ライフサイエンスコーパス: Ala

1 Ala replacement at Ser(46), Ser(162), Ser(181), Ser(269)

2 Ala substitutions for aromatic residues at the alphaM4-a

3 Ala substitutions for most alphaM4 residues, including t

4 Ala tailing thus follows mechanistic principles surprisi

5 Ala-tRNAPro is specifically hydrolyzed by the editing do

6 e well-tolerated, with Val(1)-Val(2), Ile(1)-Ala(2), and Leu(1)-Val(2) variants exhibiting ProT(QQQ)

7 PR-selective ligand [d-Phe(6), beta-Ala(11), Ala(13), Nle(14)]Bn(6-14) (sBB2L) generating peptide con

8 lytic MIO prosthetic group created from (189)Ala-Ser-Gly(191) residues and the bound l-phenylalanine

9 ions on mutant D1-His-198-Ala and D2-His-197-Ala RCs, our simulated absorption-difference spectra rep

10 sults with calculations on mutant D1-His-198-Ala and D2-His-197-Ala RCs, our simulated absorption-dif

11 ected with PyC(2)-Gly, PyC(3)-Gly and PyC(2)-Ala at quantifiable concentrations.

12 wild-type SLN and a pair of mutants, Asn(4)-Ala and Thr(5)-Ala, which yielded gain-of-function behav

13 and a pair of mutants, Asn(4)-Ala and Thr(5)-Ala, which yielded gain-of-function behavior comparable

14 ocycles c[Pro(1)-Arg(2)-Phe(3)-Phe(4)-Xaa(5)-Ala(6)-Phe(7)-dPro(8)], where Xaa was Dap(5) or Asn(5),

15 (177)Lu-DOTA-PP-F11 ((177)Lu-DOTA-(dGlu)(6)-Ala-Tyr-Gly-Trp-Met-Asp-Phe-NH(2)), and whether the use

16 (177)Lu-DOTA-PP-F11N ((177)Lu-DOTA-(dGlu)(6)-Ala-Tyr-Gly-Trp-Nle-Asp-Phe-NH(2)) performs better than

17 d minigastrin analog (177)Lu-DOTA-(d-Glu)(6)-Ala-Tyr-Gly-Trp-Nle-Asp-PheNH(2) ((177)Lu-PP-F11N) is a

18 olysis occurs at Glu-729-Val-730 and Glu-732-Ala-733 in the ADAMTS7 Spacer domain, which was corrobor

19 Replacing Asn(7), Ser(8), Ala(19), and Ile(21) with the corresponding residues fro

20 Patients with the A4V (Ala-Val) SOD1 mutation (SOD1(A4V)), the largest mutation

21 -mer peptide variants containing amino acids Ala, Asn, Gln, His, Ile, and Lys at positions equivalent

22 f the affinity and selectivity by additional Ala to Xaa substitutions; 6) protection of the charged f

23 Oxidation of Tyr-Ala-Ala-Ala-Arg (YAAAR) produces Tyr-O radicals by combined elec

24 Alanine (Ala) accumulated to about 35% of total amino acids in ne

25 osteric binding sites for inhibitor alanine (Ala) and activator fructose-1,6-bisphosphate (Fru-1,6-BP

26 egrees C from d-glucose (Glc) and l-alanine (Ala) as well as from fructosylalanine - the correspondin

27 d lower ratios of (13)C Bicar/Lac + alanine (Ala), and (13)C Bicar/tC than those of the sham-operated

28 9A, containing a threonine (Thr) to alanine (Ala) substitution at amino acid 79, failed to induce the

29 Interestingly, although Ala-tRNAThr mischarging is not known to occur in bacteri

30 r, a linear molecule, N-alanyl-aminoacetone (Ala-AA), also bound and activated VqmA.

31 An Ala mutation of the distal C-terminal Arg-354 or Ser-357

32 Although an Ala substitution locally destabilized hydrogen bonding a

33 This suppressor variant and an Ala-substituted beta-hairpin PriA variant displayed wild

34 e severe effects than replacing Cys276 by an Ala residue in the active site of the enzyme, as encount

35 periments with subtype B HIV-1 identified an Ala-to-Val mutation at SP1 residue 1 and a Pro-to-Ala mu

36 We substituted Val285 with Ala (V285A) in an Ala-Val dipeptide, to mimic the conserved Ala-Ala in man

37 the complete protein sequence and located an Ala/Thr difference between the two species that explaine

38 major HLA-B*51 subpeptidomes with Pro-2 and Ala-2, the former one was significantly reduced, and the

39 In this study, the Asn and Ala positions of a reported AGRP macrocyclic scaffold (c

40 Asp and Ala, in the selectivity motif DEKA, line the walls of th

41 igand-binding analyses revealed that DPO and Ala-AA occupy the same binding site.

42 ntly inhibit the R(N) stimulation by Pro and Ala but not PEP.

43 entified phosphoenolpyruvate (PEP), Pro, and Ala as the most potent stimulators of plant leaf R(N) Us

44 nhibitory effects of amino acids on Pro- and Ala-stimulated R(N) were mitigated by inhibition of the

45 One among the synthesized analogue, Ac-Arg-Ala-[d-Cys-Arg-Phe-His-Pen]-COOH (19), displayed subnano

46 selective, and plasma stable peptide, Ac-Arg-Ala-[d-Cys-Arg-Phe-Phe-Cys]-COOH (3).

47 h five arginyl dipeptides: Ala-Arg (AR), Arg-Ala (RA), Arg-Pro (RP), Arg-Glu (RE), and Glu-Arg (ER);

48 Cleavage of S generates a polybasic Arg-Arg-Ala-Arg carboxyl-terminal sequence on S1, which conforms

49 DP, and RhoGAP, which has the mutation Arg85'Ala.

50 substituted by other small residues such as Ala and Ser without affecting RAT of TM4SF20.

51 op composed of six residues (Arg-Phe-Phe-Asn-Ala-Phe) that is imperative for binding and function.

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

53 ncy at the mMC4R, c[Pro-His-DPhe-Arg-Trp-Asn-Ala-Phe-DPro] and c[Pro-His-DPhe-Arg-Trp-Dap-Ala-DPro],

54 we found that this non-canonical cleavage at Ala-470-Asn-471 is instrumental for the onset of catalys

55 amino acids, amino tetrazolyl alanines ((ATz)Ala = Ata), in a very good yield was subsequently achiev

56 to the GRPR-selective ligand [d-Phe(6), beta-Ala(11), Ala(13), Nle(14)]Bn(6-14) (sBB2L) generating pe

57 id agonist tetrapeptide H-Dmt-d-Arg-Aba-beta-Ala-NH(2) (KGOP01) was fused to NT(8-13) analogues.

58 and the three achiral amino acids Gly, beta-Ala, and GABA).

59 exhibited modest effects on coupling between Ala and PEP binding.

60 at gives rise to the silent coupling between Ala and phosphoenolpyruvate.

61 (R)-Aic(NN)-Ala-OMe and the hexapeptide Boc-[Ala-(R)-Aic(NN)-Ala]2-OMe as well.

62 10.3 mum The improvements obtained with both Ala(101) and Leu(106) have implications regarding glypho

63 yclic hexapeptide with replacement of Cys by Ala.

64 gulation of rabbit muscle pyruvate kinase by Ala to demonstrate that this effector reduces substrate

65 [(13)C2]Ala and [(13)C2]Pro were the most abundant and rapidly l

66 Xp-ala is another editing domain that clears Ala-tRNAPro in trans.

67 nicked Pre2 derivative with a single cleaved Ala-470-Asn-471 bond.

68 We also show that a conserved Ala residue limits thymine excision by hindering nucleot

69 an Ala-Val dipeptide, to mimic the conserved Ala-Ala in many members of the basic leucine-zipper fami

70 ouble disulfide-bonded Wnt peptide contained Ala substituted for the Ser acylation site.

71 ellaran/gelatin hydrolysate films containing Ala-Tyr peptide were developed and characterised for the

72 In contrast, Ala substitution of Lys-57, Glu-77, and Lys-96, located

73 ing of 85 scalemic samples of Pro, Met, Cys, Ala, methylpyrrolidine, 1-(2-naphthyl)amine, and mixture

74 D-Ala-D-Ala ligase, encoded by ddl genes, is responsible f

75 ve antagonist arodyn (Ac[Phe(1,2,3),Arg(4),d-Ala(8)]dynorphin A(1-11)-NH(2)) by ring closing metathes

76 -muramyl-l-Ala-gam ma-d-Glu-meso-DAP-d-Ala-d-Ala and 1,6-anhydro-N-acetyl-beta-d-muramyl-l-Ala-gamma-

77 d-muramyl-l-Ala-gamma-d-Glu-meso-DAP-d-Ala-d-Ala and binds to two activator muropeptides, N-acetyl-be

78 D-Ala-D-Ala ligase, encoded by ddl genes, is responsible for the

79 In contrast, D-Ala-D-Ala limitation caused a dramatic increase in expression

80 Addition of D-Ala-D-Ala to the medium inactivated DdlR, reducing dipeptide b

81 of peptidoglycan (PG) stem terminal d-Ala-d-Ala with d-Ala-d-Lac.

82 le for the synthesis of a dipeptide, D-Ala-D-Ala, an essential precursor of bacterial peptidoglycan.

83 d-muramyl-l-Ala-gamma-d-Glu-meso-DAP-d-Ala-d-Ala, as assessed by non-denaturing mass spectrometry.

84 x laboratory media in the absence of D-Ala-D-Ala.

85 rminating in D-Ala-D-Lac in place of D-Ala-D-Ala.

86 difications designed to provide dual d-Ala-d-Ala/d-Ala-d-Lac binding that directly overcome the molec

87 f action, only one of which requires d-Ala-d-Ala/d-Ala-d-Lac binding.

88 ism of action that is independent of d-Ala-d-Ala/d-Ala-d-Lac binding.

89 nisms of action, both independent of d-Ala-d-Ala/d-Lac binding.

90 tions designed to provide dual d-Ala-d-Ala/d-Ala-d-Lac binding that directly overcome the molecular b

91 on, only one of which requires d-Ala-d-Ala/d-Ala-d-Lac binding.

92 action that is independent of d-Ala-d-Ala/d-Ala-d-Lac binding.

93 -diaminopimelic acid (mDAP) and d-alanine (d-Ala) with cross-links occurring either between d-Ala and

94 sphorylated muOR bound to the morphine and D-Ala(2), N-MePhe(4), Gly-ol]-enkephalin (DAMGO) nonbiased

95 E. coli mutants lacking mepK and another d-Ala-mDAP-specific endopeptidase (mepS) were synthetic si

96 with cross-links occurring either between d-Ala and mDAP or two mDAP residues.

97 In contrast, D-Ala-D-Ala limitation caused a dramatic increase in expre

98 ylated analogues of the stem peptide cyclo(d-Ala-Ala5 ); 2) selection of cyclic peptides with the hig

99 beta-d-muramyl-l-Ala-gam ma-d-Glu-meso-DAP-d-Ala-d-Ala and 1,6-anhydro-N-acetyl-beta-d-muramyl-l-Ala-

100 -beta-d-muramyl-l-Ala-gamma-d-Glu-meso-DAP-d-Ala-d-Ala and binds to two activator muropeptides, N-ace

101 -beta-d-muramyl-l-Ala-gamma-d-Glu-meso-DAP-d-Ala-d-Ala, as assessed by non-denaturing mass spectromet

102 ponsible for the synthesis of a dipeptide, D-Ala-D-Ala, an essential precursor of bacterial peptidogl

103 ket modifications designed to provide dual d-Ala-d-Ala/d-Ala-d-Lac binding that directly overcome the

104 s were found to be l-configured except for d-Ala.

105 nings, which revealed extraordinarily high d-Ala contents of up to 99% in all samples.

106 synthesis to use precursors terminating in D-Ala-D-Lac in place of D-Ala-D-Ala.

107 on PG units that have stems terminating in d-Ala-d-Lac, serving as markers to prevent both the PG-ste

108 ith a pentapeptide stem that terminated in d-Ala-d-Lac.

109 d MX-2401, maintained the incorporation of D-Ala during peptidoglycan biosynthesis while the incorpor

110 an biosynthesis while the incorporation of D-Ala into teichoic acids was inhibited.

111 Addition of D-Ala-D-Ala to the medium inactivated DdlR, reducing dipep

112 complex laboratory media in the absence of D-Ala-D-Ala.

113 ors terminating in D-Ala-D-Lac in place of D-Ala-D-Ala.

114 mechanism of action that is independent of d-Ala-d-Ala/d-Ala-d-Lac binding.

115 mechanisms of action, both independent of d-Ala-d-Ala/d-Lac binding.

116 MOR activation by morphine or [d-Ala(2),N-MePhe(4), Gly-ol]enkephalin (DAMGO) causes diff

117 isms of action, only one of which requires d-Ala-d-Ala/d-Ala-d-Lac binding.

118 s enzyme in both the removal of C-terminal d-Ala residues from stem peptides and the cleavage of cros

119 cement of peptidoglycan (PG) stem terminal d-Ala-d-Ala with d-Ala-d-Lac.

120 The d-Ala-d-Lac incorporation can affect both the fitness and

121 In Escherichia coli, the d-Ala-mDAP cross-links whose cleavage by specialized endop

122 ysis of a model strain predominantly using D-Ala-D-Lac precursors for peptidoglycan biosynthesis duri

123 glycan (PG) stem terminal d-Ala-d-Ala with d-Ala-d-Lac.

124 by substitution of C-capping glycines with d-Ala.

125 n obtained when glycines are replaced with d-Ala.

126 Ala-Phe-DPro] and c[Pro-His-DPhe-Arg-Trp-Dap-Ala-DPro], and may be further developed to generate nove

127 namely (177)Lu-DOTA-MG11 ((177)Lu-DOTA-dGlu-Ala-Tyr-Gly-Trp-Met-Asp-Phe-NH(2)) and (177)Lu-DOTA-PP-F

128 ubtilis RQC complexes representing different Ala tail synthesis steps.

129 ae (HBO) cells with five arginyl dipeptides: Ala-Arg (AR), Arg-Ala (RA), Arg-Pro (RP), Arg-Glu (RE),

130 tagenesis of a beta-arrestin binding domain (Ala-Ser-Lys) within the intracellular C terminus of 5-HT

131 C-A-8E progressively increased the Km Double Ala substitutions for Ser-497 and either Thr-500, Ser-51

132 hains of different polarity and length (i.e. Ala, Arg, Cys, His, Glu, and Leu) on transporter stabili

133 Even Ala substitutions for coevolved pairs of residues at the

134 analysis of a set of 25 analogues featuring Ala(1) or His(1) and a variety of aromatic side chains a

135 Substitution of Tyr for Ala and Gly in ADS1.2 and ADS1.4, respectively, blocked

136 es, while beta-ketosulfonamides derived from Ala, Phe, or hPhe gave the hydrates of the imino beta-ke

137 structures suggested that the solvent-front Ala-810 makes hydrophobic contacts with a methyl group a

138 mino acid as compared to melanoidin from Glc/Ala and exhibit higher absorption in the UV/Vis.

139 Consequently, melanoidins formed from Glc/Ala contain more sugar degradation products with lower a

140 ngement in contrast to the reaction from Glc/Ala.

141 teins 3 and 4 (LTBP3/4) at a Glu-Val and Glu-Ala site, respectively.

142 lation of the gene encoding the sole Asp-Glu-Ala-Asp (DEAD)-box RNA helicase in Synechocystis sp. PCC

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

144 Methods: DOTA-D-Glu-Ala-Tyr-Gly-Trp-(N-Me)Nle-Asp-1-Nal-NH(2) (DOTA-MGS5) ra

145 gregation of the hexapeptide VEALYL (Val-Glu-Ala-Leu-Tyr-Leu), the B-chain residue 12-17 segment of i

146 than observed for influx; 3) mutant Glu325 - Ala does little or no efflux in the absence or presence

147 of the 20 common amino acids, including Gly, Ala, Ser, Thr, Asp, and Glu, which are relatively silent

148 erically hindered amino acid junctions (Gly, Ala, Trp, Glu).

149 tide H(2)N-(CH(2))(4)-CO-Pro-Leu-Arg-Phe-Gly-Ala-NH-CH(2)-Fc is the optimal probe for cathepsin B.

150 n permeation pathway and buttresses the 'Gly-Ala-Ser' (GAS) constriction, thus providing a structural

151 code PORB mutant proteins with defined Cys-->Ala exchanges.

152 e of the enzyme, as encountered in (Cys276-->Ala)-PORB plants.

153 oenzyme, PORA, as encountered with (Cys303-->Ala)-PORB plants, caused more severe effects than replac

154 or Leu(14)) and incorporated specific [(2)H]Ala labels within the helical core sequence.

155 On the other hand, Ala substitutions for Thr422 and Arg429 caused relativel

156 m Arabidopsis, ADS1.2 and ADS1.4, which have Ala and Gly, respectively, in place of the gatekeeping T

157 ection of the non-phosphorylatable hRXRalpha Ala-260 mutant.

158 cted with the non-phosphorylatable hRXRalpha Ala-260 mutant.

159 ncentration of a conjugated form of IAA (IAA-Ala).

160 e domains; and (iii) a single, inconspicuous Ala-to-Ser substitution in the catalytic site was key to

161 The functional effects of individual Ala substitutions in alphaM4 were found to be additive,

162 the subcellular localization of PC7 and its Ala variants of Leu-725 and Glu-719 and Glu-721 revealed

163 ides mimicking this region of the CT and its Ala variants revealed that the three exposed residues ar

164 abiotic samples (seven enantiomer pairs d/l-Ala, -Asp, -Glu, -His, -Leu, -Ser, -Val and the three ac

165 1-->4)-1,6-anhydro-N-acetyl-beta-d-muramyl-l-Ala-gam ma-d-Glu-meso-DAP-d-Ala-d-Ala and 1,6-anhydro-N-

166 pressor ligand UDP-N-acetyl-beta-d-muramyl-l-Ala-gamma-d-Glu-meso-DAP-d-Ala-d-Ala and binds to two ac

167 la and 1,6-anhydro-N-acetyl-beta-d-muramyl-l-Ala-gamma-d-Glu-meso-DAP-d-Ala-d-Ala, as assessed by non

168 ind to 1,6-anhydro-N-acetyl-beta-d-muramyl-l-Ala-gamma-d-Glu-meso-DAP.

169 selection resulting in a critical error of L-Ala mischarged onto tRNA(Thr), which is proofread by Ani

170 of the native L3P as D-Phe-N-Methyl-L-Val-L-Ala-OMe attached in N-ter to a 20-carbon fatty acid chai

171 ed with pH levels, whereas (13)C Bicar/Lac + Ala and (13)C Bicar/tC levels were positively correlated

172 ac/tC, and lower ratios of (13)C Bicar/Lac + Ala and (13)C Bicar/tC than those of the AMI/R group.

173 Keratin mutation (Arg-to-Lys/Ala) at the methylation sites, but not the acetylation s

174 wed estimation of the following metabolites: Ala, NAA, Glu, Gln, Ins, Cho, Cr, PCr, Tau, GABA, Lac, N

175 nthetase (ProRS) misactivates and mischarges Ala and Cys, which are similar in size to cognate Pro.

176 ted with azide and alkyne at its termini, N3-Ala-Val-NHCH2-C identical withCH, which is designed to s

177 ural amino acid, isothiocyanyl alanine ((NCS)Ala = Ita), for the synthesis of another class of unnatu

178 Next, Ala-scanning of the five Asp residues preceding the acti

179 rystal structures of ligase-defective NgrRnl-Ala mutants in complexes with ATP/Mn2+.

180 tapeptide Boc-(R)-Aic(NN)-(Ala)2-(R)-Aic(NN)-Ala-OMe and the hexapeptide Boc-[Ala-(R)-Aic(NN)-Ala]2-O

181 OMe and the hexapeptide Boc-[Ala-(R)-Aic(NN)-Ala]2-OMe as well.

182 and i+3 of the pentapeptide Boc-(R)-Aic(NN)-(Ala)2-(R)-Aic(NN)-Ala-OMe and the hexapeptide Boc-[Ala-(

183 tistical significance in the distribution of Ala/Val genotype between suicide attempters and non-atte

184 of vascular nitrate supply had no impact on Ala accumulation during secretion, suggesting that necta

185 oriented lipid bilayers by using (2)H-NMR on Ala-d3-labeled peptides, which yielded orientation-depen

186 s residue, which is a Tyr in LodA, to Tyr or Ala eliminates the cooperativity and destabilizes the di

187 Analyzed in aggregate, both PEP/Ala and PEP/Fru-1,6-BP coupling were again fully tunable

188 The Phe, Ala, and Dap/Asn residues were successively removed to g

189 A and RhsB effectors of ECL both contain Pro-Ala-Ala-Arg (PAAR) repeat domains, which bind the beta-s

190 To our knowledge, the peptides Gly-Pro-Ala-Val, Val-Cys, and Phe-Phe have not been previously i

191 on of a long, defined-length, N-terminal Pro/Ala/Ser (PAS) random-coil polypeptide with IL-1Ra.

192 n synthase kinase (GSK3beta) site in the Pro/Ala-rich linker of C0-C2 did not significantly affect th

193 yielded potent MC4R ligands, while replacing Ala with Ser maintained MC4R potency.

194 TMSs) and cytoplasmic domains, with residues Ala(463) and Cys(466) buried within the trimer interface

195 ergy when RhoA is complexed with RhoGAPArg85'Ala relative to wild-type (WT) RhoGAP.

196 hate measurements confirmed that single-site Ala substitutions reduced receptor phosphate levels more

197 dentified as changing in this silent system (Ala as the effector) were included in changes previously

198 stalled peptide, as shown during C-terminal Ala and Thr addition (CAT-tailing) in yeast.

199 Moreover, the N-terminal Ala-1-Ser-30 region of cE5 (which includes an RGD tripep

200 odifies stalled NCs with a carboxy-terminal, Ala- and Thr-containing extension-the 'CAT tail'.

201 buffer at 37 degrees C; 45-fold faster than Ala-AMP and 120-fold faster than Phe-AMP.

202 y of channel activity, and here we show that Ala or Cys substitutions of the functionally equivalent

203 ntial sites of phosphorylation, we show that Ala substitutions of Ser-561 and Ser-641/Thr-642 recapit

204 Positions near the Ala binding site had rheostatic outcomes on allosteric c

205 deprotonation, His-123 acts to protonate the Ala-enamine intermediate, and Arg-56 facilitates catalys

206 therein that supplied the codons for one Thr-Ala-Ala unit from which the extant repetitive AFGP-codin

207 c residues in the activation peptide through Ala mutagenesis results in a mutant activated by thrombi

208 l with a phosphorylation-defective Ser-16 to Ala-16 substitution in AMELX.

209 osphorylation sites at Thr-70 and Ser-166 to Ala resulted in a loss of KIN10-dependent phosphorylatio

210 Substitutions of Lys-20 and Lys-31 to Ala in the FABP1 helical cap affected neither its nuclea

211 The Trp-38 to Ala substitution resulted in increased off-rates and dec

212 Using GSK3beta Ser(389) to Ala mutant mice, we show that failure to inactivate nucl

213 Dual substitution of Asp-219 and Glu-447 to Ala sustained pH-independent activity over a broad range

214 Site-directed mutagenesis of Thr-48 to Ala (T48A) to prevent phosphorylation enhanced dopamine

215 lso show that mutating Thr(60) or Ser(64) to Ala increases the half-life of UNG2, reduces the rate of

216 Interestingly, mutation of Arg99 to Ala had no impact on the overall structure and affinity

217 We engineered a DUB mutation (Asp1772 to Ala) into a murine coronavirus and evaluated the replica

218 agenesis of all six Cys residues in ATIII to Ala resulted in its efficient secretion even though the

219 d NBP35 protein in combination with Cys14 to Ala substitution had distorted leaf development and decr

220 E2 interaction was not disrupted by Cys14 to Ala substitution.

221 Substitution of Cys14 to Ala, which destabilized the N-terminal Fe4 S4 cluster in

222 b' domain of PDI, and mutation of His256 to Ala abolishes BAP2 analogue activity.

223 Systematic mutagenesis of His583 to Ala, Asp, Asn, Glu, Gln, Lys, Phe, Tyr, and Trp showed t

224 A Leu to Ala amino acid substitution approximately 10 A from the

225 Substitution of Lys51 to Ala in LC3B abrogates binding of a phosphomimetic Nix mu

226 r multiple residues of hERG1 were mutated to Ala or Cys and the resulting mutant channels were hetero

227 c mice in which Ser367 of PS1 was mutated to Ala, show dramatic increases in Abeta peptide and in bet

228 Mutation to Ala of specific residues in the S1 (Tyr420), S2 (Leu452,

229 f this tyrosine was confirmed by mutation to Ala, leading to drastic loss of enzymatic activity.

230 e to ASP loop residues, an additional Phe to Ala substitution was synthesized and observed to maintai

231 Mutation of each amino acid in PSLFQ to Ala identified both Leu and Phe as independently essenti

232 rsion of the five key amino acids (PSLFQ) to Ala, or deletion of PSLFQ in the context of full-length

233 Thus, mutation of any of these residues to Ala abrogated zinc transfer from AztD.

234 Substitution of Arg 289 in Rrp9 to Ala (R289A) specifically reduced cleavage at sites A1 an

235 lation sites to non-phosphorylatable (Ser to Ala, SA) or phosphomimetic residues (Ser to Glu, SE) red

236 n sites identified, the mutation of Ser68 to Ala (Ser68Ala) was sufficient to inhibit Panx3-mediated

237 Mutation of Thr233 to Ala disrupts this elaborated interaction network, and de

238 el mouse line harboring a knock-in Thr607 to Ala (Kv4.2TA) mutation that abolished dynamic Pin1 bindi

239 mutation of the conserved N-terminal Trp8 to Ala both promote an inward-facing state.

240 d ubiquitin variant that contains two Val to Ala mutations.

241 Mutating CcpA Val301 to Ala (strain 2221-CcpA-V301A) abolished interaction betwe

242 Site-directed (Arg-to-Ala) mutagenesis of this cleavage site abolished matript

243 Ten single Asn-to-Ala substitutions at the predicted N-glycosylation sites

244 hosphoesterase activity, we generated His-to-Ala variants and examined their ability to negatively re

245 o-Val mutation at SP1 residue 1 and a Pro-to-Ala mutation at CA residue 157 within the major homology

246 f Ser-314 phosphorylation either with Ser-to-Ala substitution or with a specific inhibitor of CDK4/6

247 -in mice bearing phospho-deficient Ser999-to-Ala (S999A) and phospho-mimetic (S999D) mutations.

248 iciently mischarged, no corresponding Thr-to-Ala mistranslation is detectable.

249 cer was specifically tested by p27 Thr187-to-Ala knockin (p27T187A KI), it was found dispensable for

250 wild-type Rca-beta or Rca-beta with Thr78-to-Ala (T78A) or Thr78-to-Ser (T78S) site-directed mutation

251 The Thr92-to-Ala substitution (Ala92-D2) caused ER stress and activat

252 were evaluated along with two control Val-to-Ala substitutions.

253 obust proofreading activity of ThrRS towards Ala-tRNAThr.

254 NA synthetase (AlaRS) and can form BMAA-tRNA(Ala) by escaping from the intrinsic AlaRS proofreading a

255 conditions, yeast tRNA(Phe) and E. coli tRNA(Ala) transcripts fold in a single, cooperative transitio

256 over, DTD's activity on non-cognate Gly-tRNA(Ala) is conserved across all bacteria and eukaryotes, su

257 ure can efficiently edit mischarged Gly-tRNA(Ala) species four orders of magnitude more efficiently t

258 The structures explain how tRNA(Ala) is selected via anticodon reading during recruitmen

259 ively selects the universally invariant tRNA(Ala)-specific G3*U70.

260 ng hinge-like movements in RqcH leading tRNA(Ala) into a hybrid A/P-state associated with peptidyl-tr

261 or, senses the obstruction and recruits tRNA(Ala(UGC)) to modify nascent-chain C termini with a polya

262 nomethylaniline-diglycolic acid-DPhe-Gln-Trp-Ala-Val-Gly-His-Leu-NHEt), showing excellent tumor local

263 ino-1-carboxymethyl-piperidine-d-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2 ((68)Ga-RM2) is a synthetic

264 atural amino acids, thioureayl alanines ((TU)Ala = Tua).

265 three dipeptides, Tyr-Gly, Phe-Gly, and Tyr-Ala, from raw water demonstrates a useful application of

266 3,5-Di-I-Tyr-Ala and N-Br-Tyr-Ala were detected in treated water but not in the corres

267 -Cl-Phe-Gly, N-Cl-Tyr-Ala, and N,N-di-Cl-Tyr-Ala along with their corresponding dipeptides were detec

268 -Cl-Phe-Gly, N-Cl-Tyr-Ala, and N,N-di-Cl-Tyr-Ala were identified as the major products based on accur

269 y, N,N-di-Cl-Tyr-Gly, N-Cl-Phe-Gly, N-Cl-Tyr-Ala, and N,N-di-Cl-Tyr-Ala along with their correspondin

270 y, N-Cl-Phe-Gly, N,N-di-Cl-Phe-Gly, N-Cl-Tyr-Ala, and N,N-di-Cl-Tyr-Ala were identified as the major

271 3,5-Di-I-Tyr-Ala and N-Br-Tyr-Ala were detected in treated water but

272 n surrounding the C-terminal Glu-Pro-Ile-Tyr-Ala (EPIYA) motifs as well as the number of EPIYA motifs

273 Oxidation of Tyr-Ala-Ala-Ala-Arg (YAAAR) produces Tyr-O radicals by combi

274 We show that the loss of the C-terminal Tyr-Ala-Met-Leu motif is responsible for P0 mislocalization,

275 yrosylglycine (Tyr-Gly), tyrosylalanine (Tyr-Ala), and phenylalanylglycine (Phe-Gly), reacted with so

276 alanylglycine (Phe-Gly), tyrosylalanine (Tyr-Ala), and tyrosylglycine (Tyr-Gly), under chloramination

277 his exquisite fine specificity, we undertook Ala substitution assays revealing that the p7 residue (L

278 sed VH4-34-encoded antibodies with unmutated Ala-Val-Tyr and Asn-His-Ser motifs, which recognize both

279 talled translation, during which untemplated Ala/Thr residues are added C terminally to stalled pepti

280 by changing every amino acid residue to Val, Ala, or Gly, and then screening the drug resistance phen

281 estigated three mutant forms (I14X; X = Val, Ala, Gly) of the enzyme that have increased active site

282 ould produce the tripeptide Phe-N-Methyl-Val-Ala with a lipid moiety, termed lipotripeptide (L3P).

283 CL-derived peptide with the sequence Ser-Val-Ala-Phe-Ser (SVAFS) displayed robust blocking activity a

284 ubstitutions had no effect or increased Vmax Ala but not Glu substitution for Ser-497 increased the M

285 eplacement of either Leu-395 or Phe-396 with Ala led to inactivation of MGAT4D-L inhibitory activity.

286 titution of Arg-8 in subunit e (eArg-8) with Ala or Glu or of Glu-83 in subunit g (gGlu-83) with Ala

287 Glu or of Glu-83 in subunit g (gGlu-83) with Ala or Lys destabilized the digitonin-extracted F-ATP sy

288 sitioned because of a significant clash with Ala-558.

289 plants expressing PORB mutant proteins with Ala substitutions of Cys276 or Cys303 are hypersensitive

290 5G variants in which Tyr-15 is replaced with Ala or Gly, respectively, are monomeric.

291 fully maintained when Cys63 is replaced with Ala or Val.

292 nverted Cys-Pro motif had been replaced with Ala residues fails to bind hemin with high affinity.

293 in the binding tunnel had been replaced with Ala.

294 Replacement of a conserved Lys residue with Ala abolished the in vitro RNA-binding and TATase activi

295 d seven C-terminal Lys and Arg residues with Ala and added a Cys residue at either position 289 or 27

296 n of four aromatic/hydrophobic residues with Ala dramatically impairs both IAPP self-assembly and het

297 We substituted Val285 with Ala (V285A) in an Ala-Val dipeptide, to mimic the conser

298 e differential susceptibility of X-Pro and X-Ala bonds to ERAP1 trimming and together resulted in a s

299 ) with previously reported Gly -> Xaa (Xaa = Ala, Arg, or Val) vEDS substitutions within a high-affin

300 active loop derivative c[Pro-Arg-Phe-Phe-Xxx-Ala-Phe-DPro], where Xxx was the native Asn of AGRP or a