interface of the heterotetrameric complex exhibits

222 The modulators bind within the dimer interface of the ligand-binding domain (LBD) and s

223 Peculiarities include the wrapping at the dimer interface of the N-terminal elongations from the t

224 to a rigid body rotational motion within the dimer interface of the regulator.

225 chain of the T-cell receptor but also to the dimer interface of the T-cell costimulatory receptor CD2

226 for molecules of cholesterol at the dimer + dimer interface of the tetramer, which is consistent wit

227 e reveal the importance of the D-loop at the dimer interface of the two nucleotide-binding domains (N

228 l extension that structurally mimics a dimer-dimer interface of these enzymes that are canonically or

229 ar preferred supramolecular organization and dimer interfaces of ORs across the different receptor su

230 he preferred supramolecular organization and dimer interfaces of ORs in a cell membrane model.

231 l membrane Bax proteins form a BH3-in-groove dimer interface on the MOM surface similar to that obser

232 e existence of two structurally distinct M3R dimer interfaces, one involving i2/i2 contacts (TM4-TM5-

233 ve led to distinctly different proposals for dimer interfaces, one involving interactions of ABED bet

234 ulators acting at the agonist-binding domain dimer interface or ion channel pore.

235 CLCNKB mutations in barttin-binding sites, dimer interface or selectivity filter often have severe

236 DeltaE2-4 SV gave an alternative, neomorphic dimer interface 'orthogonal' to that of native TyrRS.

237 by engineering glycosylation sites into the dimer interface; other interface mutants remained dimeri

238 imer epitope (EDE), readily exposed at the E dimer interface over the region of the conserved fusion

239 The dimer interface overlaps with RIP2 CARD but not RhoGDI b

240 Importantly, we find that a dimer interface peptide can effectively block Raf dimeri

241 presence of structural plasticity at the CTD dimer interface permits pleiotropic HIV-1 capsid assembl

242 units are "bolted" together to form a stable dimer interface permitting slight relative rotation but

243 only residues in the hydrophobic core of the dimer interface perturbed the I(2)* population.

244 tional selectivity and plasticity at the NTD dimer interface play a role in the pH-dependent transiti

245 but T.th. RuvC has a more tightly associated dimer interface possibly reflecting its thermostability.

246 RuvC has a more tightly associated dimer interface possibly reflecting its thermostability.

247 ing tRNA and instead repurposes it to form a dimer interface presenting a DNA-binding groove.

248 This DBD-LBD interaction masked CAR's dimer interface, preventing CAR homodimer formation.

249 ylation events directed to the extracellular dimer interface provide another mechanism to regulate th

250 ex hexagons, allosteric communication across dimer interfaces provides a pathway for receptor-generat

251 located at the surface and/or within the NS5 dimer interface, providing a functional significance to

252 ship between ligand binding, LBD closure and dimer interface rearrangement in activation remains uncl

253 an engineered disulfide bond across the NBD dimer interface reduces conformational fluctuations and

254 Genetic disruption of the predicted IpaH9.8 dimer interface reduces the solution molecular weight an

255 ing induces closure of the LBDs, followed by dimer interface reorientation.

256 Variability of the dimer interface residues likely ensures selective homodi

257 structure of the STAT3 NTD and identified a dimer interface responsible for cooperative DNA binding

258 Destabilizing the dimer interface resulted in the loss of RSV filament for

259 own, using a specific antibody [SOD1 exposed dimer interface (SEDI) antibody], that the dimer interfa

260 whereas targeting an allosteric site in the dimer interface selects an inactive conformation that co

261 ineered Toc159 with a cysteine placed at the dimer interface showed increased cross-linking to bound

262 ease with allosteric inhibitors bound to the dimer interface site.

263 l loop II-strand 3, rather than the proposed dimer interface site.

264 tructure reveals that ParB binds at the ParA dimer interface, stabilizing the ATPase-competent ATP sa

265 its form a remarkable, tryptophan-dominated, dimer interface stitched together by a complex salt-brid

266 it that acts in trans; tRNAs bind across the dimer interface such that Trm6 from the opposing heterod

267 er by approximately 33 A across an extensive dimer interface, suggesting a mechanism in which polyhyd

268 been determined, each displaying a different dimer interface, suggesting that SecA may adopt differen

269 , we identified a ligand-binding site in the dimer interface, suggesting that the cavity in the dimer

270 scussed in the context of a Trp49-containing dimer interface that acts as a conduit for thermally act

271 helical and beta-sheet domains at the native dimer interface that becomes exposed upon mutated SOD1 m

272 ion of a flexible loop proximal to the dimer-dimer interface that is essential for catalysis (i.e. th

273 he active conformation reveals an asymmetric dimer interface that is essentially the same as that in

274 n highly conserved residues across the RNase dimer interface that place key catalytic residues poised

275 d" SelA variants with mutations at the dimer-dimer interface that prevent pentamerization.

276 sults in a helix to strand transition at the dimer interface that reorients both DNA-binding domains,

277 londelta/gamma heterodimer revealed a unique dimer interface that results in a heterodimer with consi

278 ructural determinants at the GluN1/GluN2 NTD dimer interfaces that critically dictate UV-controlled i

279 the location of the structural motifs in the dimer interface, thereby establishing that both sequence

280 coli beta-sliding clamp that destabilize the dimer interface to determine whether the formation of an

281 imeras and PAR4 point mutants has mapped the dimer interface to hydrophobic residues in transmembrane

282 fluorescence of a tryptophan located at the dimer interface to show that dimer dissociation occurs s

283 (residues 333-366), which is located at the dimer interface, undergo a rapid transition on the sub-m

284 ation of ligand-dependent signals across the dimer interface via an unknown structural mechanism.

285 nd N749A) or in residues that disrupted Ire1 dimer interface (W426A or R697D).

286 Another dimer interface was formed inside the MOM by two interse

287 obe the functional significance of the Mre11 dimer interface, we have generated and characterized a d

288 Drawing on structural analysis of the dimer interface, we identified a bacteriophytochrome in

289 s canonical role it maintains the synthetase dimer interface, whereas in its function in tRNA primer

290 nd binding are linked to the dynamics of the dimer interface, whereas the low activity and affinity f

291 with the two transmembrane helices being the dimer interface, whereas the N-terminal cytoplasmic doma

292 picted decreased hydrophobic contacts at the dimer interface, whereas the Nle-29-HD5 crystal structur

293 eproteins was observed preferentially at the dimer interface, whereas the transit peptide was found a

294 that residue 178 was located near the dimer-dimer interface, which may affect VP1 assembly and oligo

295 hin or directly adjacent to CDR3 loop at the dimer interface, which remarkably include both destabili

296 veal remarkable structural similarity of the dimer interface with 3CL(pro) from HKU4-CoV and HKU5-CoV

297 ein-1 (MCP-1) by substituting Thr(10) at the dimer interface with Cys.

298 s that form an unusual helical bundle at its dimer interface with some resemblance to the helical tra

299 ergetic coupling between residues across the dimer interface with spontaneous pore opening/closure in

300 first example of a functionally important TM dimer interface within an HCV nonstructural protein and