ライフサイエンスコーパス: Asn

1 Asn-110 replacement with Gln completely abrogated rhDAO

2 Asn-401 and Thr-381 each form hydrogen bonds with two at

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

4 geometry with His(117), His(257), Asp(116), Asn(216), and a water/hydroxide as ligands.

5 bserved upon simultaneous mutation of the 16 Asn sites.

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 iganded form, the EndoBT-3987-Man(9)GlcNAc(2)Asn substrate complex, and two EndoBT-3987-Man(9)GlcNAc

10 auses the substrate of MGAT1 (Man(5)GlcNAc(2)Asn) to accumulate on glycoproteins, a change that is de

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

12 Because Val-17, Gly-22, Leu-25, Asn-26, and Pro-29 are predicted to reside along the sam

13 y conserved residues - Gln(232/585)-Asp(262)/Asn(623)-Tyr(322/666) (the constriction triads).

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

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

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

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

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

19 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

20 l ligands in MPE: Asp(33), His(35), Asp(78), Asn(112), His(124), His(146), and His(158) A swath of po

21 Therefore, the Asn(81)-Asn(149) fragment can be considered as the site of IgE r

22 Grafting of the Asn(81)-Asn(149) fragment within the primary structure of yeast

23 ion mutants, a conserved 69-residue (Asn(81)-Asn(149)) fragment at C terminus of Rhi o 2 was identifi

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

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

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

27 An Asn residue (N191) that is critical for caC excision is

28 A nanobody containing an Asn-Pro-Phe peptide within the complementarity-determini

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

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

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

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

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

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

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

36 contrast, that the nearby sites Asn-145 and Asn-160 contain lower levels of sialylated N-glycans and

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

38 an rhodopsin is N-glycosylated on Asn(2) and Asn(15), whereas human (h) red and green cone opsins (hO

39 n OTUB2, the catalytic residues His(224) and Asn(226) formed a stable hydrogen bond.

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

41 cific hydrogen bonding between Ser(5.46) and Asn(6.55), and the aromatic head group of the ligands.

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

43 determined that glycosylation of Asn-471 and Asn-1030 is necessary for ACLP secretion and identified

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

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

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

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

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

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

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

51 gh Michael addition, including Gln, Arg, and Asn, which are inaccessible to existing chemical crossli

52 post-translational hydroxylation of Asp and Asn residues in epidermal growth factor-like domains (EG

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

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

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

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

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

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

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

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

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

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

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

64 ed antibodies with unmutated Ala-Val-Tyr and Asn-His-Ser motifs, which recognize both erythrocyte I/i

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

66 We also investigated another Asn residue (N140) that is catalytically essential and s

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

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

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

70 decomposition of labile amino acids such as Asn, Gln, Trp, Cit, and theanine.

71 with the amino acid data rich in Asx (Asp + Asn) and Glx (Glu + Gln) typical of invertebrate skeleta

72 ystematic mutagenesis of His583 to Ala, Asp, Asn, Glu, Gln, Lys, Phe, Tyr, and Trp showed that althou

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

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

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

76 se (AspH) catalyses the hydroxylation of Asp/Asn-residues in epidermal growth factor-like domains (EG

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

78 The M6 asparagine Asn-905 stood out as being essential for the lipid subst

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

80 EPs) are cysteine proteases which break Asx (Asn/Asp)-Xaa bonds in acidic conditions.

81 in the extracellular N terminus of PAR(2) at Asn(30) Arg(31), proximal to the canonical trypsin activ

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

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

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

85 ated VEGFR2 displays sialylated N-glycans at Asn-247 and, in contrast, that the nearby sites Asn-145

86 on, specifically the capping of N-glycans at Asn-247 by sialic acid, tunes ligand-dependent activatio

87 d hOPSG, respectively) are N-glycosylated at Asn(34) Here, utilizing a monoclonal antibody (7G8 mAB),

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

89 leads to diminished PrP(Sc) glycosylation at Asn-196, resulting in an unshielded PRC7 epitope that is

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

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

92 42, 66, and 74, becoming sialylated only at Asn-42.

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

94 fy the unique N-linked glycosylation site at Asn(297), either through chemical and enzymatic methods

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

96 at multiple N-linked sites, one of which at Asn-126 was adjacent to a putative GalNAc transfer motif

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

98 e bond moieties due to cross-linking between Asn or Gln and Lys side chains.

99 The results also indicate that both Asn and Asp can restore the activity of Val-inhibited PK

100 ion of the proton-coupling residue Asp309 by Asn, similar inward-open structures were captured.

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

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

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

104 d in solution, and that the highly conserved Asn-76 of the AhpD core motif is important for SpAhpD fo

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

106 les, are impacted by depleting the conserved Asn, informing its role in binding and addition of the n

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

108 In contrast, Asn-21 substitution with the conformationally constraine

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

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

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

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

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

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

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

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

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

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

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

120 the Amadori compound fructose-asparagine (F-Asn) as a nutrient through the successive action of thre

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

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

123 ediated genome editing abolished growth on F-Asn.

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

125 s, but here the Trp interacts with the first Asn.

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

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

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

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

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

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

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

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

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

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

136 a-GalA-(1-2)-]-alpha-GalAN-(1-3)-beta-GalNAc-Asn.

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

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

139 hydrogen bonds involving sidechains of Gln, Asn, Ser, and Tyr residues, both along and transverse to

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

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

142 Legumain cannot cleave after glycosylated Asn residues, which enabled the robust identification an

143 tro Sequence analysis revealed a rare His -> Asn variation adjacent to the CysRS catalytic pocket.

144 ys codons in vivo We surmise that the His -> Asn variation can be introduced into any CysRS to provid

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

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

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

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

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

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

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

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

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

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

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

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

157 er major cell surface glycan types including Asn(N)-linked glycans.

158 a- and intermolecular interactions involving Asn-21 promote IAPP primary nucleation events by modulat

159 In contrast, SETD3 and its Asn(255) substituted derivatives did not methylate gluta

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

161 iously proposed mechanism of hydrolysis of L-Asn by the type II L-asparaginase from E. coli (EcAII),

162 n in the presence of the native substrate, L-Asn.

163 showing that the same mechanism applies to L-Asn and L-Gln, we postulate that it is common for all th

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

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

166 pS2, or pS(T) However, the betaA-betaB loop Asn-55-His and Lys-57-Ser substitutions in the pS3-subun

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

168 20 positions 23, 45, 47, and 70 (Ile-Ala-Lys-Asn [I-A-K-N]) emerged as signatures of mucosal transmis

169 Mammalian Asn-linked glycans are extensively processed as they tra

170 We found that FIH1 modifies Asn(35) within the uncharacterized N-terminal ubiquitin-

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

172 terized wild-type SLN and a pair of mutants, Asn(4)-Ala and Thr(5)-Ala, which yielded gain-of-functio

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

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

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

176 If a substrate bears, for example, Nt-Asn, its targeting involves deamidation of Nt-Asn, argin

177 n which a substrate bearing, for example, Nt-Asn, would be captured by a complex-bound Nt-amidase, fo

178 We discovered that the human Nt-Asn-specific Nt-amidase NTAN1, Nt-Gln-specific Nt-amidas

179 sn, its targeting involves deamidation of Nt-Asn, arginylation of resulting Nt-Asp, binding of result

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

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

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

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

184 412-423) complex, such that glycosylation of Asn-415 would not prevent antibody binding.

185 genesis, we determined that glycosylation of Asn-471 and Asn-1030 is necessary for ACLP secretion and

186 ncanonical surface and that hydroxylation of Asn(35) inhibits ubiquitin binding.

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

188 Maturation of Asn-linked oligosaccharides in the eukaryotic secretory

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

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

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

192 xcB, accepts several amino acids in place of Asn and introduces unnatural beta-thioether linkages at

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

194 imulations provided insight into the role of Asn-285 for Gb4 and phenylurea-galabiose binding, sugges

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

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

197 Substitution of Asn(255) with phenylalanine (N255F), together with subst

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

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

200 Human rhodopsin is N-glycosylated on Asn(2) and Asn(15), whereas human (h) red and green cone

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

202 rected mutagenesis revealed that Asp(147) or Asn(169) of RIPK1 are key for ceramide binding and that

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

204 (6)-Phe(7)-dPro(8)], where Xaa was Dap(5) or Asn(5), to explore the functional effects of these natur

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

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

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

208 In cone Pgamma, Asn-13 and Gln-14 significantly enhanced Gt(alpha)*-GTPg

209 n loop composed of six residues (Arg-Phe-Phe-Asn-Ala-Phe) that is imperative for binding and function

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

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

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

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

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

215 le 9-fluorenylmethyl chloroformate-protected Asn moiety.

216 genesis of the Fc, that disrupts the protein-Asn(297) carbohydrate interface.

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

218 nce at the catalytic cavity-defining residue Asn-98.

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

220 Previous studies have suggested that residue Asn-21 plays a critical role in the in vitro self-assemb

221 of deletion mutants, a conserved 69-residue (Asn(81)-Asn(149)) fragment at C terminus of Rhi o 2 was

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

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

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

225 DNF carries a single N-glycosylation sequon (Asn-127) that remains virtually unstudied despite being

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

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

228 Ten single Asn-to-Ala substitutions at the predicted N-glycosylatio

229 In the SETD3 active site, Asn(255) engages in a unique hydrogen-bonding interactio

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

231 -247 and, in contrast, that the nearby sites Asn-145 and Asn-160 contain lower levels of sialylated N

232 Strikingly, Asn-905 aligns with key ion-binding residues of P-type A

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

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

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

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

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

238 ialylated glycans attached to the N-terminal Asn(221) sequon bound influenza virus hemagglutinin and

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

240 We found that Asn (polar) and Asp (charged) activate PKM2 and that Val

241 ous structural studies, we hypothesized that Asn-169, a conserved residue in the AAG active-site pock

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

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

244 sing site-directed mutagenesis, we show that Asn-26 in the motif is crucial for RAT of TM4SF20, as it

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

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

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

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

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

250 we demonstrate that N-linked glycans at the Asn-247 site in VEGFR2 hinder VEGF ligand-mediated recep

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

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

253 Grafting of the Asn(81)-Asn(149) fragment within the primary structure o

254 We found that mutation of the Asn-127 prevents intracellular maturation and secretion,

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

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

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

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

259 d transmission EM analysis revealed that the Asn-21 amide side chain is not required for IAPP nucleat

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

261 Therefore, the Asn(81)-Asn(149) fragment can be considered as the site

262 Thus, the Asn-285-mediated molecular mechanism of type P(N) SadP b

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

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

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

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

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

268 from detection when glycans are attached to Asn-196.

269 major module engaging gamma8 by an H-bond to Asn-172 (gamma8).

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

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

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

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

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

275 d residue 17 from the N terminus from Thr to Asn by site-directed mutagenesis, making it constitutive

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

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

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

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

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

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

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

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

284 can undergo nonenzymatic deamidation on two Asn residues.

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

286 ter deglycosylation or removal of the unique Asn(297) N-X-(T/S) sequon.

287 hiol group to the beta-carbon of an upstream Asn residue.

288 Two compounds 19 (c(Bua-Cpa-Thi-Val-Asn-Cys)-Pro-Agm) and 38 (c(Bua-Cpa-Thi-Val-Asn-Cys)-Pro

289 -Asn-Cys)-Pro-Agm) and 38 (c(Bua-Cpa-Thi-Val-Asn-Cys)-Pro-d-Arg-NEt(2)) have been selected for clinic

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

291 Furthermore, we report that VEGFR2 Asn-247-linked glycans capped with sialic acid oppose li

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

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

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

295 he simultaneous substitution of Asp-163 with Asn, and characterized these transporter variants in ele

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

297 (HOAsn) or 3-methoxyaspartate (MeOAsp) with Asn or Asp, respectively, in A5D is more detrimental to

298 here both HOAsn and MeOAsp are replaced with Asn or Asp, respectively.

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

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