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 possibly through disruption of the E138-K101 salt bridge.

5 accommodated by formation of an interfacial salt bridge.

6 obic interactions, 14 hydrogen bonds and one salt bridge.

7 tent with expectations for the strength of a salt bridge.

8 ontrols the formation and disruption of this salt bridge.

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

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

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

12 they have different capabilities of forming salt bridges.

13 which is stabilized by multiple intersubunit salt bridges.

14 endritic guest via the formation of multiple salt bridges.

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

16 be linked with formation and maintenance of salt bridges.

17 ve to reference electrodes with conventional salt bridges.

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

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

20 zation on chromosome involving inter-protein salt-bridges.

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

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

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

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

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

26 This Amp-Asp salt bridge allowed for the rational design of strands t

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

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

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

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

31 12 amino acid residues forming intersubunit salt bridges and 21 amino acid residues forming hydrogen

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

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

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

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

36 l of the thin filament displays a paucity of salt bridges and hydrophobic complementarity between the

37 ther show that the heterodimers interact via salt bridges and hydrophobic forces, which apparently ma

38 eraction with tropomyosin contained abundant salt bridges and intimately integrated hydrophobic netwo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

54 of the hydrophobic core and the existence of salt bridges at the periphery of the interface affect sl

55 that competes with a critical intermolecular salt-bridge at the native UBC13/TRAF6(RING) interface.

56 Here, we present an interstrand salt bridge between (4S)-aminoproline (Amp) and aspartic

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

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

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

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

61 lso observed that for release from the ER, a salt bridge between Asp-17 and Arg-57 is essential.

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

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

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

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

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

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

68 nique P-loop conformation characterized by a salt bridge between R41 and the carboxylic acid of the i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

85 th talin results in a complete disruption of salt bridges between R995 on alphaIIb and D723/E726 on b

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

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

88 Additional salt bridges between the phosphoserines and SUMO account

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

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

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

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

93 ofilaments which interact via intermolecular salt-bridges between amino acids K45, E57 (polymorph 2a)

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

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

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

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

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

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

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

101 Moreover, the salt-bridge competition prevents transient interactions

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

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

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

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

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

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

108 gy well of the E46K fold because the E46-K80 salt bridge diverts alpha-synuclein into a kinetic trap-

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

110 Due to multiple, strong hydrogen bonding and salt bridge effects, CP/Ad-SS-GD well interact with Cas9

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

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

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

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

115 Mutations eliminating salt bridge formation in RGS8 and RGS4 decreased thermal

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

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

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

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

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

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

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

123 These results show that the alpha (4) salt bridge-forming residue controls flexibility in seve

124 A single salt bridge-forming residue determines differences in fl

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

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

127 finity DNA and triggers the loss of a distal salt bridge (Glu-343/Arg-378) via a large side-chain mot

128 strong interpeptide interactions, including salt bridges, H-bonds, and polar interactions.

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

130 They are often depicted as single conformer salt bridges (hydrogen-bonded ion pairs) in crystal stru

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

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

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

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

135 Molecular dynamics simulations with an added salt bridge in RGS19 (L118D) showed reduced RGS19 flexib

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

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

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

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

140 this effect to the formation of a gas-phase salt bridge in the first activated conformation.

141 d K80, a residue pair which form the E46-K80 salt bridge in the wild-type fibril structure.

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

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

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

145 2+) interaction and consequent disruption of salt bridges in the open hemichannels.

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

147 Deamidation creates a new intramolecular salt-bridge in UBC13 that competes with a critical inter

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

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

150 protonated ligand to deprotonated RNA within salt bridges initiates loss of the ligand, but that prot

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

152 alytic Fe(II) Upon BH(4) binding a polar and salt-bridge interaction network links the three PAH doma

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

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

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

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

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

158 further identified inter- and intramolecular salt-bridge interactions of Orai subunits as a core elem

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

160 ggest important contributions of interdomain salt-bridge interactions to the stabilization of differe

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

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

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

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

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

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

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

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

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

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

171 497D or R712L, implying that abolishing this salt bridge is one cause of the human disease.

172 Furthermore, a salt bridge is shielded by actively reducing its surface

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

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

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

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

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

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

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

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

181 clusively in the region where the sample and salt bridge mixed.

182 the alpha (4) helix of RGS4, 8, and 19 with salt bridge-modifying mutations.

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

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

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

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

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

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

189 sed by conserved hydrophobic residues, and a salt bridge network, braced by tyrosines.

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

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

192 of Glu-818 in an intricate hydrogen-bonding/salt-bridge network, connecting it to key residues invol

193 ment, leading to changes in the VSD internal salt-bridge network, resulting in a reshaping of the per

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

195 tch which induces disruption of a tripartite salt-bridge network.

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

197 t on either side of the membrane and involve salt-bridge networks.

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

199 identified the highly conserved E339...R416 salt bridge of the nucleoprotein trimer as a target and

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

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

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

203 ns stable while the bond is substituted by a salt bridge or disulfide bond, whereas disruption of the

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

205 Their dynamic salt bridge pairing creates the exceptional stiffness of

206 ted H(+) to the conserved Lys-300 residue, a salt bridge partner of Asp-163.

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

208 Furthermore, replacement of both salt bridge partners in the ion-binding site of EcNhaA p

209 Although salt-bridge patterns and electrostatic potential profile

210 B and ABC-type heterotrimers with only three salt bridges per triple helix.

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

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

213 ity, interfacial wettability, and asymmetric salt-bridging propensity.

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

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

216 The designed compounds containing such a salt bridge reached high oral bioavailability and oral e

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

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

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

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

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

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

223 Mixing of sample and salt bridge solutions-and in particular penetration of s

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

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

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

227 ound-state a two-fold symmetric H-bond and a salt bridge stitch the double-rings together, whereas on

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

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

230 of the mutation site, while D233N disrupts a salt bridge that contributes to Hsc70's nucleotide-induc

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

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

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

234 3-3 dimers are predicted to be stabilized by salt bridges that are largely conserved across the 14-3-

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

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

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

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

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

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

241 ometers but, despite the use of concentrated salt bridges, this is enough to affect the extent of ele

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

243 90RhoGAP; rather, it makes an intramolecular salt bridge to an aspartic acid.

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

245 fy arginine-49 as a key residue that forms a salt bridge to aspartate-25 in the patient protein fibri

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

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

248 02 due to the formation of a critical anchor salt bridge to HLA-C.

249 Nature uses salt bridges to control the folding and stability of man

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

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

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

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

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

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

260 be improved by the formation of an internal salt bridge, which helped in shielding the two opposite

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

262 hey do not include the previously identified salt bridges, which are less important.

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 with the ATP-pocket and mediates a critical salt bridge with a glutamate (Glu130) of alphaC helix, w

267 erization of alphaBAsp-109 disrupted a vital salt bridge with alphaBArg-120, a contact that when brok

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

269 nd compound 1 as an inhibitor disrupting the salt bridge with an EC(50) = 2.7 muM against influenza A

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

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

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

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

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

275 the conserved FLVR motif that forms a direct salt bridge with bound phosphotyrosine.

276 FG-Asp is moved into a back pocket forming a salt bridge with catalytic Lys, which can be tested in s

277 e protonated amino moiety forms a persistent salt bridge with E172.

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

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

280 l(2) into the ProT Ile(16) pocket, forming a salt bridge with ProT's Asp(194), thereby stabilizing th

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

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

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

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

285 the side chain of Arg259 H-bonds and forms a salt bridge with the carboxylate group of glucuronic aci

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

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

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

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

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

291 ne whereas R.RKTR forms specific multivalent salt bridges with PA.

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

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

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

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

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

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

298 ion strongly depends on the newly identified salt bridge within TMD0.

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