ライフサイエンスコーパス: Asp

1 Asp-2 increases reactive site polarity, reducing DeltaCp

2 o84 in which a residue adjacent to Tyr(179), Asp(178), is protonated revealed a conformational change

3 nserved negatively charged residues Glu-179, Asp-180, and Asp-181 that could contribute to non-bonded

4 3) The DC pair residue Asp(196) (Asp(156) in CrChR2) deprotonates in N --> O transition.

5 We conclude that CaV1.2 Asp-181 anchors the physical interaction that facilitate

6 Substitutions of CaV1.2 Asp-181 impaired the co-immunoprecipitation of CaVbeta/C

7 e active site containing the Ser-101-His-237-Asp-212 catalytic triad.

8 2) The counter-ion Asp(293) (Asp(253) in CrChR2) receives the retinal Schiff base pro

9 ence and levels of IgE responses to Asp f 3, Asp f 4, and Asp f 6 helped distinguish allergic broncho

10 both thrombin exosite I with segment Glu-35-Asp-47 and the catalytic site with the region Pro-49-Arg

11 tative active site residues reveals Asn(37), Asp(52), and Thr(68) are important for catalysis, and si

12 upled to its local protonation by the His-38/Asp-139 ion pair and Tyr-87 of subunit Nqo4.

13 ired active site conserved residues Tyr(40), Asp(181), and Arg(100)and a reacting duplex 5'-phosphate

14 in a hydrogen bond network including His-47, Asp-129, Thr-171, and Ser-202, all shown to be functiona

15 (NPY1-9, Tyr(1)-Pro(2)-Ser(3)-Lys(4)-Pro(5)-Asp(6)-Asn(7)-Pro(8)-Gly(9)-NH2) and a tachykinin-relate

16 Three aspartate residues in Cx30 (Asp-50, Asp-172, and Asp-179) have been implicated previously in

17 Moreover, we identify the residues Ala-519/Asp-520 of EHD1 and Asn-519/Glu-520 of EHD3 as defining

18 omain, that replacement of the aspartic acid Asp-396 with cysteine prevents proton transfer.

19 analogues bearing basic (Lys, Orn) or acid (Asp or Glu) function.

20 onds to the alphaIIb-subunit, and the acidic Asp side chain coordinates to a metal ion held by the be

21 The amino acids Asp and Glu accumulate to high concentrations during rip

22 ion of the protein, encompassing amino acids Asp-31-Arg-62, is the region mainly responsible for alph

23 simply by adding chiral acidic amino acids (Asp and Glu).

24 De novo biosynthesis was shown for Ala, Asp, Ser, and Thr at high rates and for Gly, Lys, Phe, T

25 ic samples (seven enantiomer pairs d/l-Ala, -Asp, -Glu, -His, -Leu, -Ser, -Val and the three achiral

26 recombinase driven by the DEAD (Asp-Glu-Ala-Asp) box protein 4 (Ddx4) gene promoter.

27 re, we have identified the DEAD (Asp-Glu-Ala-Asp) box RNA helicase 24 (DDX24) as a novel regulator of

28 and a homologous aspartate aminotransferase (Asp-AT) from Escherichia coli as a control.

29 An Asp-Lys SF behaved like the Asp-Arg one and was experime

30 atalytic dyad (His(99) and Cys(136)), and an Asp (Asp(134)) in the potential S1 binding site.

31 The P domain contains an Asp-His-Ser catalytic triad that is, together with five

32 etween open and closed conformations plus an Asp residue carboxylate shift between monodentate and bi

33 s residue, followed by phosphotransfer to an Asp residue of the response regulator DosR.

34 rved residues equivalent to SOD5 Glu-110 and Asp-113.

35 , whereas an interaction between Arg-126 and Asp-49 is essential for catalysis.

36 -45 and Asp-49 in the second and His-153 and Asp-157 in the fifth transmembrane segments coordinate z

37 alytic triad comprising Cys-73, His-162, and Asp-182.

38 SF region (Pro(165), Tyr(166), Ser(167), and Asp(168)) of apoA-I are critical for both LCAT binding t

39 rtate residues in Cx30 (Asp-50, Asp-172, and Asp-179) have been implicated previously in the Ca(2+) s

40 sis of Nef amino acids Arg-134, Glu-174, and Asp-175, which stabilize Nef for AP-2 alpha-sigma2 bindi

41 ively charged residues Glu-179, Asp-180, and Asp-181 that could contribute to non-bonded interactions

42 e hypothesis that replacement of Arg-213 and Asp-143 with the corresponding RF1 residues will reduce

43 ained by a rearrangement of the Arg(222) and Asp(385) residues, which are crucial for specific collag

44 active site residues identified Asn(24) and Asp(39) as being essential for activity.

45 component system and identified His(241) and Asp(61) as conserved phosphorylation sites in NarS and N

46 -43 and Asp-47 in the second and His-244 and Asp-248 in the fifth transmembrane segments.

47 ines in catalysis and identified Tyr-322 and Asp-323 as critical determinants involved in the hydroxy

48 er, and amino acid residues Ser/Arg(339) and Asp/Asn(421) in CTLD domain contribute to their differen

49 ent cleavage of the propeptide at Asn-38 and Asp-54.

50 ls of IgE responses to Asp f 3, Asp f 4, and Asp f 6 helped distinguish allergic broncho-pulmonary as

51 olished manganese efflux, that of Asn-43 and Asp-47 did not.

52 0, the corresponding residues are Asn-43 and Asp-47 in the second and His-244 and Asp-248 in the fift

53 In YiiP, side chains of residues Asp-45 and Asp-49 in the second and His-153 and Asp-157 in the fift

54 ative ligands for cation binding (Asp-55 and Asp-59 in helix II).

55 ding required key residues Asp-179(4.60) and Asp-275(6.58) (residue numbering follows the Ballesteros

56 omers through the interaction of Arg-742 and Asp-113 is essential for catalytic activity and nuclear

57 torial proton path in BR in which Asp-85 and Asp-96 serve as acceptor and donor, respectively, of the

58 tions identified two amino acids (Lys-98 and Asp-100 in LRRC8A and equivalent residues in LRRC8C and

59 d that Asp-7 acts as the catalytic base, and Asp-176 acts as the catalytic acid.

60 structures of the Eb/O-PLP-AFPA complex and Asp-AT-PLP-AFPA complex revealed that GabR is incapable

61 a pI of 5.3 in the boundary between cSer and Asp-His.

62 Gln- and Asp-150-substituted versions of ACO further confirmed th

63 We analyzed the role of HA and Asp in the B. cinerea-T. arundinaceum interaction, inclu

64 dition to the membrane-bound Asp-His-His and Asp-His-His-associated (DHH/DHHA1) domain-containing pho

65 n N-terminal extension containing a His- and Asp/Glu-rich hypervariable region followed by a highly c

66 not conserved in E. coli OtsA (His, Leu, and Asp, respectively), providing a rationale for the purine

67 Another similar pair is Leu-126 in RF1 and Asp-143 in RF2, which are also conserved within their re

68 inhibited upon binding of Ala, Tyr, Trp and Asp to the protein.

69 ts of Ala-978 (to Leu, Pro, Phe, or Tyr) and Asp-1028 (to Tyr or Trp) with larger side chains showed

70 interaction between Arg 54 on ubiquitin and Asp 143 on Ube2R1/2.

71 ) triggers rapid dissociation of the anionic Asp-139 toward the membrane domain that couples to confo

72 vely charged residues (either Glu(-)/Arg(+), Asp(-)/Arg(+), or Glu(-)/Lys(+)).

73 Third, an Arg-Asp dipeptide immediately preceding the ZF helix, conser

74 FTERD3) (where CFTERD is Cys-Phe-Thr-Glu-Arg-Asp) was developed for chymase detection.

75 This Arg-Asp conformational switch allows identical ZF modules to

76 Seven synthetases, Ala-, Arg-, Asp-, Asn-, Leu-, Lys- and TyrRS, appear to associate wi

77 We show that arrayed Asp-Pro-Phe (DPF) motifs within the early-arriving endoc

78 2 and His-305 is particularly interesting as Asp-302 is the site of a temperature-sensitive-folding m

79 tic dyad (His(99) and Cys(136)), and an Asp (Asp(134)) in the potential S1 binding site.

80 in self-processing and decreased aspartate (Asp) content.

81 Biosynthesis of aspartate (Asp)-derived amino acids lysine (Lys), methionine (Met),

82 els of the polyketide compounds aspinolides (Asp) B and C.

83 roteins are cleaved by caspases-1 and -11 at Asp-276.

84 imers, but feedback cleavage by caspase-3 at Asp-330 removed the linker entirely and partially restor

85 eolysis of Bid and mono-ubiquitinated Bid at Asp-52 increasing the release of cytochrome c and caspas

86 Intramolecular self-cleavage at Asp-193 evoked higher solvent exposure in the regions of

87 nducing selective intramolecular cleavage at Asp-315.

88 aspartyl-tRNA synthetase (ND-AspRS) attaches Asp to tRNA(Asn) and the amidotransferase GatCAB transam

89 he distance between the catalytic acid/base (Asp-315) and the ligand anomeric carbon is unusually sho

90 at the tip of the second beta-strand (beta2-Asp/Glu).

91 ancestor) ancestor that possessed the beta2-Asp/Glu motif.

92 A hydrogen-bonded salt bridge between Asp-302 and His-305 is particularly interesting as Asp-3

93 identified a network of salt bridges between Asp(1261) and the rest of A1 that lock the N-terminal li

94 position of the proton that resides between Asp-222 and the pyridinyl nitrogen.

95 nd human beta1c subunits preferentially bind Asp and Leu in their S1 pockets, while Glu and large hyd

96 e three putative ligands for cation binding (Asp-55 and Asp-59 in helix II).

97 let (aspirin/Plavix [clopidogrel bisulfate]; Asp/Pla) therapy achieved nearly half the patency observ

98 show that in addition to the membrane-bound Asp-His-His and Asp-His-His-associated (DHH/DHHA1) domai

99 structure highlights the key role played by Asp-558 at the extended loop of the CBS2 motif of CNNM2

100 mes complementary to trypsin, such as Glu-C, Asp-N, Lys-N, Arg-C, LysargiNase has been reported.

101 ir (G-Arg interaction) to a G:C base pair (C-Asp interaction).

102 -His-D-Nal(2')-Arg-Trp-Lys]-NH2 (Ac-Nle(4)-c[Asp(5),D-Nal(2')(7),Lys(10)]-NH2), a nonselective cyclic

103 backbone N-methylation approach on Ac-Nle-c[Asp-His-D-Nal(2')-Arg-Trp-Lys]-NH2 (Ac-Nle(4)-c[Asp(5),D

104 A conserved catalytic Asp residue is required for Gdh1's functions in telomeri

105 resulting contact signaling network connects Asp-49 to distal residues involved in GSH binding and is

106 the Zn(2+) ion is coordinated by a conserved Asp residue only observed to date as a metal ligand in M

107 features, mainly the presence of a conserved Asp(246), allow MtHPP to bind HOLP specifically.

108 Roles are identified for conserved Asp-24 in the formation of the first intermediate and fo

109 mediated motility, (ii) two highly conserved Asp residues are crucial for enzymatic activity of the p

110 in the alpha1 helix alters how the conserved Asp-20 interacts with ADP-ribose and may explain the eff

111 PX2) overcomes the reliance on the conserved Asp-His hydrogen bonding interaction, leading to a catal

112 ations to reposition a universally conserved Asp (D) residue involved in catalysis.

113 Three aspartate residues in Cx30 (Asp-50, Asp-172, and Asp-179) have been implicated previ

114 Mammals synthesize d-Ser and d-Asp, primarily in the central nervous system, where d-Se

115 sing brain slices to Glut and D-aspartate (D-Asp) before recording resulted in an increase in frequen

116 preexposure to the amino acid D-aspartate (D-Asp).

117 analogue zyklophin ([N-benzyl-Tyr(1)-cyclo(d-Asp(5),Dap(8))]dynorphin A(1-11)NH2) is a kappa opioid r

118 Using D-Asp as a "false" GT, we determined the extent of local n

119 Using D-Asp, it was possible to investigate the effects of speci

120 The finding indicates that D-[Asp/Glu] may have the potential for removing IgE or redu

121 in using cre recombinase driven by the DEAD (Asp-Glu-Ala-Asp) box protein 4 (Ddx4) gene promoter.

122 Here, we have identified the DEAD (Asp-Glu-Ala-Asp) box RNA helicase 24 (DDX24) as a novel

123 PRUNE is a member of the DHH (Asp-His-His) phosphoesterase protein superfamily of mole

124 tained its dimeric structure, but diminished Asp f3's peroxidase activity, and extended the alpha-hel

125 lu-Arg (ER); and two non-arginyl dipeptides: Asp-Asp (DD) and Glu-Asp (ED).

126 the vacuole in exchange for import of either Asp or Glu.

127 c and polar residues, substitution of either Asp-219 or Glu-447 with any other residues resulted in r

128 y additional in silico digestion with either Asp-N, Arg-C, Glu-C, Lys-C, or Lys-N.

129 ments generated by trypsin plus endoprotease-Asp-N.

130 ttenuation of a fraB mutant stems from 6-P-F-Asp toxicity.

131 tabolite: 6-phosphofructose-aspartate (6-P-F-Asp).

132 nfirm that the fraB mutant accumulates 6-P-F-Asp.

133 Substituting Asn for Asp at equivalent positions in the alpha-, beta-, and -s

134 ellular vestibule with an important role for Asp-101.

135 sults suggest a putative pH-sensing role for Asp-219 and Glu-447 in hENT3 and that the size, ionizati

136 es even when using the central cE5 fragment (Asp-31-Arg-62) alone.

137 peptide (corresponding to the sequence from Asp(15) to Phe(19) of human calcitonin and reported as t

138 tional Asp kinases (AKs) and dual-functional Asp kinase-homoserine dehydrogenases (AK-HSDHs).

139 f preselected to carry at least one A118G G (Asp) allele, were randomized to naltrexone (50 mg) or pl

140 tal muscle and plasma of UCP3 Tg mice (e.g., Asp, Glu, Lys, Tyr, Ser, Met) were significantly reduced

141 r charge conservative mutations Arg-126-Gln, Asp-49-Asn, and Arg-126-Lys, we inferred that a crystall

142 en assayed in counterexchange mode with Glu, Asp, or GABA.

143 non-arginyl dipeptides: Asp-Asp (DD) and Glu-Asp (ED).

144 r, bound adjacent to a conserved Glu-Arg-Glu/Asp ionic network in the enzyme's active site.

145 pha3 domain of HLA-A2 and -B8, including Glu/Asp at position 177, Gln/Glu at position 180, Gly/Arg at

146 Although Arg-Gly-Asp (RGD) integrin ligand and matrix softening confer re

147 ependently of IGF binding through an Arg-Gly-Asp (RGD) integrin-binding motif.

148 C3 harbors an Arg-Gly-Asp (RGD) motif, which is the major integrin-binding sit

149 ration by targeting integrins, using Arg-Gly-Asp (RGD) peptide-functionalized gold nanorods.

150 Cyclic peptides containing the Arg-Gly-Asp (RGD) sequence have been shown to specifically bind

151 Peptides containing the Arg-Gly-Asp (RGD) sequence have high affinity for alphavbeta3 in

152 intermediates for the preparation of Arg-Gly-Asp (RGD)-based cyclopentapeptides (cRGD) with nanomolar

153 We previously demonstrated that Arg-Gly-Asp (RGD)-containing ligand-mimetic inhibitors of integr

154 higher affinity compared with other Arg-Gly-Asp binding integrins.

155 tion was effectively blocked by RGD (Arg-Gly-Asp) peptide and neutralizing alphavbeta3 antibodies, ex

156 stresses on the cell surface via an Arg-Gly-Asp-coated magnetic bead.

157 pid domains increased beta1-integrin-Arg-Gly-Asp-peptide affinity and valency, thus implicating Ld do

158 l cells, BA increased beta1-integrin-Arg-Gly-Asp-peptide affinity by 18% with a transition from singl

159 erine O-acetyltransferase uses a similar Gly-Asp-Gly-Ile motif to form the "cysteine synthase" comple

160 ighly preferred for binding to conserved Gly:Asp:Asn residues.

161 intact Glu-Arg-Glu network, as only Glu --> Asp substitutions retain activity.

162 ild up H2N-Pro-Gly-Ala-CONHL and H2N-Cys-His-Asp-CONHL (where L = organic struts) amino acid sequence

163 is an esterase/lipase with catalytic Ser-His-Asp triad.

164 tically inactive Phe substitution in the His-Asp catalytic dyad of CurJ-DH to elucidate substrate-enz

165 carriers, glutamic acid, aspartyl-histidine (Asp-His), cycloserine (cSer), and arginine, which provid

166 orms indole-3-acetic acid aspartic acid (IAA-Asp) and indole-3-acetic acid glutamic acid (IAA-Glu) of

167 After the addition of IDL (Ile-Asp-Leu) to the C terminus of CHR peptide WQ or MT-WQ, t

168 ln653, named CP), but with an innovative Ile-Asp-Leu tail (IDL) that dramatically increased the inhib

169 2) The counter-ion Asp(293) (Asp(253) in CrChR2) receives the retinal Schif

170 s that deviated from the expected 3:1 isoAsp/Asp ratio.

171 s indicate that conversion of l-aspartate (l-Asp) to N-carbamoyl-l-aspartate by PyrB may reduce the a

172 aspartate by PyrB may reduce the amount of l-Asp available for PG synthesis and thus cause the appear

173 thesize that the concurrent utilization of l-Asp for pyrimidine and PG synthesis may be part of the r

174 The fact that l-Asp availability is dependent on nucleotide metabolism,

175 ilk bioactive peptides, Ile-Asn-Tyr-Trp, Leu-Asp-Gln-Trp, and Leu-Gln-Lys-Trp, and different bile sal

176 o bind the minimal FLAG peptide (Asp-Tyr-Lys-Asp) were grafted onto a single-chain variable fragment

177 tains an aspartate that aligns with lysozyme Asp-52 (a residue critical for catalysis), a conservatio

178 eaving enzyme 1 (BACE1) cleaves APP at minor Asp(1) site to generate C99 for amyloid beta protein (Ab

179 he SCID/bg mouse (NK Ab: 0.356 +/- 0.151 mm, Asp/Pla: 0.452 +/- 0.130 mm).

180 Thr), and isoleucine involves monofunctional Asp kinases (AKs) and dual-functional Asp kinase-homoser

181 yses reveal that a conserved diacidic motif (Asp-Glu) in these proteins is necessary for their export

182 re not separated from peptides with multiple Asp or Glu residues, interfering with the identification

183 The mutated Asp residue, which determines the disease phenotype, is

184 G synthesis and thus cause the appearance of Asp/Asn-less stem peptides in PG.

185 ng morphology is induced by L-enantiomers of Asp and Glu, whereas 'left-handed' (clockwise) morpholog

186 er narrowed to the protonation equilibria of Asp(309) with a parallel set of spectroscopic studies us

187 olds and yeasts prompts future evaluation of Asp f3 as a potential therapeutic target.

188 The conserved expression of Asp f3 homologs in medically relevant molds and yeasts p

189 enotype was rescued by ectopic expression of Asp f3.

190 to interrogate the conformational impact of Asp isomerization and Met oxidation in the CDRs of a mod

191 The increases of Asp, Lys, and Met in ak-hsdh2 were also observed in ak1-

192 tal structure and the catalytic mechanism of Asp f3, a two-cysteine type peroxiredoxin.

193 th mass spectrometry showed that mutation of Asp(21) promoted disorder in the N-terminal helices of 1

194 s to bind nitric oxide, a single mutation of Asp-96 to Val in mitoNEET or Asp-123 to Val in Miner1 fa

195 tion triggered by the Glu-145 replacement of Asp.

196 is enzyme shed light on the critical role of Asp(309) in substrate binding and catalysis.

197 hENT3 revealed that the ionization states of Asp-219 and Glu-447, and not His, strongly determined th

198 Substitution of Asp(362) for His resulted in a general increase in prote

199 Dual substitution of Asp-219 and Glu-447 to Ala sustained pH-independent acti

200 rprisingly, although alanine substitution of Asp-248 abolished manganese efflux, that of Asn-43 and A

201 Thus, pushing by the beta3-subunit on Asp is sufficient for headpiece opening and ligand slidi

202 he small subunit with Ser, Val, Gln, Gly, or Asp, and we analyzed the effects of these mutations on t

203 gle mutation of Asp-96 to Val in mitoNEET or Asp-123 to Val in Miner1 facilitates nitric oxide bindin

204 and Val) are similar in S. venezuelae OtsA (Asp, Ser, and Phe, respectively) but not conserved in E.

205 used IQF substrates to re-investigate the P1-Asp characteristic of caspases, thus demonstrating that

206 predicted to bind the minimal FLAG peptide (Asp-Tyr-Lys-Asp) were grafted onto a single-chain variab

207 Here we show that the peroxiredoxin Asp f3 of Aspergillus fumigatus inactivates ROS.

208 Although the aspartate at position Asp-50 was indispensable for divalent cation-dependent g

209 s of the urotensin II (UII, 1, H-Glu-Thr-Pro-Asp-c[Cys-Phe-Trp-Lys-Tyr-Cys]-Val-OH) fragment 4-11 wer

210 ysates, we explored the use of the proteases Asp-N and Glu-C and a nonenzymatic acid induced cleavage

211 modification of tRNA(UUC)(Glu) and tRNA(QUC)(Asp) increases errors, suggesting that the modifications

212 al of the crucial Na(+)-coordinating residue Asp(926) This mechanistic model is consistent with exper

213 a mutant DD with the phospho-mimetic residue Asp at this position is impaired in both signalling and

214 3) The DC pair residue Asp(196) (Asp(156) in CrChR2) deprotonates in N --> O tr

215 Mutations at active site residue Asp-185 compromise binding of both compounds.

216 The presence of acidic residues Asp and Glu near the peptide N-terminus is by far the mo

217 Although residues Asp(220) and Arg(327) are found necessary for compound I

218 Charged residues Asp-997, Glu-998, Arg-1000, and Lys-1001 in M10, partici

219 This network, which involves residues Asp-222, His-143, Thr-139, His-189, and structural water

220 mutant lacking all LHCSR isoforms, residues Asp(117), Glu(221), and Glu(224)were shown to be essenti

221 CXCL12 binding required key residues Asp-179(4.60) and Asp-275(6.58) (residue numbering follo

222 th assays demonstrate that MazF-mt6 residues Asp-10, Arg-13, and Thr-36 are critical for RNase activi

223 In YiiP, side chains of residues Asp-45 and Asp-49 in the second and His-153 and Asp-157

224 Both are induced by the C-terminal residues Asp-78-Trp-82 of EcMazE, which are also responsible for

225 ate maltose, we identified several residues (Asp-1028 and Asn-1029 from domain A, as well as Leu-938,

226 Two active site residues, Asp-547 and His-466, were also examined and shown by sit

227 tably, the pyrimidine containing prodrug (S)-Asp-FPMPC is the only congener within this series to dem

228 ion mechanism of AMSDH, we created Ala, Ser, Asp, and Gln mutants and studied them using biochemical,

229 Several Asp residues are racemized in Abeta plaque, with residue

230 FXI binding motifs containing the signature Asp-Phe-Pro (DFP) tripeptide.

231 s amine group with the conserved active-site Asp is essential for activity and likely dictates its or

232 SOD5 Asp-113 connects to the active site in a manner similar

233 DHHC3), a cellular Golgi apparatus-specific Asp-His-His-Cys (DHHC) zinc finger protein.

234 known as DHHC3), a Golgi apparatus-specific Asp-His-His-Cys (DHHC) zinc finger protein; (ii) a GODZ

235 be catabolised to form Glu and subsequently Asp, and the requirement for the fruit to maintain osmot

236 y inspired by previous work on 3-substituted Asp analogues, we designed and synthesized a total of 32

237 d synthesized a total of 32 beta-sulfonamide Asp analogues and characterized their pharmacological pr

238 ctural differences in these beta-sulfonamide Asp analogues provide analogues with diverse EAAT subtyp

239 ctrostatic interaction between an N-terminal Asp of the pheromone and Arg-153 within the proposed phe

240 ction effect of the side chain of N-terminal Asp reduces the basicity of the N-terminal amino group a

241 Racemization of the original N-terminal Asp to l-isoAsp was also detected and loss of one amino

242 -arginylated by R-transferase are N-terminal Asp, Glu, and (oxidized) Cys.

243 carboxyl groups of internal (non-N-terminal) Asp and Glu; and (iii) that some isoforms of Ate1 are sp

244 d mutagenesis and kinetics demonstrated that Asp-7 acts as the catalytic base, and Asp-176 acts as th

245 Quantum chemical calculations indicate that Asp-222, which is directly coupled to the pyridinyl nitr

246 d free-energy surface studies indicated that Asp-168 is important in anchoring Arg-155 for ligand bin

247 tracentrifugation, our results revealed that Asp(21) and Glu(89) both play key roles in dimer dynamic

248 The Asp-His-His-Cys-Cys-rich domain-containing Protein S-Acy

249 tance of 5-HT2A/1A receptor subtypes and the Asp system in the control of social functioning, and as

250 We found that mutations at the Asp-184 residue gave mutants that demonstrated significa

251 leaves along with mutual effects between the Asp family and SMM pathways operating in these tissues.

252 onation of the GtCCR2 SB occurs not from the Asp-96 homolog, but by proton return from the earlier pr

253 An Asp-Lys SF behaved like the Asp-Arg one and was experimentally verified to be proton

254 Replacement of the Asp f3 cysteines with serine residues retained its dimer

255 ion or stability in vitro The effects of the Asp-302-His-305 salt bridge are thus complex and context

256 In GtCCR2, deprotonation of the Asp-96 homolog is required for cation channel opening an

257 vides valuable insights into the role of the Asp-His-Fe triad of heme peroxidases.

258 all proteins showed favored cleavage of the Asp-X bond.

259 ic channel to cations in GtCCR2 requires the Asp-96 homolog to be unprotonated, as has been proposed

260 , because molecular modeling showed that the Asp-426 side chain in CNNM3 buries into the catalytic ca

261 of BACE1 in APP from the Glu(11) site to the Asp(1) site both in male and female transgenic mice in v

262 BACE1 cleavage site from the Glu(11) to the Asp(1) site, resulting in much higher C99 level and C99/

263 e SB chromophore rapidly deprotonates to the Asp-85 homolog, as in BR.

264 he amidotransferase GatCAB transamidates the Asp to Asn on the tRNA.

265 of the ligand forming salt bridges with the Asp(127) and Glu(229) receptor residues.

266 Mutation of this Asp residue in nSMase2 disrupts catalysis, allosteric ac

267 n amino acids, including Gly, Ala, Ser, Thr, Asp, and Glu, which are relatively silent with regard to

268 ts with the carboxylic moiety of these three Asp residues.

269 A dual mutation of Glu-181 to Asp in the double E loop and Gln-329 to Ala in the canon

270 hereas phosphomimetic mutation of Ser-357 to Asp did not.

271 In addition to Asp-335, the catalytic essentiality of Glu-216 was revea

272 ins of charged or polar residues adjacent to Asp-248 in the first (Glu-25) or fourth (Asn-127) transm

273 the H-bond network, although certain Arg to Asp salt bridges create highly localized rigidity increa

274 results in the formation of a salt bridge to Asp-4938.

275 ging Glu(-)/Arg(+) rotamer pairs compared to Asp(-)/Arg(+) and Glu(-)/Lys(+).

276 the N terminus at position 1 (equivalent to Asp-221 in the Fc of IgG1) dramatically enhances overall

277 th prevalence and levels of IgE responses to Asp f 3, Asp f 4, and Asp f 6 helped distinguish allergi

278 48 in RPE65, a site in which substitution to Asp has been associated with loss of enzymatic function

279 owed a striking selectivity of Pmt1 for tRNA(Asp) methylation, which distinguishes Pmt1 from other Dn

280 enzymes were thought to be specific for tRNA(Asp).

281 e deafness-associated mitochondrial(mt) tRNA(Asp) 7551A > G mutation.

282 A failure in metabolism of mt-tRNA(Asp) caused the variable reductions in mtDNA-encoded pol

283 oacylation and steady-state level of mt-tRNA(Asp) in mutant cybrids, compared with control cybrids.

284 ltered the structure and function of mt-tRNA(Asp) The primer extension assay demonstrated that the m.

285 created the m(1)G37 modification of mt-tRNA(Asp) Using cybrid cell lines generated by transferring m

286 oding RNAs and reduced the stability of tRNA(Asp(GTC)) We also demonstrate the importance of m(5)C in

287 eny revealed that discrimination toward tRNA(Asp) by AspRS has evolved independently multiple times.

288 domain and implicate a previously unexamined Asp-Thr dyad in catalysis of the cyclodehydration reacti

289 ine the vectorial proton path in BR in which Asp-85 and Asp-96 serve as acceptor and donor, respectiv

290 Phosphomimetic substitution of Thr-38 with Asp increased co-immunoprecipitation of the CAR DBD with

291 we report that substitution of Gly-4941 with Asp or Lys results in functional channels as indicated b

292 to E88D selectins that replaced Glu-88 with Asp.

293 for instance, appeared to be associated with Asp(808) protonation.

294 rg-742 of a monomer forms a salt bridge with Asp-113 of another monomer.

295 modulated by its respective interaction with Asp-49.

296 Because exemestane interacts with Asp(309) based on its co-crystal structure with the enzy

297 tonated and forms an electrostatic pair with Asp(76) from the catalytic loop, triggering the decameri

298 f the possible antiparallel structures (with Asp(15) and Phe(19) aligned), are highly stable and orde

299 , Ser-3 modification (i.e. substitution with Asp or phosphorylation) "undocks" and repositions the co

300 amate (YNB + Glu), or YNB + aspartate (YNB + Asp).