ライフサイエンスコーパス: Asn

1 Asn(7.32) is affected by modifications on position Arg(3

2 Asn-110 replacement with Gln completely abrogated rhDAO

3 Asn-538/745 double and Asn-168/538/745 triple substituti

4 bserved upon simultaneous mutation of the 16 Asn sites.

5 B/c and C57 residues revealed that Trp(166), Asn(167), and Cys(251) are of major importance for cI bi

6 rted that the N-glycosylation sites Asn-168, Asn-538, and Asn-745 in recombinant hDAO (rhDAO) carry c

7 Mutations of Asn-168, Asn-538, and Asn-745 reduced rhDAO secretion by 13, 71,

8 mannose(1-3)fucose(0-1)N-acetylglucosamine(2)Asn).

9 s transition state stabilization by Arg-248, Asn-249, His-255, and Arg-349.

10 from the asparagine residue at position 25 (Asn-25) is located within the trans homophilic-binding i

11 t not other N-glycosylation sites (Asn(260), Asn(371), and Asn(394)), result in collagen I-independen

12 Asp(32), and Trp(59) in FKBP12 and Gln(31), Asn(32), and Phe(59) in FKBP12.6.

13 uggested that three residues (i.e. Arg(338), Asn(347), and Asp(360)) might be important for stabilizi

14 p(360); ACm2A), or three residues (Arg(338), Asn(347), and Asp(360); ACm3A) were substituted with Ala

15 that Asn-663 and to a lesser extent Asn-348, Asn-468, and Asn-812 contribute to protein stability/syn

16 ln-384/Leu-349, Gln-390/Glu-355, and Glu-392/Asn-357) that contribute to selective interactions betwe

17 e cluster of N-glycosylation sites (Asn-467, Asn-473, and Asn-494) was required for immunoreactivity

18 re2 derivative with a single cleaved Ala-470-Asn-471 bond.

19 that this non-canonical cleavage at Ala-470-Asn-471 is instrumental for the onset of catalysis in si

20 e conservative mutations Arg-126-Gln, Asp-49-Asn, and Arg-126-Lys, we inferred that a crystallographi

21 ee relay loop amino acid residues (Ile(508), Asn(509), and Asp(511)) in communicating with converter

22 Arg-528/Asp-575 < Lys-528/Asp-575 < Arg-528/Asn-575 < Lys-528/Asn-575, indicated that the relative a

23 Lys-528/Asp-575 < Arg-528/Asn-575 < Lys-528/Asn-575, indicated that the relative activity of variant

24 Residues Tyr(2.64), Asp(2.68), Asn(6.55), Asn(7.32), and Phe(7.35) of Y4R are found to be importan

25 9, Tyr(1)-Pro(2)-Ser(3)-Lys(4)-Pro(5)-Asp(6)-Asn(7)-Pro(8)-Gly(9)-NH2) and a tachykinin-related pepti

26 irmed four N-glycosylazhytion sites (Asn-67, Asn-91, Asn-436, and Asn-612) in human ADAM8.

27 Residues Tyr(2.64), Asp(2.68), Asn(6.55), Asn(7.32), and Phe(7.35) of Y4R are found to

28 ur N-glycosylazhytion sites (Asn-67, Asn-91, Asn-436, and Asn-612) in human ADAM8.

29 ether, the results show that Trp-81, Tyr-97, Asn-140, and Met-149 play similarly important roles in t

30 idate under conditions mimicking accelerated Asn aging.

31 A single amino acid (Asn to Ile) substitution in the homeodomain abolished th

32 peptide variants containing amino acids Ala, Asn, Gln, His, Ile, and Lys at positions equivalent to 7

33 residues containing a small side chain (Ala, Asn, and Gln), but not with a bulky side chain.

34 ins of mammalian GT6, but has an Asn(95)-Ala-Asn(97) (NXN) sequence substituted for the DXD motif and

35 of succinyl-CoA, Rhodobacter capsulatus ALAS Asn-85 has a proposed role in regulating the opening of

36 ing aromatic (Phe, Trp, Tyr, and His)/amide (Asn and Gln)/Guanidine (Arg)) side-chains and charged hy

37 revealing a strict requirement for either an Asn or Gln residue.

38 -binding interface, suggesting a role for an Asn-25-associated glycan in PECAM-1 homophilic interacti

39 talytic domains of mammalian GT6, but has an Asn(95)-Ala-Asn(97) (NXN) sequence substituted for the D

40 ure of our synthetic scheme is the use of an Asn-specific butelase-mediated cyclization of their line

41 Asn synthetase genes knocked out is still an Asn prototroph.

42 the consensus T:A base pair H-bonds with an Asn that replaces His in ZnF10.

43 we identified several residues (Asp-1028 and Asn-1029 from domain A, as well as Leu-938, Ala-978, and

44 ed that the residues adjacent to Asn-110 and Asn-137 form a highly conserved hydrophobic cleft intera

45 mass measurement has shown that Asn(16) and Asn(45) underwent a nonenzymatic deamidation, the sequen

46 have N-linked glycosylations at Asn(208) and Asn(310).

47 leavage site was mapped between Asp(342) and Asn(343).

48 curred equally well at Thr(345)-Leu(346) and Asn(347)-Leu(348), was abolished by the presence of Asn(

49 glycosylation sites (Asn(260), Asn(371), and Asn(394)), result in collagen I-independent constitutive

50 N-glycosylation was observed on Asn-436 and Asn-612 in the active and remnant forms.

51 azhytion sites (Asn-67, Asn-91, Asn-436, and Asn-612) in human ADAM8.

52 alytic residues, and Trp(270), Tyr(461), and Asn(462) were involved in the substrate-binding site for

53 and to a lesser extent Asn-348, Asn-468, and Asn-812 contribute to protein stability/synthesis of CaV

54 N-glycosylation sites (Asn-467, Asn-473, and Asn-494) was required for immunoreactivity in one patien

55 we found specific residues like Arg-476 and Asn-425 that were associated with differences in bystand

56 locations in the DAO structure, Asn-538 and Asn-745 glycosylations might be important for efficient

57 to tetra-antennary branches, and Asn-538 and Asn-745 had similar complex-type glycans with some tissu

58 N-glycosylation sites Asn-168, Asn-538, and Asn-745 in recombinant hDAO (rhDAO) carry complex-type g

59 Mutations of Asn-168, Asn-538, and Asn-745 reduced rhDAO secretion by 13, 71, and 32%, resp

60 wo highly conserved asparagines (Asn-638 and Asn-652).

61 The Asn-67 and Asn-91 prodomain sites contained high mannose, whereas c

62 contribute to cation selectivity (Val-86 and Asn-258), the transition between the two open states (Va

63 The Asn-91 and Asn-612 sites were essential for its correct processing

64 transmembrane residues (Val-86, Lys-93, and Asn-258) that form a putative barrier to ion translocati

65 Third, mutation of Leu-981 and Asn-1029 significantly affected the transglycosylation r

66 ed with bi- to tetra-antennary branches, and Asn-538 and Asn-745 had similar complex-type glycans wit

67 from Aspergillus niger in deglycosylated and Asn-linked N-acetylglucosamine-stub forms reveal a 10(2/

68 Asn-538/745 double and Asn-168/538/745 triple substitutions reduced rhDAO secre

69 ify the residues Ala-519/Asp-520 of EHD1 and Asn-519/Glu-520 of EHD3 as defining the selectivity of t

70 encode AsnRS for Asn-tRNA(Asn) formation and Asn synthetases to synthesize Asn and GatCAB for Gln-tRN

71 1 at positions Asp-18 and Asp-200 to His and Asn exhibit dominant autoimmune phenotypes associated wi

72 equivalent to Asn-297 in the Fc of IgG1) and Asn-236 (equivalent to Asn-563 in the tail piece of IgM)

73 actions that involve Tyr(L32), Tyr(L92), and Asn(L27d) that directly interact with Arg(315), thus elu

74 unique to Abeta40 include Lys16, Leu17, and Asn 27, whereas sites unique to Abeta42 include Phe20 an

75 ontaneously at near-neutral and basic pH and Asn(16)-Gly(17) rather at basic pH.

76 -MS/MS to determine the cleavage site(s) and Asn(347) glycosylation as a function of digestion time.

77 (90)-TMD2, Leu(290)-TMD7, Ser(407)-TMD11 and Asn(411)-TMD11) in the predicted gate were substituted w

78 ), Arg-144 (helix V), His-322 (helix X), and Asn-272 (helix VIII) interact directly with the galactop

79 In SLC30A10, the corresponding residues are Asn-43 and Asp-47 in the second and His-244 and Asp-248

80 drophobic peptide of NSP, lacking Arg or Arg-Asn with -4 charge, induced early thrombosis and mortali

81 rta, selected peptides containing Arg or Arg-Asn, not Arg-Met, with a 0 or +1 charge, significantly r

82 Seven synthetases, Ala-, Arg-, Asp-, Asn-, Leu-, Lys- and TyrRS, appear to associate with ES7

83 ere rich in Lys, Glu/Gln, Gly, Pro, Ala, Asp/Asn, and Arg.

84 and amino acid residues Ser/Arg(339) and Asp/Asn(421) in CTLD domain contribute to their differential

85 ophobicity (retention on C18 columns) of Asp/Asn (or Glu/Gln) peptide analogues among all naturally o

86 nthesis and thus cause the appearance of Asp/Asn-less stem peptides in PG.

87 y preferred for binding to conserved Gly:Asp:Asn residues.

88 simultaneously separate Gln and asparagine (Asn) deamidation products even for those peptides showin

89 ic acid (Asp) isomerization, and asparagine (Asn) deamidation.

90 cystine (dimer of cysteine), and asparagine (Asn) did not show signs of racemization at the irradiati

91 from Escherichia coli deamidates asparagine (Asn) and glutamine, with an ~10(4) higher specificity (k

92 n contains two highly conserved asparagines (Asn-638 and Asn-652).

93 ce of the unique N-linked glycan attached at Asn-297 on the structure and function of IgG1-Fc is well

94 simulations indicate that deglycosylation at Asn-163 of CD16 removes the steric hindrance for the CD1

95 n N-glycan in the HA binding Link domain (at Asn(2280)), and cells expressing membrane-bound HARE(N22

96 Glycans at Asn-168 were predominantly sialylated with bi- to tetra-

97 vely displayed high-mannose glycosylation at Asn-137.

98 We report here that glycosylation at Asn-297 is critical for interactions with Fc receptors a

99 ors and complement and that glycosylation at Asn-563 is essential for controlling multimerization.

100 uctures that have N-linked glycosylations at Asn(208) and Asn(310).

101 Mutations at Asn-101 alter the cation dependence of the transporter,

102 a pH-dependent cleavage of the propeptide at Asn-38 and Asp-54.

103 Hexa-Fc contains two N-linked sites at Asn-77 (equivalent to Asn-297 in the Fc of IgG1) and Asn

104 In particular, hydrogen bonding between Asn(462) and xylose at the nonreducing end subsite +2 wa

105 ans likely reflects the ancient link between Asn biosynthesis and its use in translation that enabled

106 and alpha1,6-fucosylation) and augmented by Asn(347) NeuAc-type sialylation (all p < 0.05).

107 held within the porphyrin is coordinated by Asn-211 residue.

108 ignificance of the hydrogen bond provided by Asn-169 to the reaction mechanism of AMSDH, we created A

109 which the distal His has been substituted by Asn.

110 tential N-glycosylation sites of E-cadherin, Asn-554 is the key site that is selectively modified wit

111 e N1 and N2 positions adjacent to the N-cap (Asn, Asp, Ser, Thr, Gly), followed by Glu, Gln, or Asp i

112 Residues at the B-type channel (Asn-34, Glu-66, Asp-132, and Asp-139) of E. coli bacteri

113 and structural measures, such as NH(Gly)-CO(Asn-sc) distances.

114 p in splicing involves attack of a conserved Asn side-chain amide on the adjacent backbone amide, lea

115 hythmic drug, to probe the role of conserved Asn residues in the S6s of DIII and DIV in NaV1.5 and Na

116 Mutation of the conserved Asn residue (N890A) in the MARCH6 CTE stabilized the nor

117 est that multiple PrP(C) segments containing Asn/Gln residues may act in concert along a replicative

118 dase (ClbP)-mediated cleavage of an N-acyl-d-Asn side chain, and all isolation efforts have employed

119 We substituted the D1-Asn(87) residue in the cyanobacterium Synechocystis sp.

120 iant strains to probe the function of the D1-Asn(87) residue in the water-oxidation mechanism.

121 provide new insight into the role of the D1-Asn(87) site in the water-oxidation mechanism and explai

122 The Phe, Ala, and Dap/Asn residues were successively removed to generate a 14-

123 straction being achieved using a diphosphate-Asn-Ser relay.

124 op C ((148)TM(149) and His(151)) and loop E (Asn(226) and Glu(228)).

125 lar loop 2, ECL2 (Thr-141/Ile-142) and ECL2 (Asn-148/Asp-149, Leu-150/Thr-151, Arg-157/Tyr-158), were

126 or-like effector nucleases containing either Asn-Asn (NN) or Asn-Lys (NK) repeat variable di-residues

127 esis and its use in translation that enabled Asn to be added to the genetic code.

128 ntly antagonized by several volume-enhancing Asn(347) glycan features (i.e. occupancy, triantennary G

129 orks from side chain amides forming extended Asn/Gln ladders.

130 onstrate that Asn-663 and to a lesser extent Asn-348, Asn-468, and Asn-812 contribute to protein stab

131 us, which encodes the fructose-asparagine (F-Asn) utilization pathway, are highly attenuated in mouse

132 cific nutrient source fructose-asparagine (F-Asn), to the probiotic bacterium Escherichia coli Nissle

133 Here, we report that F-Asn is bacteriostatic to a fraB mutant (IC50 19 muM), bu

134 The amide group of Asn(95), the first Asn of the NXN motif, interacts with the ribose moiety o

135 the i-2, i-1, i+1, and i+2 residues flanking Asn at the i position.

136 ncluding acidic domain 1 (AD1), the flanking Asn/Ser/Thr-rich (NST) domain and AD2] are transiently t

137 urans and Bacillus subtilis encode AsnRS for Asn-tRNA(Asn) formation and Asn synthetases to synthesiz

138 that, with the exception of isoacceptors for Asn, Glu, and Ile, the majority of 48 synthetic Escheric

139 eria are predicted to use only one route for Asn-tRNA(Asn) formation.

140 ains, and that Ala and Cys substitutions for Asn in both S6s result in uncoupling of the pore domains

141 made for NaV1.4, although substitutions for Asn in DIII-S6 showed somewhat less uncoupling.

142 to Asp-248 in the first (Glu-25) or fourth (Asn-127) transmembrane segments were required.

143 PrP, we show that mutating residue 173 from Asn to Thr alters protein stability and misfolding only

144 sialic acid-containing glycan emanating from Asn-25 reinforces dynamic endothelial cell-cell interact

145 s associated with a glycosylation shift from Asn-417 to Asn-415 that enables HCV to escape neutraliza

146 We purified to homogeneity functional Asn, Glu, and Ile tRNAs from the native E. coli tRNA mix

147 e specificity toward alpha1,6-fucosyl-GlcNAc-Asn or alpha1,6-fucosyl-GlcNAc-polypeptide in transglyco

148 oduction of distinguishably protected GlcNAc-Asn building blocks during automated solid phase peptide

149 city and kinetics of binding to Man9 GlcNAc2 Asn and a synthetic nonamannoside.

150 Asp with Glu, Gln, or Cys and R175 with Gln, Asn, or Cys.

151 taGly-141 mutants, the backbone amide of Glu/Asn-142 forms an H-bond to the N5 of the oxidized flavin

152 utyric acid > Gln, Thr, Ser > Glu, Ala, Gly, Asn, Asp.

153 erine-to-asparagine substitution [Ser(139)-->Asn(139) (S139N)] in the viral polyprotein substantially

154 e (22-27) fragment (with a C-terminal Gly, H-Asn-Phe-Gly-Ala-Ile-Leu-Gly-NH2) and acyl carrier protei

155 gh number of Asn and Gln residues and a high Asn:Gln ratio.

156 bstituted one of four amino acids (Asp, His, Asn, Gln) at each of the 12 ligating positions because t

157 the peptide hormone by binding to an Arg-His-Asn motif in IDA.

158 present the structure of the ZRANB3 HNH (His-Asn-His) endonuclease domain and provide a detailed anal

159 s obtained for the pentapeptides Cys-Ile-His-Asn-Pro and Cys-Ile-Gln-Pro-Val while low response was a

160 (cysteinylglycine, glutathione, Cys-Ile-His-Asn-Pro, Cys-Ile-Gln-Pro-Val, Cys-Arg-Gln-Val-Phe) vs. 1

161 Eco94GmrSD is proposed to belong to the His-Asn-His (HNH)-nuclease family by the identification of a

162 His78 (Asn in UPPS) is essential for catalysis and is proposed

163 A conserved asparagine in the oxyanion hole, Asn-169, is found to be H-bonded to substrate-derived in

164 s non-lysosomal glycoproteins with identical Asn-linked glycans.

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

166 int mutations of variant residues identified Asn-16 and Ser-23 as important contributors to the time

167 racted with the most hydrophobic peptide Ile-Asn-Tyr-Trp.

168 raction between milk bioactive peptides, Ile-Asn-Tyr-Trp, Leu-Asp-Gln-Trp, and Leu-Gln-Lys-Trp, and d

169 fragment (H-Val-Gln-Ala-Ala-Ile-Asp-Tyr-Ile-Asn-Gly-OH), following the solid-phase peptide synthesis

170 The results explain why B. subtilis with its Asn synthetase genes knocked out is still an Asn prototr

171 ia can be formed either by directly ligating Asn to tRNA(Asn) using an asparaginyl-tRNA synthetase (A

172 We document that RCL-localized Asn(347) glycosylation fine-tunes the RCL cleavage rate

173 The Asn-473 is positioned on a short loop (Asn-Gln-Gly-Glu-Pro) instead of an alpha-helix and forms

174 20 positions 23, 45, 47, and 70 (Ile-Ala-Lys-Asn [I-A-K-N]) emerged as signatures of mucosal transmis

175 es [DOTA-Ala(1)]SS14 (DOTA-Ala-Gly-c[Cys-Lys-Asn-Phe-Phe-Trp-Lys-Thr-Phe-Thr-Ser-Cys]-OH), PanSB1 (DO

176 allotypes at three amino acid positions (Lys/Asn-392, Val/Met-397, Lys/Arg-409) to alter the strength

177 a high-affinity site, formed by the Gly-Met-Asn signature sequence (Gly312 and Asn314) at the extrac

178 rms of uncleaved CBG indicated that multiple Asn(347) glycan features are modulating the RCL digestio

179 on sites in HeV G by conservative mutations (Asn to Gln) and found that six out of eight sites were a

180 drolysis of the yam tuber, dioscorin-namely, Asn-Trp (NW), and its analogue, Gln-Trp (QW)-were synthe

181 -Xxx-Ala-Phe-DPro], where Xxx was the native Asn of AGRP or a diaminopropionic (Dap) acid residue pre

182 Significantly, NS3:Asn-570 to alanine mutation introduced into an infectiou

183 , [Cu4 (S-Cys)6 ](2-) , and [Cu4 (S-Cys)5 (O-Asn)](-) clusters.

184 fficient in vitro synthesis allowing >90% of Asn-linked beta-N-GlcNAc-ylated peptide and proteins.

185 y promoting N-acetylglucosamine branching of Asn (N)-linked glycans.

186 The change of Asn at position 460 to His, which corresponds to the nat

187 The characterization of Asn deamidated residues by LERLIC-MS/MS also uncovered n

188 sly in proteins during aging; deamidation of Asn-Gly-Arg (NGR) sites can lead to the formation of iso

189 412-423) complex, such that glycosylation of Asn-415 would not prevent antibody binding.

190 We conclude that N-glycosylation of Asn-594 of COX-2 occurs in the ER, leading to anterograd

191 ollowing post-translational glycosylation of Asn-594.

192 The amide group of Asn(95), the first Asn of the NXN motif, interacts with

193 Introduction of Asn into the PqsC active site led to significant activit

194 of these residues was tolerated, but loss of Asn-638 resulted in the synthesis of truncated LAM, whic

195 Maturation of Asn-linked oligosaccharides in the eukaryotic secretory

196 m metabolism, revealing onward metabolism of Asn by the photorespiratory nitrogen cycle and accumulat

197 Mutation of Asn-43 resulted in an increased tendency to form dimers,

198 By contrast, mutations of Asn(233), Arg(235), Glu(237), and Glu(255) exosite resid

199 Mutations of Asn-168, Asn-538, and Asn-745 reduced rhDAO secretion by

200 Bank voles have a high number of Asn and Gln residues and a high Asn:Gln ratio.

201 These findings suggest that a high number of Asn and Gln residues at specific positions may stabilize

202 The side-chain orientation of Asn is a key determining factor; if it is turned away fr

203 )-Leu(348), was abolished by the presence of Asn(347) glycosylation but was enhanced by sialoglycans

204 conclude that the evolutionary selection of Asn-150 was significant for optimizing the forward enzym

205 a glycyl residue is at the carboxyl side of Asn and leads to formation of aspartyl and isoaspartyl r

206 Substitution of Asn-610 with either Asp or Glu within the transposase do

207 By comparison, substitutions of Asn for Ile-136 (I136N) and Thr for Ile-142 (I142T) in a

208 Asp-248 abolished manganese efflux, that of Asn-43 and Asp-47 did not.

209 ere it was stable and slowly glycosylated on Asn-594.

210 complex type N-glycosylation was observed on Asn-436 and Asn-612 in the active and remnant forms.

211 cterization of three AC variants, where one (Asn(347); ACm1A), two (Arg(338) and Asp(360); ACm2A), or

212 In contrast, mutations of Val(168) or Asn(171) in the upper site, which are unique to ROMK wit

213 Alanine substitution of Glu(68), Tyr(92), or Asn(139), which interact with arabinose and xylose side

214 he 5 Glu and Asp residues replaced by Gln or Asn in our experiments, none of the mutant pigments shif

215 ted from apoA-I mutants (Tyr(166) --> Glu or Asn), which showed preservation in both LCAT binding aff

216 ine at positions 92 and 96; Z = Val, Gly, or Asn at position 95)).

217 nucleases containing either Asn-Asn (NN) or Asn-Lys (NK) repeat variable di-residues (RVDs) and 3- a

218 Unlike Met oxidation, Asn deamidation and Asp isomerization mostly had very li

219 AGRP macrocyclic scaffold (c[Pro-Arg-Phe-Phe-Asn-Ala-Phe-DPro]) were explored with 14-compound and 8-

220 The most potent scaffold, c[Pro-Arg-Phe-Phe-Asn-Ala-Phe-DPro], comprised the hexa-peptide beta-hairp

221 In particular, mutations at cohesin position Asn(37) show dramatic variability in their effect on doc

222 For two of the four positions, Asn and Gln residues were not interchangeable, revealing

223 s site-specific glycosylation, by preventing Asn-554 from receiving the deleterious branched structur

224 le 9-fluorenylmethyl chloroformate-protected Asn moiety.

225 Replacing Asn(7), Ser(8), Ala(19), and Ile(21) with the correspond

226 r-homing peptide containing a representative Asn-Gly-Arg (NGR) motif.

227 esidues with the isosteric but polar residue Asn (L267N/L270N) stabilized channels in a fully open st

228 changing the allosteric sodium site residue Asn 131 to an alanine or a valine augments constitutive

229 e identification of a third crucial residue, Asn-88.

230 ECL2 residues Asn-173 and Thr-174 are essential for quinine binding.

231 the wild type glycopeptide fraction revealed Asn-732 peptide fragments linked to the sulfoquinovose-c

232 sis of putative active site residues reveals Asn(37), Asp(52), and Thr(68) are important for catalysi

233 e) and the additional C-terminal serine-rich Asn-63-Glu-82 region (absent in orthologues from anophel

234 ent a nonenzymatic deamidation, the sequence Asn(45)-Gly(46) being deamidated spontaneously at near-n

235 cross sections of hydrophilic residues (Ser, Asn, Trp) tend to stay on or fall below the isotropic mo

236 Q mutations in the non-operational sextuplet Asn mutant protein partially restored CaValpha2delta1 fu

237 We found that a single N-glycosylation site (Asn(8)) was important for MICA018 surface expression.

238 ntly reported that the N-glycosylation sites Asn-168, Asn-538, and Asn-745 in recombinant hDAO (rhDAO

239 motif, but not other N-glycosylation sites (Asn(260), Asn(371), and Asn(394)), result in collagen I-

240 d that the cluster of N-glycosylation sites (Asn-467, Asn-473, and Asn-494) was required for immunore

241 sis confirmed four N-glycosylazhytion sites (Asn-67, Asn-91, Asn-436, and Asn-612) in human ADAM8.

242 use of their locations in the DAO structure, Asn-538 and Asn-745 glycosylations might be important fo

243 Substituting Asn for Asp at equivalent positions in the alpha-, beta-

244 formation and Asn synthetases to synthesize Asn and GatCAB for Gln-tRNA(Gln) synthesis, their AspRS

245 ng and can be used with GatCAB to synthesize Asn.

246 l-tRNA synthetase (AsnRS) or by synthesizing Asn on the tRNA.

247 Asp-575 conferred lower activity than Asn-575, but the difference depended on residue 528.

248 These results demonstrate that Asn-663 and to a lesser extent Asn-348, Asn-468, and Asn

249 ng the gating currents, we demonstrated that Asn residues in the S6s of DIII and DIV are important fo

250 Mass spectrometry revealed that Asn-95 carries a core glycan, consisting of two GlcNAc a

251 Here, we show that Asn-110 in native hDAO from amniotic fluid and Caco-2 ce

252 les accurate mass measurement has shown that Asn(16) and Asn(45) underwent a nonenzymatic deamidation

253 The Asn(95) peptide displayed specific efflux inhibition and

254 The Asn-473 is positioned on a short loop (Asn-Gln-Gly-Glu-P

255 The Asn-67 and Asn-91 prodomain sites contained high mannose

256 The Asn-91 and Asn-612 sites were essential for its correct

257 Among the Asn(297) mutants that result in lack of glycosylation an

258 nopropionic acid (Dap), DDap, and His at the Asn position yielded potent MC4R ligands, while replacin

259 Here, we report that N-glycosylation at the Asn(211) residue plays a unique role in the control of D

260 n alpha1,6-fucose moiety specifically at the Asn-linked GlcNAc moiety not only to GlcNAc-peptide but

261 Even though substitutions for the Asn in DIV-S6 in NaV1.5, N1764A and N1764C, produce litt

262 d Na(+) illicit 5-HT-induced currents in the Asn-101 mutants and reveal that, although Ca(2+) promote

263 nt protomers binding the first GlcNAc of the Asn(340) N-linked glycan on the other independent protom

264 the endoplasmic reticulum or mutation of the Asn-24 glycosylation site decreased GC activity, but nei

265 To verify the contribution of the Asn-25 glycan to endothelial barrier function, we genera

266 In contrast, mutation of the Asn-67 site had only modest effects on enzyme stability

267 In this study, the Asn and Ala positions of a reported AGRP macrocyclic sca

268 pt for the ~10 amino acids that surround the Asn(154) glycosylation site in each of the 180 envelope

269 fine-tuning Gd(3+)-sensitivity, and that the Asn-584 residue determines Ca(2+) permeability of the TR

270 ade movement of COX-2 to the Golgi where the Asn-594-linked glycan is trimmed prior to retrograde COX

271 The mechanism by which the Asn side-chain becomes activated as a nucleophile is not

272 rements for N-glycosylation have yielded the Asn-X-Ser/Thr (NXS/T) sequon and the enhanced aromatic s

273 single, highly conserved asparagine on TM1 (Asn-101) to provide several lines of evidence demonstrat

274 ess this model, five residues (Gln(45)-TMD1, Asn(90)-TMD2, Leu(290)-TMD7, Ser(407)-TMD11 and Asn(411)

275 d with a glycosylation shift from Asn-417 to Asn-415 that enables HCV to escape neutralization by mAb

276 tures revealed that the residues adjacent to Asn-110 and Asn-137 form a highly conserved hydrophobic

277 otransferase GatCAB transamidates the Asp to Asn on the tRNA.

278 egnenolone and progesterone hydrogen bond to Asn(202) in orientations consistent with production of 1

279 containing a repeating SQ-Hex unit bound to Asn-732 of the H. volcanii S-layer glycoprotein, a posit

280 explained by differences in flux from CN to Asn caused by altered beta-cyanoalanine nitrilase activi

281 two N-linked sites at Asn-77 (equivalent to Asn-297 in the Fc of IgG1) and Asn-236 (equivalent to As

282 n the Fc of IgG1) and Asn-236 (equivalent to Asn-563 in the tail piece of IgM).

283 ange the 558-encoding amino acid from Lys to Asn (K558N).

284 sfolding only subtly, whilst changing Ser to Asn at codon 169 causes instability in the protein, prom

285 shield created by the glycosylation shift to Asn-415, we determined the structure of this broadly neu

286 Also, a proton transfers spontaneously to Asn, advancing a new hypothesis that the substrate's alp

287 Synthesis of asparaginyl-tRNA (Asn-tRNA(Asn)) in bacteria can be formed either by direc

288 Bacillus subtilis encode AsnRS for Asn-tRNA(Asn) formation and Asn synthetases to synthesize Asn and

289 predicted to use only one route for Asn-tRNA(Asn) formation.

290 Synthesis of asparaginyl-tRNA (Asn-tRNA(Asn)) in bacteria can be formed either by directly ligat

291 A synthetase (ND-AspRS) attaches Asp to tRNA(Asn) and the amidotransferase GatCAB transamidates the A

292 rmed either by directly ligating Asn to tRNA(Asn) using an asparaginyl-tRNA synthetase (AsnRS) or by

293 potency at the mMC4R, c[Pro-His-DPhe-Arg-Trp-Asn-Ala-Phe-DPro] and c[Pro-His-DPhe-Arg-Trp-Dap-Ala-DPr

294 Moreover, we mapped two Asn residues within CRD4 that are N-linked glycosylated

295 ies show that catalysis depends on a Lys-Tyr-Asn-Tyr tetrad that emerged adjacent to a computationall

296 Molecular dynamics simulations of various Asn(347) glycoforms of uncleaved CBG indicated that mult

297 ids associated with binding guanine in VldE (Asn, Thr, and Val) are similar in S. venezuelae OtsA (As

298 Whereas Asn-415 is buried by HCV1 and AP33, it is solvent-expose

299 (rhDAO) carry complex-type glycans, whereas Asn-110 carries only mammalian-atypical oligomannosidic

300 itution of a Lys residue at position 68 with Asn in MUG not only accelerates the removal of uracil fr

301 uon and the enhanced aromatic sequons (Phe-X-Asn-X-Thr and Phe-X-X-Asn-X-Thr), which can be efficient

302 romatic sequons (Phe-X-Asn-X-Thr and Phe-X-X-Asn-X-Thr), which can be efficiently N-glycosylated.