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1 ant role in maintaining structure across the dimer interface.
2 hat both occurs through the crystallographic dimer interface.
3 eases the side chain of His23 from the dimer-dimer interface.
4 domain reveal the molecular nature of the CC dimer interface.
5 ith neonatal microcephaly, is located at the dimer interface.
6 es a central hydrogen bonding network at NS1 dimer interface.
7 tein motions, consistent with a destabilized dimer interface.
8 ing two modulator-binding sites at the GluK1 dimer interface.
9 hat it can be activated by disruption of the dimer interface.
10 ween specific charged amino acids across the dimer interface.
11 homodimer of ACT folds with Phe bound at the dimer interface.
12 nces in how the subunits are arranged at the dimer interface.
13 ent manner to form a ferroxidase center at a dimer interface.
14 ue quaternary epitope on the E protein dimer-dimer interface.
15 ium with the Cys(257) residue located on the dimer interface.
16 e protruding Jalpha helix and on the LOV-LOV dimer interface.
17 interactions observed at the N. clavipes NTD dimer interface.
18 r identifies subunits e and g at the lateral dimer interface.
19 d cooperatively recognize the antigen in the dimer interface.
20 ent active dimers and revealed the preferred dimer interface.
21 ces in aromatic-aromatic interactions at the dimer interface.
22  value and is located within the hydrophobic dimer interface.
23 nsport core and TM11-TM12 helices lining the dimer interface.
24 quely in RECQ1) is buttressed by the protein dimer interface.
25 rk of hydrogen bonds and salt bridges at the dimer interface.
26 ent of conserved proline residues across the dimer interface.
27 outer edges, and basic side grooves near the dimer interface.
28 kp1-Rnl-Hen1 heterotrimer fused at the Pnkp1 dimer interface.
29  a number of sites near the crystallographic dimer interface.
30 f the dimer, we mutated five residues on the dimer interface.
31 id the design of inhibitors that bind at the dimer interface.
32 etrical dimer with a large deep cleft at the dimer interface.
33 otential Zn(2+)-binding sites outside of the dimer interface.
34 h recapitulating the role of Phe(B24) at the dimer interface.
35 cal frame-work with protruding spikes at the dimer interface.
36 f transmembrane helix IV, is observed at the dimer interface.
37 t this site restricts its involvement at the dimer interface.
38 r part of, or allosterically coupled to, the dimer interface.
39 lly coupled, conveying inhibition across the dimer interface.
40  which forms part of the mariner transposase dimer interface.
41 g of protomers through two histidines at the dimer interface.
42 on of binding kinetics by mutations at the X-dimer interface.
43 cooperativity due to steric hindrance at the dimer interface.
44 nt, with two nucleotides "sandwiched" at the dimer interface.
45 phate (Fru-6-P), binds along the other dimer-dimer interface.
46 on of the chemokine, which overlaps with the dimer interface.
47 etworks in the active-site cavity and at the dimer interface.
48 g the C-terminal residues that stabilize the dimer interface.
49 lectrostatic interactions that stabilize the dimer interface.
50  dimer by introducing a disulfide across the dimer interface.
51 entire active site, as well as 3 hits at the dimer interface.
52 iminished with disruption of the BRAF kinase dimer interface.
53 ut Trp/Arg side chains that stack across the dimer interface.
54 ons of the surface residues that mediate the dimer interface.
55 ing site on SLIP1 for SLBP lies close to the dimer interface.
56 hibitor binds in an allosteric manner at the dimer interface.
57 dimer with two (p)ppGpp binding sites at the dimer interface.
58 mental data that suggest coordination in the dimer interface.
59 omodimer with a dicopper Cu(A) center at the dimer interface.
60 eveals a binding site for the 3' cRNA at the dimer interface.
61  GyrA WHD and GyrB TOPRIM domains across the dimer interface.
62 on of the C domains that disrupts the normal dimer interface.
63 ward the ligand fingertips and away from the dimer interface.
64  immunity are conformational epitopes at the dimer interface.
65         Instead, TM2, TM6, and TM11 line the dimer interface.
66 ATPase, positions of the main domains, and a dimer interface.
67 PP2A/RACK1 binding site is buried within its dimer interface.
68 ) in the predicted, tightly packed TM domain dimer interface.
69 dine (HAP) pocket between core protein dimer-dimer interfaces.
70 kinetics of receptor association at specific dimer interfaces.
71 ral rearrangements specifically at the dimer-dimer interfaces.
72 ry to confirm APJ homo-dimer and explore the dimer-interfaces.
73 an R-state conformation with a lysine at the dimer-interface acting as a peg in a hole, locking the a
74                      Disrupting the observed dimer interface affects particle assembly and overall sp
75 d modeling, we find that the subunits form a dimer interface along the entire length of S1, and also
76 soflurane and sevoflurane bound to both TLR9 dimer interface and 5'-xCx DNA binding site.
77 a homologous BH4-binding site located in the dimer interface and a conserved tryptophan residue that
78 ng in the rearrangement of the kinase domain-dimer interface and a rotation of the RNase domains away
79 both AtPRK and CrPRK have a strongly reduced dimer interface and an increased number of random-coiled
80  in the amino acids located primarily at the dimer interface and at the C-terminal region of IFN-gamm
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 that structurally stabilized the EGFR kinase dimer interface and conferred sensitivity to kinase inhi
85  mutations of BRCA1 are found to disrupt the dimer interface and dimer formation.
86 ed stabilization of aromatic clusters at the dimer interface and enhancement of intersubunit hydrogen
87 ovine rhodopsin (Rho) to investigate the Rho dimer interface and functional consequences of its disru
88 a positively charged Arg residue at the beta-dimer interface and high NaCl concentrations destabilize
89 A positively charged cavity is formed on the dimer interface and involves several strictly conserved
90 nating in the epicenter further disrupts the dimer interface and leads to dimer dissociation.
91 H1 indicates that the inhibitor binds at the dimer interface and makes direct contact with a residue
92 iochemical analysis, reveal a lipid mediated dimer interface and mechanism for coordinating structura
93  in live cells confirm that mutations at the dimer interface and peripheral site produce effects comp
94 hat disrupts the BC-loop regions at the P450 dimer interface and results in a CYP126A1 monomeric crys
95 lly those residing at barttin binding sites, dimer interface and selectivity filter.
96  and PHF19 associate with PRC2 at around the dimer interface and stabilize the dimer.
97 rs of thymidylate synthase (hTS) bind to the dimer interface and stabilize the inactive form of the p
98 nally to the interhelical axis and spans the dimer interface and that heparin binding enhances the st
99 lay of more than one amino acid at the dimer-dimer interface and the C-terminal unstructured tail.
100 lex) confirm structural coupling between the dimer interface and the catalytic center.
101         The structure suggests that ATM/Tel1 dimer interface and the consecutive HEAT repeats inhibit
102 are non-native oligomers in which the native dimer interface and the electrostatic loop mediate the f
103        Our results show that residues at the dimer interface and the switch II region of Toc159G are
104 alcohol dehydrogenase (ht-ADH): Y25A (at the dimer interface) and V260A (at the cofactor-binding doma
105 5 was identified as being located in the A52 dimer interface, and consistent with that, A52-M65E was
106 ate altered hydrogen-bonding patterns at the dimer interface, and cross-correlation analysis showed t
107 These mutations resided in the dorsal flaps, dimer interface, and GTP-binding regions of the catalyti
108 dy binds to E proteins residues at the intra-dimer interface, and the virus quaternary structure-depe
109 onserved ATP-binding pocket that lies at the dimer interface, and we identify key residues in this bi
110 ingle position of the allosteric site of the dimer interface, and we show that the enzyme activity va
111                We noted that residues at the dimer interface are also present in LsdB, another lignos
112 monstrate that the KAR M3-S2 linkers and LBD dimer interface are critical determinants for Neto2 modu
113 a10/I24N), in which the beta1-strands at the dimer interface are extruded and available to bind MinD,
114 dues in the C-terminal CA subdomain (CA-CTD) dimer interface are needed for the stability of the firs
115                      We also identify the D1 dimer interface as a novel site of Neto2 modulation and
116 f channel opening by F508del and support the dimer interface as a target for cystic fibrosis therapeu
117 d for Raf function, thus identifying the Raf dimer interface as a therapeutic target.
118 harmacophore, binds at the same GluN1/GluN2B dimer interface as ifenprodil but adopts a remarkably di
119 mission of conformational changes across the dimer interface as the most probable mechanism of altere
120 erivatives target a similar pocket at the IN dimer interface as the quinoline-based ALLINIs, the lead
121 ensitizing conditions, the largely decoupled dimer interface at the agonist-binding domain as seen in
122 nd cross-linking studies show that the dimer-dimer interface at the agonist-binding domain mediates t
123 onal and structural studies suggest that the dimer interface at the agonist-binding domain plays a ke
124 c IN inhibitors (ALLINIs) that engage the IN dimer interface at the binding site for the host protein
125 ic acid derivatives that bind at the CCD-CCD dimer interface at the principal lens epithelium-derived
126  As expected, a peptide corresponding to the dimer interface became more solvent exposed over time at
127 kbone H-bonding interactions by substituting dimer interface beta-strand residues with proline (Pro)
128 he SelA catalytic site is close to the dimer-dimer interface, but the significance of the dimer penta
129                            We confirmed this dimer interface by double electron-electron resonance me
130  the protein, where it is coordinated at the dimer interface by main chain carbonyl oxygen atoms from
131  of the mutants can facilitate access to the dimer interface by small molecules and thereby aid the d
132 tion of the beta3- and beta3'-strands at the dimer interface; changes in the second are more extensiv
133 ntified a possible lipid binding site at the dimer interface comprising residues Arg265, Arg267, Arg4
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        These various sites and the conserved dimer interface could be exploited for the development o
140 interface, suggesting that the cavity in the dimer interface could serve as an allosteric site of hTS
141 istent with the experimental data from which dimer interfaces could be deduced.
142 Structure-guided mutational analyses of RopB dimer interface demonstrated that single alanine substit
143    Ten years after the definition of the RAF dimer interface (DIF) by crystallography, this review fo
144 imeric in solution and in crystals, with the dimer interface displaying a surface groove that is line
145  region at triosephosphate isomerase (TIM)'s dimer interface, distant from its catalytic site, is a t
146 region at the active state asymmetric kinase dimer interface do not affect the stability of ligand-in
147 eas a CatC mutant with a disrupted CRAF-CRAF dimer interface does not.
148 ), which is also formed at the S100A8/S100A9 dimer interface, does not provide a high-affinity Mn(II)
149 nts--to the extracellular ligand binding and dimer interface domains of the EGFR can induce EGFR dime
150 ergoes dynamic motion that exposes the dimer-dimer interface during catalysis.
151 lts indicate that tryptophan residues at the dimer interface engage in photoinduced proton coupled el
152 that methylation of R198 and R200 within the dimer interface enhances growth factor ligand binding an
153  targeting the disulfide-bond stabilized LRX dimer interface fail to rescue lrx infertility phenotype
154                         A large antiparallel dimer interface formed by the first 4 extracellular cadh
155 upies the UDG DNA-binding cleft, whereas the dimer interface forms a hydrophobic box to trap a mechan
156 hough CT263 lacks the active site-associated dimer interface found in prototypical MTANs, co-crystal
157 ivation also involves a reorientation of the dimer interface from a 'relaxed' to an 'active' state, b
158 ing dynamics to the substitution site in the dimer interface; G194C and G426E both led to minor struc
159 e lowest potential energy although its intra-dimer interface has the least free energy of formation.
160 Substituting a critical residue of the dimer-dimer interface, His-110, altered the tetramer dissociat
161                         Substitutions at the dimer interface impaired IreB function and stability in
162  We demonstrate that a mutation at the GAPDH dimer interface impairs formation of the second RNA-GAPD
163                               Mutating these dimer interfaces implicates one of them (dimer 1) in sol
164                      A mutation at the dimer-dimer interface in a thermolabile psychrophilic homologu
165 dentified the structural determinants of the dimer interface in the active receptor, and validated th
166 ion mode is distinct from the widely studied dimer interface in the CA domain and from protein intera
167 sidues on the Escherichia coli SecA (ecSecA) dimer interface in the cytosol of intact cells.
168 ast, detergent-resistant lipids bound at the dimer interface in the leucine transporter show decrease
169 ciation, suggesting that stability of the D1 dimer interface in the ligand-binding domain (LBD) is an
170 nd C termini, subunit exchange, and variable dimer interfaces in ABC.
171  also reveal by crystallography two distinct dimer interfaces in the BTN3A1 full-length intracellular
172 t factors contribute to the stability of the dimer interfaces in the closed conformation and how clam
173 resolution shows distinct asymmetry near the dimer interface, in the region harboring catalytically i
174                                          The dimer interface includes hydrophobic and hydrophilic int
175 al-binding sites formed at the S100A8/S100A9 dimer interface, including a histidine-rich site compose
176 ific effects of oxidative "mutations" at the dimer interface, including lysine, arginine, proline and
177 ts are at a serotype-invariant site at the E-dimer interface, including the exposed main chain of the
178  aims to understand how the stability of the dimer interface influences clamp-opening dynamics and cl
179 me B prosthetic group present at the subunit dimer interface influences the stability and pressure la
180  the TREX1 Arg-62 residues extend across the dimer interface into the active site of the opposing pro
181       The purified protein was a dimer whose dimer interface involves interactions between the coiled
182                      Finally, mutations at a dimer interface, involving fusion domains associated in
183 ced bending of a long signaling helix at the dimer interface is counteracted by the ligand-induced st
184  of the intermolecular disulfide, the Rgg2Sd dimer interface is destabilized and Rgg2Sd can adopt mul
185 hat the CC3 forms a parallel homodimer whose dimer interface is formed by a small number of hydrophob
186 P7B, does not disrupt dimerization, i.e. the dimer interface is formed by the domains that are conser
187                                          The dimer interface is formed entirely by phylum-specific co
188  cotranslational interactions until the LuxB dimer interface is fully exposed.
189  here suggested that a properly aligned RopB dimer interface is important for GAS pathogenesis and hi
190 x-ray scattering analysis indicated that the dimer interface is located at the C terminus and provide
191                                          The dimer interface is more efficient for attracting and bin
192 nformational states in which Domain 1 at the dimer interface is more flexible and prone to unfolding.
193                                          The dimer interface is suited to resist hydrodynamic force a
194 ) motif (site 2) formed at the S100A8/S100A9 dimer interface is the site of high-affinity Mn(II) coor
195  important than specific amino acids and the dimer interface is unique from other A3 enzymes.
196 ollowing model: Gag dimerizes via the CA-CTD dimer interface just before or during membrane targeting
197 N1/GluN2B N-terminal domain (NTD) upper lobe dimer interface leads to an irreversible allosteric inhi
198  mutated three conserved residues in the Nef dimer interface (Leu(112), Tyr(115), and Phe(121)) and d
199 dded in a pocket immediately adjacent to the dimer interface, linking the phosphorylation status of t
200                                        The X-dimer interface lowers the energy barrier associated wit
201    The A3G dimer structure has a hydrophobic dimer-interface matching with that of the previously rep
202 ackbone amide carbonyl positioned across the dimer interface may be responsible for the altered behav
203 he nonconserved amino acids distant from the dimer interface may control MERS-CoV 3CL(pro) dimerizati
204           The isoform-specific RI-holoenzyme dimer interface mediated by N3A-N3A' motifs defines mult
205                                   Short B7-2 dimer interface mimetic peptides bind diverse superantig
206                                          Nef dimer interface mutants also failed to trigger internali
207                           A CA inter-hexamer dimer interface mutation led to a loss of induced PIP2 c
208 dies indicated that Cys-20 is located at the dimer interface near the DNA-binding surface.
209 e destabilization through mutagenesis of the dimer interface of a bacterial F(-)/H(+) antiporter, ClC
210 ate, but variation in B-cell epitopes at the dimer interface of DBP leads to induction of strain-limi
211 observation is that lithium ions bind to the dimer interface of GluK2/K5 heteromers and slow their de
212                            We found that the dimer interface of HSPB5 is destabilized over physiologi
213 tigen receptor for chemokines (DARC) and the dimer interface of P. vivax DBP.
214 ents indicate that AXXXG motif is not on the dimer interface of p75-TM-WT, suggesting that the confor
215 d site-specific mutations into the BC domain dimer interface of Staphylococcus aureus PC (SaPC), equi
216                                          The dimer interface of Ste2 is formed by the N terminus, the
217 reveal that the PLPLRT/SD motif binds to the dimer interface of TBK1.
218                    Last, we propose that the dimer interface of the BRAF(D594G):CRAF heterodimer may
219 4I) directly weaken inhibitor binding at the dimer interface of the catalytic core domain but at the
220            NVR-010-001-E2 binds at the dimer-dimer interface of the core proteins, forms a new intera
221                 The compound is bound at the dimer interface of the CT domain, at a site equivalent t
222         This alpha-hairpin is located in the dimer interface of the Ec-NhaA homodimer together with a
223  revealed a binding site at the GluN1-GluN2A dimer interface of the extracellular ligand-binding doma
224 CSP-NMR-guided HADDOCK modeling of the dimer-dimer interface of the heterotetrameric complex exhibits
225               The modulators bind within the dimer interface of the ligand-binding domain (LBD) and s
226 chain of the T-cell receptor but also to the dimer interface of the T-cell costimulatory receptor CD2
227  for molecules of cholesterol at the dimer + dimer interface of the tetramer, which is consistent wit
228 e reveal the importance of the D-loop at the dimer interface of the two nucleotide-binding domains (N
229 l extension that structurally mimics a dimer-dimer interface of these enzymes that are canonically or
230 ar preferred supramolecular organization and dimer interfaces of ORs across the different receptor su
231 he preferred supramolecular organization and dimer interfaces of ORs in a cell membrane model.
232 l membrane Bax proteins form a BH3-in-groove dimer interface on the MOM surface similar to that obser
233 e existence of two structurally distinct M3R dimer interfaces, one involving i2/i2 contacts (TM4-TM5-
234 ve led to distinctly different proposals for dimer interfaces, one involving interactions of ABED bet
235   CLCNKB mutations in barttin-binding sites, dimer interface or selectivity filter often have severe
236                             Mutations in the dimer interface, or of residues along an inhibitory path
237 DeltaE2-4 SV gave an alternative, neomorphic dimer interface 'orthogonal' to that of native TyrRS.
238  by engineering glycosylation sites into the dimer interface; other interface mutants remained dimeri
239 imer epitope (EDE), readily exposed at the E dimer interface over the region of the conserved fusion
240                                          The dimer interface overlaps with RIP2 CARD but not RhoGDI b
241                  Importantly, we find that a dimer interface peptide can effectively block Raf dimeri
242 tional selectivity and plasticity at the NTD dimer interface play a role in the pH-dependent transiti
243 ing tRNA and instead repurposes it to form a dimer interface presenting a DNA-binding groove.
244        This DBD-LBD interaction masked CAR's dimer interface, preventing CAR homodimer formation.
245 ylation events directed to the extracellular dimer interface provide another mechanism to regulate th
246 ex hexagons, allosteric communication across dimer interfaces provides a pathway for receptor-generat
247 located at the surface and/or within the NS5 dimer interface, providing a functional significance to
248 ship between ligand binding, LBD closure and dimer interface rearrangement in activation remains uncl
249  an engineered disulfide bond across the NBD dimer interface reduces conformational fluctuations and
250  Genetic disruption of the predicted IpaH9.8 dimer interface reduces the solution molecular weight an
251 ing induces closure of the LBDs, followed by dimer interface reorientation.
252                                    The dimer-dimer interface requires an intricate hydrogen bonding n
253  structure of the STAT3 NTD and identified a dimer interface responsible for cooperative DNA binding
254                            Destabilizing the dimer interface resulted in the loss of RSV filament for
255  whereas targeting an allosteric site in the dimer interface selects an inactive conformation that co
256 ineered Toc159 with a cysteine placed at the dimer interface showed increased cross-linking to bound
257 cal stability with core regions close to the dimer interface showing lower protection but some other
258 tide requires binding of cations to an intra-dimer interface site in the RCK dimer.
259 l loop II-strand 3, rather than the proposed dimer interface site.
260 ease with allosteric inhibitors bound to the dimer interface site.
261 tructure reveals that ParB binds at the ParA dimer interface, stabilizing the ATPase-competent ATP sa
262                   Conserved loops at the CBD dimer interface straddle a conserved peripheral NBD heli
263 it that acts in trans; tRNAs bind across the dimer interface such that Trm6 from the opposing heterod
264 er by approximately 33 A across an extensive dimer interface, suggesting a mechanism in which polyhyd
265 , we identified a ligand-binding site in the dimer interface, suggesting that the cavity in the dimer
266 scussed in the context of a Trp49-containing dimer interface that acts as a conduit for thermally act
267 helical and beta-sheet domains at the native dimer interface that becomes exposed upon mutated SOD1 m
268 igher affinity is due to the residues in the dimer interface that create an attractive electrostatic
269 ion of a flexible loop proximal to the dimer-dimer interface that is essential for catalysis (i.e. th
270 he active conformation reveals an asymmetric dimer interface that is essentially the same as that in
271 n highly conserved residues across the RNase dimer interface that place key catalytic residues poised
272 d" SelA variants with mutations at the dimer-dimer interface that prevent pentamerization.
273 hat single amino acid mutations at the IL-37 dimer interface that result in the stable formation of I
274 londelta/gamma heterodimer revealed a unique dimer interface that results in a heterodimer with consi
275 ructural determinants at the GluN1/GluN2 NTD dimer interfaces that critically dictate UV-controlled i
276                             Of all the inter-dimer interfaces, the CB interface has the least area an
277 eside closely on a loop that constitutes the dimer interface; their sidechains interact with the Pro7
278 ps leads to a compaction of the intersubunit dimer interface, thereby bringing the cysteine-rich doma
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        However, besides 8 tryptophans at the dimer interface to form two critical pyramid perception
282                              Mutation of the dimer interface to make Set1C monomeric abolished H3K4me
283  fluorescence of a tryptophan located at the dimer interface to show that dimer dissociation occurs s
284 dues along an inhibitory pathway linking the dimer interface to the enzyme's active site, favour BiP
285 ve effect allosterically propagated from the dimer interface to the inhibitory Glu234, thereby permit
286 - and (p)ppGpp-bound tetramer, where a dimer-dimer interface triggers allosteric structural rearrange
287 ation of ligand-dependent signals across the dimer interface via an unknown structural mechanism.
288                                      Another dimer interface was formed inside the MOM by two interse
289        Drawing on structural analysis of the dimer interface, we identified a bacteriophytochrome in
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 eproteins was observed preferentially at the dimer interface, whereas the transit peptide was found a
293 red an additional nickel-binding site at the dimer interface, which binds Ni(II) with an affinity of
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 ergetic coupling between residues across the dimer interface with spontaneous pore opening/closure in
298 ing is found between V(L)-V(L) and C(L)-C(L) dimer interfaces, with destabilization of one interface
299 first example of a functionally important TM dimer interface within an HCV nonstructural protein and
300 meric complexes on Psi RNA require an intact dimer interface within Gag.

 
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