ライフサイエンスコーパス: salt bridge

1 that are capped at the end of the chain by a salt bridge.

2 ed by a turn stabilized by a Asp(25)-Lys(30) salt bridge.

3 ere connected through the Arg(102)-Glu(1032) salt bridge.

4 ontrols the formation and disruption of this salt bridge.

5 possibly through disruption of the E138-K101 salt bridge.

6 accommodated by formation of an interfacial salt bridge.

7 subconductance state does not require either salt bridge.

8 rmation, and identified a novel load-bearing salt bridge.

9 ccluded than in kindlins-2 and -3 due to its salt bridge.

10 ed by Glu(317) is largely independent of the salt bridge.

11 inding that this substitution eliminates the salt bridge.

12 endritic guest via the formation of multiple salt bridges.

13 dimer is held together by arginine-aspartate salt bridges.

14 o form a network of inter- and intraprotomer salt bridges.

15 be linked with formation and maintenance of salt bridges.

16 ve to reference electrodes with conventional salt bridges.

17 ferred to collagen by axial lysine-aspartate salt bridges.

18 Lys (K) residues, and stabilized by multiple salt bridges.

19 ix, as well as by intramolecular H-bonds and salt bridges.

20 they have different capabilities of forming salt bridges.

21 ip bonds mediated by force-induced K113:E195 salt-bridges.

22 ced movement that disrupts the Glu167/Arg290 salt bridge, a comparison of the closed and open rat P2X

23 We further find that the D23-K28 salt-bridge, a major feature of the Abeta40 fibrils and

24 the core domain, which may be involved in a salt bridge, abolished virion assembly and cell-to-cell

25 The salt bridge accounts for the nonphysiological cation(s)

26 Mutations aimed at disrupting any of these salt bridges activated binding unless the mutated residu

27 ics simulations suggest that the interdomain salt bridge acts as a steric barrier regulating ligand b

28 Instead, a labile salt bridge acts as an incessantly active "agitator" tha

29 148 at the C-terminus of CaM forms transient salt bridges alternating between Glu side chains in the

30 s of UVR8 and show that mutations of several salt-bridge amino acids affect dimer/monomer status, int

31 rmed that rho-TIA binding was dominated by a salt bridge and cation-pi between Arg-4-rho-TIA and Asp-

32 inding site, facilitating the formation of a salt bridge and freeing a tyrosine-containing strand.

33 Non-covalent bonds, more likely salt bridge and ionic interactions, played a major role

34 diated by arginine residue switching between salt bridge and pi-pi stacking interactions.

35 cket, stabilizing a network of extracellular salt bridges and blocking transmembrane helix motions ne

36 A redistribution of salt bridges and cation-pi interactions at the N-termina

37 with breakage of the E247-R135 and R135-E134 salt bridges and concomitant release of the E134 side ch

38 amic-acid mutation leads to the loss of both salt bridges and destabilizes interactions with Ig-2D1.

39 l of resolution, and we identify a number of salt bridges and hydrogen bonds at the interface of myos

40 those five residues form a stable network of salt bridges and hydrogen bonds, leaving the Asp side ch

41 nd E56, which we attribute to the effects of salt bridges and hydrogen bonds.

42 est fit for the interaction reveals multiple salt bridges and hydrophobic contacts between the two pr

43 eptide lysine-aspartate and lysine-glutamate salt bridges and maintains good thermal stability with a

44 ple sensitivity and clogging of conventional salt bridges and the often poorly controlled loss of bri

45 eractions have unique aspects, including two salt bridges and weak recognition of the peptide C termi

46 to engage in tertiary polar contacts such as salt bridging and hydrogen bonding, providing evidence t

47 Bifurcated and intermediary salt-bridge and hydrogen-bond interactions play a role i

48 interference in oxidoreductase interactions, salt-bridge and hydrogen-bonding networks, and nonconser

49 attention compared to ion-ion interactions (salt bridges) and dipole-dipole interactions (hydrogen b

50 eimer's disease: the N-terminus, the central salt bridge, and the C-terminus.

51 ced by intrachain hydrogen bonds, side-chain salt bridges, and a row of seven stacked tyrosines on th

52 ecting the two rungs, buried polar residues, salt bridges, and asparagine ladders.

53 ites were the largest in size, involved many salt bridges, and were the most compact and least planar

54 c mimics employ a range of hydrogen bonding, salt bridging, and hydrophobic interactions with thrombi

55 ith the membrane in terms of hydrogen bonds, salt-bridges, and nonpolar contributions.

56 in vitro The effects of the Asp-302-His-305 salt bridge are thus complex and context-dependent.

57 Two important salt bridges are found between the HAs and Ig-2D1.

58 intrapeptide interactions, particularly the salt bridge Asp(23)-Lys(28).

59 ure fibrils by disrupting the intermolecular salt bridge Asp23-Lys28 via hydrogen bonding.

60 mutation of Lys-99, which participates in a salt bridge at the SAM polymer interface, reduces self-a

61 modeling indicated that the mutation altered salt bridges at subunit interfaces, including regions im

62 ar dynamic simulations suggested that stable salt bridges at the cis side, which are susceptible to d

63 s an intricate network of hydrogen bonds and salt bridges at the dimer interface.

64 These include the previously identified salt bridge between a lysine from the beta3-strand and a

65 on may have resulted in a direct loss of the salt bridge between A-DNA and hMPG, whereas R120C substi

66 a lysine 113(K113):glutamic acid 195 (E195) salt bridge between actin subunits, thus suggesting a mo

67 conformation of Glu(76), primarily through a salt bridge between Arg(83) and Glu(76).

68 The disruption of the salt bridge between Arg155 and Glu244, which stabilizes

69 e stabilizing T4 lysozyme, that the expected salt bridge between ArgIII:26 and GluVI:-06 does form re

70 A hydrogen-bonded salt bridge between Asp-302 and His-305 is particularly

71 terferes with formation of a fibril-specific salt bridge between aspartic acid 23 and lysine 28.

72 ding the alpha-helix, are conserved, but the salt bridge between aspartic acid and arginine is lost.

73 n hydrogen bonds with D23 and a cross-region salt bridge between E22 and K28, highlighting the role o

74 The formation of a salt bridge between Glu309 and Arg494 is found to be par

75 ural configurations, one of which included a salt bridge between His-164 of cTnI and Glu-19 of cTnC.

76 The clamp over the DNA, characterized by the salt bridge between Lys369 and Glu497, undergoes reduced

77 Engineering a more polar salt bridge between p51 and p66 resulted in even greater

78 hic helix is stabilized by an intramolecular salt bridge between residues Glu(615) and Arg(152).

79 nase domain that is stabilized by an unusual salt bridge between the activation loop and alphaD helix

80 l and biochemical evidence for the role of a salt bridge between the desosamine N,N-dimethylamino fun

81 analysis and found two residues that form a salt bridge between the first and second putative transm

82 ly conserved Arg-125 on cytP450 serving as a salt bridge between the heme propionates of cytP450 and

83 M), with the predominant interaction being a salt bridge between the ligand carboxylate headgroup and

84 wo residues (Glu-816 and Arg-1229) forming a salt bridge between the NADPH/FAD and FMN domains in the

85 favirenz promotes formation of the E138-K101 salt bridge between the p51 and p66 subunits of RT, whic

86 ontain the electrolyte solution that forms a salt bridge between the sample and the reference electro

87 ontain the electrolyte solution that forms a salt bridge between the sample and the reference solutio

88 otons are examined, and the possibility of a salt bridge between the sulfate and amine groups of 3-O-

89 ding pocket toward TM5 due to absence of the salt bridge between the USB and the protonated E113 resi

90 ions in Cpx and the v-SNARE that disrupted a salt bridge between these two proteins.

91 sh the integrity of the M1 layer through new salt bridges between adjacent M1 subunits when the origi

92 A interactions requires a pair of asymmetric salt bridges between Arg52 and Asp49' that connect other

93 ding experiments, we identified a network of salt bridges between Asp(1261) and the rest of A1 that l

94 The pore complex is stabilized by salt bridges between beta-hairpins of adjacent subunits

95 cs simulations, we investigate the effect of salt bridges between different types of charged amino-ac

96 lysis of the simulations point to non-native salt bridges between helices as the source, which provid

97 erent types of charge pairs, we observe that salt bridges between side chains of Glu(-) and Arg(+) ar

98 ization by introducing several interprotomer salt bridges between the alphaC-helix and charged residu

99 cked in the closed state by the formation of salt bridges between the phosphate group of PEP and the

100 nd quantitative binding assays indicate that salt bridges between the sulfate group and two lysine re

101 hanism of dimerization involves formation of salt bridges between the two GTPase domains (G domains)

102 rge dipole moment drives the breaking of the salt bridges between the two monomer subunits.

103 we also demonstrate that two intermolecular salt bridges between TolA and pIII provide the driving f

104 g nonannular lipid binding site leading to a salt-bridge between adjacent KcsA-Kv1.3 subunits, which

105 oduced the E442A mutation, which abrogates a salt-bridge between switch I and switch II, and the G440

106 tions, and the MD simulations identified the salt-bridge between the primary amine of 5-HT and the li

107 r not only charge state isomers that include salt bridges but also protonation at nonbasic residues.

108 portions of the peptide-MHC through similar salt bridges, but their hydrophobic side-chain packings

109 imentally, we found that disruption of these salt bridges by mutations facilitates hemichannel closin

110 nteractions stabilized by hydrogen bonds and salt bridges can hinder the separation of fragments even

111 phobic core of Abeta and breaks an essential salt-bridge characteristic of the beta-hairpin conformat

112 try, active site residues, and a stabilizing salt bridge cluster, (ii) is thermostable and shows a fo

113 Here we identify a salt-bridge competition or "theft" mechanism that enable

114 ng a beta-hairpin loop that forms a critical salt-bridge contact with the 3'-terminal adenylate of aa

115 the present study, we determined how the two salt bridges cooperate to maintain the open pore archite

116 H-bond network, although certain Arg to Asp salt bridges create highly localized rigidity increases.

117 rine-to-asparagine mutation coincided with a salt bridge destabilization, hydrogen bond losses, and a

118 Substitutions that abolish the salt bridge destabilize coat protein monomers and impair

119 for this proof of concept that one specific salt bridge determines the formation of pentamers or hex

120 ionic strength (to modulate stability of the salt bridges) did not affect the rotational correlation

121 The associated release of the Glu167/Arg290 salt bridge during channel opening allows a strong ionic

122 The use of a micro cross for positioning a salt bridge-electrode opposite the separation capillary

123 he Abeta termini can determine the fate of a salt bridge far away in the sequence, and this has signi

124 To fabricate a porous membrane as a salt bridge for free-flow zone electrophoresis, we used

125 zed trans-proline variants exist in a linear salt-bridge form where the metal ion interacts with a de

126 The major complex structure shows a salt bridge formation between Glu-213/Glu-214 of FBD and

127 Although salt bridge formation did not appear to be critical for

128 (94) residue was predicted to be involved in salt bridge formation with Glu(98), therefore causing si

129 formation through compensatory intracellular salt bridge formation, which in turn favors binding of c

130 Binding is primarily dependent on salt-bridge formation and correct folding of the intact

131 erall, we propose interstrand separation and salt-bridge formation as key reaction coordinates descri

132 EXXX, where X is K or R) expected to promote salt-bridge formation between Glu and Lys/Arg.

133 rmed by residues 54-81 and an intermolecular salt bridge formed by residues Arg67 and Glu73, indicati

134 side chains of two arginine residues and by salt bridges formed between the like-charge ion pair and

135 In particular, the salt-bridges formed between arginine 286 and aspartates

136 performed parametric studies to show how the salt bridge geometry determines equilibration between th

137 se of the larger conformational space of the salt-bridging Glu(-)/Arg(+) rotamer pairs compared to As

138 y, but the presence of zwitterionic pairs or salt bridges has previously been more difficult to detec

139 e vicinity of the interdomain Lys-99-Asp-101 salt bridge, have little or no effect on these oncogenic

140 nism that involves swapping of an intramotif salt bridge, i.e. R-E2 to R-E1, which is consistent with

141 The Glu(403)-Lys(118) salt bridge in C-domain ACE was shown to stabilize the h

142 genesis experiments confirm the role of this salt bridge in controlling the dissociation kinetics of

143 perimental data suggest that the role of the salt bridge in maintaining the alignment of the two part

144 pNCSF was also used to replace a native salt bridge in myoglobin with an intramolecular crosslin

145 amics simulations suggest that the loss of a salt bridge in SLO and a cation-pi interaction are deter

146 Abeta, which are known to form a stabilizing salt bridge in some fibril morphologies.

147 ed by these mutations form an intramolecular salt bridge in SPARC and are essential for the binding o

148 ntacts for a network of hydrogen bonds and a salt bridge in the core of binding.

149 ture, is that the disruption of a linker/CBD salt bridge in the R:C complex unexpectedly leads to inc

150 part of the Cp F2-G2 loop, formed a putative salt bridge in the virion.

151 adjacent subunit's backbone alpha-helix form salt bridges in hexamers and pentamers.

152 Previous studies have identified two salt bridges in human CFTR chloride ion channels, Arg(35

153 e sequence of events with the same nonnative salt bridges in the encounter complex.

154 mulations identified three novel interdomain salt bridges in the lymphomagenic virus HR1 that could a

155 2+) interaction and consequent disruption of salt bridges in the open hemichannels.

156 orylation destabilizes this highly conserved salt-bridge in temporal and physical space.

157 Our results indicate that stabilizing salt bridges (in which the interacting residues are spac

158 The Arg(352)-Asp(993) salt bridge, in contrast, is involved in stabilizing bot

159 ic, competes for a lysine from a preexisting salt bridge, initiating a partial unfolding event and pr

160 f 1a.H, by the formation of an unprecedented salt-bridge interaction.

161 single E35D substitution leads to diminished salt bridge interactions between residues 35 and 57 and

162 d with the goal of understanding how altered salt bridge interactions between the hinge and flap regi

163 transport that highlights the importance of salt bridge interactions in orchestrating alternating ac

164 mbrane helices via dynamic hydrogen bond and salt bridge interactions.

165 re stabilized by networks of hydrophobic and salt bridge interactions.

166 ucture-guided mutagenesis that the conserved salt-bridge interactions (R75:D155 and R88:D157) on the

167 ed UVR8 show that the dimer is maintained by salt-bridge interactions between specific charged amino

168 activated beta2 adrenergic receptor and form salt-bridge interactions that inhibit ionic lock formati

169 of lysine side chains that form stabilizing salt-bridge interactions with substituted and native res

170 osed at the matrix side by three interdomain salt-bridge interactions, one of which is braced by a gl

171 ds to the SH3 domain through hydrophobic and salt-bridge interactions.

172 e closed state is stabilized by a tripartite salt bridge involving the 627-NLS interface and the link

173 m with a K(d) of 8.83muM, and intermolecular salt bridges involving E60 and K64 within the folded dom

174 ceptor (FcRn) receptor primarily arises from salt bridges involving IgG histidine residues, resulting

175 ion shift in the hydrogen-bonded network and salt bridges involving side chains on ligand binding.

176 k in the S4 voltage-sensor helix, altering a salt-bridge involving K525.

177 onformational sampling and dynamics when the salt bridge is disrupted, enzyme kinetic parameters and

178 Because the Arg(102)-Glu(1032) salt bridge is essential for the C3b-Factor H complex du

179 The characteristic Asp(23)-Lys(28) salt bridge is not affected upon interacting with sulind

180 497D or R712L, implying that abolishing this salt bridge is one cause of the human disease.

181 We show that the formation of the K-E salt bridge is statistically dependent upon the activati

182 A residue Arg-325 involved in one of the two salt bridges is critical for proper functioning of the T

183 eterotrimer, ABC-2, also stabilized by axial salt-bridges, is designed containing a canonical one-ami

184 barrier originates from a switch between the salt bridges K136-D118 at the LID-CORE interface and K57

185 Ligand binding opens the salt bridge leading to a high-affinity conformation.

186 detrimental because it disrupts an internal salt bridge leading to loss of protein disulfide isomera

187 Recently we showed that salt bridges located at the cytoplasmic domain subunit i

188 ther provide experimental evidence that this salt-bridge lock exists in other STKR1s, and acts as a g

189 nd 2) destabilization of the Asp(23)-Lys(28) salt bridge makes Lys(28) available for interactions wit

190 se studies suggest that the HsRAD51(Asp-316) salt bridge may function as a conformational sensor that

191 anation, demonstrating that Glu and Arg form salt bridges more commonly, utilize a wider range of rot

192 ds were improved primarily by hydrophobic or salt bridge mutagenesis and less so by elimination of ra

193 core force-sensing region suggested how the salt-bridge mutants alter the alpha-catenin conformation

194 rmation sensor demonstrated that each of the salt-bridge mutations R551A and D503N enhances alpha-cat

195 We notice an increased density of salt bridges near protein interaction surfaces that appe

196 electron density consistent with a predicted salt bridge necessary for pilus assembly.

197 At the cytoplasmic side a second salt-bridge network forms during the transport cycle, as

198 cs simulations, we have identified a dynamic salt-bridge network within the core M region of alpha-ca

199 ead, our analysis reveals a highly conserved salt-bridge network, which likely has a role for Skp fun

200 This suggests that salt bridge networks and the hydrophobic plug function a

201 mutagenesis studies demonstrated that three salt bridges, not found in other bi-component leukocidin

202 An isoform-specific salt bridge occludes the canonical phosphoinositide bind

203 being the interaction of each ligand with a salt bridge on the extracellular side of the receptor.

204 rs in the inactive state, including a set of salt bridges on the cytoplasmic side of the transmembran

205 We speculate that the observed impact of salt bridges on the folding kinetics might explain why s

206 urring interfaces, involving hydrogen bonds, salt bridges, or hydrophobic interactions between conser

207 that mutation of Asp-101, the intermolecular salt bridge partner of Lys-99, similarly blocks transfor

208 Although salt-bridge patterns and electrostatic potential profile

209 fic features, such as an interdomain Arg-Glu salt bridge, present only in subunits that bind glycine,

210 Understanding how salt bridges promote their stability is challenging as S

211 the Bw4 residue Ile(80) also disrupted this salt bridge, providing further insight into the role tha

212 Talin also interacts with an additional salt bridge (R734-E1006), which facilitates integrin act

213 ajor structural changes in the Asp-23-Lys-28 salt bridge region and near the C terminus.

214 f these fail to form proper fibrils, and the salt bridge remains disrupted.

215 In Kir2.1, mutation of one of these CD-I salt bridge residues (R204A) reduces apparent PIP2 sensi

216 have examined the contributions of conserved salt-bridging residues in stabilizing the dimeric state

217 Helix H1, stabilized by three salt bridges, resists substantial force before unfolding

218 onclude that the removal of stabilizing CD-I salt bridges results in a collapsed state of the Kir dom

219 The double phosphorylation motif forms a salt-bridged secondary structure and causes CENP-A N-ter

220 utation of a conserved buried intermolecular salt bridge showed that electrostatics govern the rapid

221 r-tiered aromatic interaction flanked by two salt bridges, significantly contributes to proper HIV-1

222 monstrate the ability of ligands to modulate salt bridge stability.

223 The simulations show that nonnative salt bridges stabilize kinetically the encounter complex

224 of His-305 is raised to 9.0, indicating the salt bridge stabilizes the I-domain by approximately 4 k

225 promotes the formation of interprotofilament salt bridges, stabilizing lateral interactions between p

226 to 0.2 (C12) nanometers, with an increase in salt bridge strength of ~3.9 kilocalories per mole.

227 dividual hydrophobic residues or a predicted salt bridge, suggesting that production was limited by l

228 from these results that the state-dependent salt bridge switching from Arg290/Glu167 to Arg290/ATP f

229 cantly higher refractive increments and more salt bridges than other proteins with Greek key domains.

230 ng a ctenophore-specific interdomain Arg-Glu salt bridge that is notably absent from vertebrate AMPA,

231 itical: in BMI1/PCGF4, these residues form a salt bridge that may limit efficient ubiquitin transfer.

232 serine chemoreceptor, Tsr, appear to form a salt bridge that spans the interfaces between neighborin

233 3-3 dimers are predicted to be stabilized by salt bridges that are largely conserved across the 14-3-

234 tics might explain why some proteins contain salt bridges that do not stabilize the final, folded con

235 dification promotes the formation of lateral salt bridges that fine-tune the association between adja

236 n the N terminus, and a potential network of salt bridges that join the N- and C-terminal poles toget

237 Removing two salt bridges that ordinarily break during the allosteric

238 ic interactions include novel intermolecular salt bridges that provide new insights into the mechanis

239 of Ka >10(5) M(-1) from ammonium-carboxylate salt bridges that typically function poorly in water.

240 ly, this structure revealed two pH-sensitive salt bridges that, when removed, rendered SPLUNC1 pH-ins

241 d Ser13 phosphorylation creates a network of salt-bridges that facilitate the interaction between the

242 phorylated residues by binding partners, the salt-bridge theft mechanism represents a facile strategy

243 red network of interactions that replace the salt bridge thus stabilizing the structural integrity be

244 G4941K variant results in the formation of a salt bridge to Asp-4938.

245 allows fibril-like structures containing the salt bridge to emerge in the mature Abeta40 aggregates,

246 r dimensions, and a polymer electrolyte film salt bridge to enable the analysis of nanoliter-scale sa

247 rate propionates has been proposed to form a salt bridge to the C-terminus rather than to the convent

248 This system illustrates the power of axial salt bridges to direct and stabilize the self-assembly o

249 r both decarboxylations, while a lysine that salt bridges to propionate 4 is required solely for the

250 high-energy inserted intermediate by forming salt bridges to the phosphates of lipid headgroups.

251 Here we use lysine-glutamate axial salt-bridges to design a heterotrimeric collagen triple

252 roton in different solutions (connected by a salt bridge), together with earlier published reference

253 Photoreception reversibly disrupts salt bridges, triggering dimer dissociation and signal i

254 that the dynamic formation of the K265-Q633 salt bridge upon actin cleft closure regulates the activ

255 in the compaction transition and also reveal salt bridging, van der Waals, and solvent hydrogen-bondi

256 This salt bridge was absent in HLA-Bw6 molecules as well as p

257 The importance of the Arg(102)-Glu(1032) salt bridge was determined using surface plasmon resonan

258 This salt bridge was recapitulated in simulations of the cTnI

259 and electrophysiology experiments, a single salt bridge was shown to function in maintaining the PLU

260 Mutations that disrupt these salt bridges were lethal for virus production, because t

261 lization by desolvation of an intramolecular salt-bridge which induces a conformational change in the

262 evealed stabilization via a lysine-phosphate salt bridge, which was disrupted by acetyl-Lys resulting

263 This structure is stabilized by several salt bridges, which have also been observed to be import

264 isease mutations all destabilize a D354-R375 salt-bridge, which normally acts as an electrostatic loc

265 ences in pathways, namely a set of conserved salt bridges whose charge-charge interactions are fully

266 acid, which is not present in Ydj1, forms a salt bridge with an arginine of the immediately adjacent

267 a novel glutamic acid finger, which forms a salt bridge with an indispensible switch II arginine tha

268 Here we show that Arg62 forms a salt bridge with another highly conserved residue, Glu38

269 dicates that phospho-Ser(297) forms a stable salt bridge with Arg(665), part of a conserved Cys-conta

270 ration in which Arg-742 of a monomer forms a salt bridge with Asp-113 of another monomer.

271 The second proton carrier Lys300 forms a salt bridge with Asp163 in the inactive state, and relea

272 ing unless the mutated residue also formed a salt bridge with GpIbalpha, in which case the mutations

273 g suggested that D169 could form an internal salt bridge with K187 and K189.

274 10 seems to form a persistent intramolecular salt bridge with R8, an interaction that can provoke a m

275 eased transcript retention by establishing a salt bridge with RNA, thereby explaining the R substitut

276 nd, upon activation, interact directly via a salt bridge with the Arg-214 gating charge residue.

277 in which the Ser33 phosphomonoester forms a salt bridge with the Arg95 guanidinium group, thereby we

278 At this bent pose, the Lys251 forms a salt bridge with the Asp252, thus making direct proton t

279 A conserved aspartate that forms a salt bridge with the ATP gamma-phosphate is found at the

280 imer stability, because this residue forms a salt bridge with the disease-related Arg(120) of the nei

281 ne side chain previously suggested to form a salt bridge with the ligand, glutamate.

282 It is seen forming a salt bridge with the negative charge on the phosphate he

283 no tail moved toward the DFG motif to form a salt bridge with the side chain of Asp831.

284 ringently conserved Arg residue that forms a salt bridge with the substrate carboxylate group.

285 wn the unfolding of the alpha-helix, whereas salt bridges with an unfavorable geometry have the oppos

286 e open state frees the essential Asp251 from salt bridges with Arg186 and Lys178 so that Asp251 can p

287 ds, two acidic residues, D111 and E113, form salt bridges with basic, coat protein side chains.

288 Glu(11), Glu(14), Glu(84), and Glu(87)) form salt bridges with key lysine residues in ER-alpha (Lys(2

289 aM (Glu-11, Glu-14, Glu-84, and Glu-87) form salt bridges with key lysine residues in ER-alpha (Lys-2

290 We propose that LysB61 and LysC58 both form salt bridges with outer acidic Ca(2+) ligands of the C1r

291 More specifically, the CoA phosphates formed salt bridges with predicted DNA-binding residues Arg36 a

292 the two basic residues of the ligand forming salt bridges with the Asp(127) and Glu(229) receptor res

293 idic and basic residues through formation of salt bridges with the charged side chains.

294 Although salt bridges with the FA carboxylate determine the FA bi

295 are present on the beta-sheet C and D, form salt bridges with the head group of PI(4,5)P2.

296 cgammaRI forms additional hydrogen bonds and salt bridges with the lower hinge region of Fc.

297 m this turn, along with Arg12, which forms a salt-bridge with Asp8, are instrumental in modulating th

298 effects can be explained by the formation of salt-bridges with the Glu600 residue.

299 This study tested predictions that salt bridges within the force-sensing core modulate alph

300 omplementary changes that restore particular salt bridges within the suggested network suppressed the