ライフサイエンスコーパス: Ala

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

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

3 ntrations of cis ALA and one isomer of trans ALA.

4 yclic hexapeptide with replacement of Cys by Ala.

5 red and unfavoured isomerisation pathways of ALA.

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

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

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

9 idues, one or two arginines were replaced by Ala.

10 ished when all Phe residues were modified to Ala.

11 iants of PEPT2 have different affinities for ALA.

12 he analysis of the adipose tissue content of ALA.

13 -L mutant, in which Pro(205) was replaced by Ala.

14 l; they shared the substitution HA2-Asp19Asn/Ala.

15 reported to mediate heme-induced turnover of ALAS.

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

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

18 ega-3 (n-3) fatty acid alpha-linolenic acid (ALA, 18:3; n-3) may reduce coronary heart disease (CHD)

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

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

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

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

23 lexes due to the evolutionary replacement of Ala(241) with Gly.

24 Thus, the alanine residue Ala(254) determines voltage-dependent rectification upon

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

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

27 assembling homotrimeric protein with [Fe(Bpy-ala)3](2+) complexes at the interface between monomers.

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

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

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

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

32 The relation between alpha-linolenic acid (ALA), a plant-derived omega-3 (n-3) fatty acid, and age-

33 Total daily intakes of ALA, AA and DHA were below, whereas LA was above the rec

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

35 During AIP, delta-aminolevulinic acid (ALA) accumulates and promotes tubular cell death and tub

36 te the association between dietary intake of ALA, adipose tissue content of ALA, and risk of incident

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

38 Oxidation of Ala-Ala-Ala-Tyr-Arg (AAAYR) produces a mixture of cation

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

40 her high-LCPUFA or low in LCPUFA but high in ALA, allowing us to separate the effects of direct LCPUF

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

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

43 A combined approach of Ala-amino acid scan, NMR, and molecular modeling unravel

44 Alas, an exact computation of the entanglement dynamics

45 -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-

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

47 responsible for the delayed metabolism of 5-ALA and accumulation of protoporphyrin IX (PpIX) in the

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

49 of a large number of amino acids, including Ala and gamma-amino butyric acid, indicating a role of o

50 evaluate the associations between intake of ALA and intermediate and advanced AMD.Seventy-five thous

51 edictor of erythrocyte concentrations of cis ALA and one isomer of trans ALA.

52 ary intake and the adipose tissue content of ALA and risk of MI, but these associations were not stat

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

54 GLY, alanine (ALA), and serine (SER) all resulted in remarkable suppre

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

56 tween adipose tissue n-3 FAs (total n-3 FAs, ALA, and EPA plus DHA) and insulin resistance in healthy

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

58 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

59 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

60 ary intake of ALA, adipose tissue content of ALA, and risk of incident myocardial infarction (MI).

61 200-residue polypeptide tag comprising Pro, Ala, and Ser (PAS200) and by fusion with an albumin-bind

62 Crystal structures of two forms of human C-Ala, and small-angle X-ray scattering of AlaRS, showed t

63 l tubular cells mediates the reabsorption of ALA, and variants of PEPT2 have different affinities for

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

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

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

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

68 stration of hybrid 13a (H-Dmt-d-Arg-Aba-beta-Ala-Arg-Tyr-Tyr-Arg-Ile-Lys-NH2) to mice resulted in pot

69 Seven synthetases, Ala-, Arg-, Asp-, Asn-, Leu-, Lys- and TyrRS, appear to

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

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

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

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

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

75 iments amended with tetrapeptide ala-val-phe-ala (AVFA), a fragment of RuBisCO.

76 o examined the behavior of PAbetaN homologs, Ala beta-naphthylamide, Arg beta-naphthylamide, and Phe

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

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

79 iation of circulating plant-origin n-3 PUFA (ALA) but no convincing association of marine-derived n3

80 Direct DNA binding by human C-Ala, but not by bacterial C-Ala, was demonstrated.

81 European researchers reported that </=40% of ALA can be present as trans forms.We aimed to evaluate t

82 increases the posttranslational stability of ALAS, causing increased ALAS protein and ALA levels, lea

83 by hPDI therefore, step-wise peptide Phe-to-Ala changes were progressively introduced and shown to r

84 lly, even with a lower dose of just 1.75mg 5-ALA, coated microneedles suppressed the growth of subcut

85 When stratified by waist circumference, ALA continued to be inversely associated [third tertile:

86 amino acid (2,2'-bipyridin-5yl)alanine (Bpy-ala) could, in principle, be used to nucleate specific m

87 the skin (~480mum) as compared to topical 5-ALA cream formulation (~150mum).

88 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-

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

111 ministration of the heme precursors PP-IX or ALA + DFO into zebrafish larvae provides a new model of

112 of zebrafish livers from larvae administered ALA + DFO showed hepatocyte autophagosomes, nuclear memb

113 %, while a topical cream containing 5mg of 5-ALA did not suppress the tumor volume and led to tumor g

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

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

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

117 spect to total fatty acid content); however, ALA dropped (from 16% to 10%).

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

119 between adipose tissue alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic a

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

121 ALA reveals that the most highly expressed, ALA-enriched genes encode neuropeptides.

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

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

124 ociated with the regional heterogeneity of 5-ALA fluorescence in GBM.

125 mechanism underlying the heterogeneity of 5-ALA fluorescence in GBM.

126 umor microenvironments (TMEs), we utilized 5-ALA fluorescence-guided neurosurgical resection and samp

127 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-

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

129 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

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

131 ed heme precursor alpha-aminolevulinic acid (ALA), generates high levels of PP-IX in zebrafish larvae

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

133 ino acids in all fractions were dominated by Ala, Gly, Glu and Ser.

134 lass I viral fusion proteins, including high Ala/Gly content, intermediate hydrophobicity, and few ch

135 This study suggests that ALA has no appreciable association with risk of incident

136 phosphorylation site by mutating Thr(89) to Ala impaired localization of LPL to the actin-rich lamel

137 compared to topical application of 20% w/w 5-ALA in a conventional cream formulation (25mg cream).

138 equence divergence of human C-Ala reshaped C-Ala in a way that changed the global architecture of Ala

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

140 We also found trans ALA in mayonnaise samples.A high intake of ALA was assoc

141 present study was to determine the effect of ALA in patients undergoing simultaneous kidney-pancreas

142 ne biosynthesis, reduction of ester-linked D-Ala in teichoic acids, and reduction of peptidoglycan cr

143 1 to Asp in the double E loop and Gln-329 to Ala in the canonical THW loop enables the enzyme to prod

144 We identify a genetic code change, CUG-Ala, in Pachysolen tannophilus in the clade sister to th

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

146 However, expedited exposure of a 10-minute ALA incubation time did not reach significantly differen

147 with microneedle pretreatment at a 20-minute ALA incubation time significantly improved AK clearance

148 acy similar to that of a conventional 1-hour ALA incubation time.

149 10-minute or 20-minute aminolevulinic acid (ALA) incubation times, after pretreatment with a microne

150 ded surgery (FGS) using aminolevulinic-acid (ALA) induced protoporphyrin IX (PpIX) provides intraoper

151 play an essential role in the enrichment of ALA-induced PpIX in cancer cells during PDT.

152 eEF1A1 was found to enrich ALA-induced PpIX in cells by competitively blocking the

153 The presence of the proximal l-Ala instead of Gly in the common configuration of the pe

154 e-adjusted HR for intermediate AMD comparing ALA intake at the top quintile to the bottom quintile wa

155 ALA intake was not associated with advanced AMD in eithe

156 n interact with protein partners, ALIS1 (for ALA-interacting subunit1) or ALIS5, leading to different

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

158 of Tree Swallows to convert their precursor, ALA, into LCPUFA.

159 In human cells, C-Ala is also a splice variant of AlaRS.

160 alpha-lipoic acid (ALA) is a potent antioxidant that is used in patients wi

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

162 uided surgery using 5-aminolevulinic acid (5-ALA) is now a widely-used modality for glioblastoma (GBM

163 5-Aminolevulinic acid (ALA) is the first committed substrate of tetrapyrrole bi

164 ALA (mean +/- SD: 0.13% +/- 0.04%) and trans ALA isomers (0.05% +/- 0.01%) in 395 erythrocyte samples

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

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

167 through Ser(389) phosphorylation in Ser(389)Ala knockin mice causes a decrease in the fitness of cel

168 A designed beta-sheet-forming l-Ala-l-Val dipeptide containing azide and alkyne at its t

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

170 f approximately 300 site-directed mutants by Ala/Leu scanning mutagenesis, the expression of each mut

171 of ALAS, causing increased ALAS protein and ALA levels, leading to abnormal accumulation of PPIX.

172 ng process was optimized to achieve higher 5-ALA loading on microneedles and a high delivery efficien

173 iquid chromatography, we identified both cis ALA (mean +/- SD: 0.13% +/- 0.04%) and trans ALA isomers

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

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

176 es agonist to the same extent as ZnTerp upon Ala mutation of Ile-116(III:16/3.40), a residue that con

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

178 the beta-9 sheet of FGF14 where an alanine (Ala) mutation of Val-160 impaired binding to Nav1.6 but

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

180 ) is regulated by cytokine activation of the ALA neuron, which releases FLP-13 neuropeptides characte

181 endent activation of the EGF receptor in the ALA neuron.

182 he opioid pharmacophore H-Dmt-d-Arg-Aba-beta-Ala-NH2 (7) was linked to peptide ligands for the nocice

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

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

185 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

186 on microscopy established that coatings of 5-ALA on microneedles of the patch were uniform.

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

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

189 Mutation of the palmitoylated Cys residue to Ala or inhibition of protein palmitoylation decreased HC

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

191 two variants of ZIP8 with either an alanine (Ala) or a threonine (Thr) at residue 391.

192 nously derived from 5-aminolevulinic acid (5-ALA) or its derivatives, is a promising modality for the

193 l, linoleic acid (LA), alpha-linolenic acid (ALA), or ratios of betaine to choline and LA to ALA.The

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

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

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

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

198 broad pH profiles were observed for Leu- and Ala-pNA as substrates.

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

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

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

202 These results show that ALA preconditioning is capable of reducing inflammatory

203 e of a cardiac event compared with Pro/Pro + Ala/Pro genotypes in multivariate analysis (odds ratio,

204 ational stability of ALAS, causing increased ALAS protein and ALA levels, leading to abnormal accumul

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

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

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

208 anslation stress in cis triggered by the gly-ala repeat sequence of Epstein-Barr virus (EBV)-encoded

209 We generated Ala replacement mutants in this region of ENaC-alpha and

210 hat the large sequence divergence of human C-Ala reshaped C-Ala in a way that changed the global arch

211 tion of Xrn2-Thr439 to a nonphosphorylatable Ala residue caused phenotypes consistent with inefficien

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

213 otrophicus (Gd), which natively possesses an Ala residue in the position of the Ser ligand to the P-c

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

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

216 Single-cell RNA sequencing of ALA reveals that the most highly expressed, ALA-enriched

217 ither the motif between C1 and C2 or the Pro/Ala-rich linker (PAL) between C0 and C1.

218 -ala,SP metabolites +/- amiodarone, but no D-ala,RP metabolites were detected.

219 ll-derived cardiomyocytes (hiPSC-CMs), but D-ala,RP produgs, including MK-3682, did not.

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

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

222 ALA-SDT activated the caspase-3 and caspase-8 pathways i

223 Taken together, our data indicate that ALA-SDT mediates the switch from necroptosis to apoptosi

224 at caspase-3 activation peaked 4 hours after ALA-SDT treatment, 2 hours earlier than maximal caspase-

225 shown that endo-Protoporphyrin IX based SDT (ALA-SDT) could induce apoptosis in human tongue squamous

226 e-3 abolished the anti-necroptotic effect of ALA-SDT.

227 the reaction mechanism of AMSDH, we created Ala, Ser, Asp, and Gln mutants and studied them using bi

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

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

230 ds from PAGE gels reveal an abundance of Gly/Ala/Ser/Thr repeats exemplified by a prominent, previous

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

232 drug metabolite formation, yet exacerbated L-ala,SP + amiodarone effects, implicating the prodrugs in

233 ifference in intracellular accumulation of L-ala,SP metabolites +/- amiodarone, but no D-ala,RP metab

234 Cathepsin A (CatA) inhibitors attenuated L-ala,SP prodrug metabolite formation, yet exacerbated L-a

235 and metabolic conversion to UTP analog are L-ala,SP prodrug-dependent in cardiomyocytes.

236 Co-applied with amiodarone, L-ala,SP prodrugs increased beating rate and decreased bea

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

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

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

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

241 The effect of the Trp-38 to Ala substitution on on-rates was strongly dependent on t

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

243 al analysis demonstrated that the Glu(3) --> Ala substitution resulted in a molecular switch that was

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

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

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

247 dues for this, a mutant peptide KYE28A, with Ala substitutions at Phe(11), Phe(19), Phe(23), and Tyr(

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

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

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

251 ct observed for the small subset of Gly-to-d-Ala substitutions which are not stabilizing.

252 r mutant Drosophila Top2 with various Ser-to-Ala substitutions.

253 Alas, surviving early hazards, like prematurity or infec

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

255 RNA reductase (GluTR) as the first enzyme of ALA synthesis is encoded by HEMA genes and tightly regul

256 lation levels, and thereby the rate-limiting ALA synthesis.

257 ption, with an appended C-terminal domain (C-Ala) that is conserved from prokaryotes to humans but wi

258 hen supplemented with o-Tyr, cognate Phe, or Ala, the latter of which is not a substrate for activati

259 ), or ratios of betaine to choline and LA to ALA.The findings supported our hypothesis that early int

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

261 poiesis, heme biosynthesis, bioconversion of ALA to PPIX, and porphyrin-mediated phototoxic cell deat

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

263 convert the precursor 5-aminolevulinic acid (ALA) to PPIX appeared to reinforce this mechanism.

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

265 r and to the recipients; and (iii) recipient ALA-treated group.

266 eated control; (ii) donor and recipient (DR) ALA-treated, in which ALA was administered both to the d

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

268 ldR-DNA complex is inhibited upon binding of Ala, Tyr, Trp and Asp to the protein.

269 e composed of Leu-Val, Leu-Tyr, Gly-Tyr, and Ala-Tyr dissolved in DMSO-d6/GL (8:2, v/v) and of an apo

270 Oxidation of Ala-Ala-Ala-Tyr-Arg (AAAYR) produces a mixture of cation radical

271 ontaining 57 microneedles were coated with 5-ALA using an in-house developed micro-precision dip coat

272 Overall, the strategy of delivering 5-ALA using coated microneedles could be a promising appro

273 ics showed that delivery of just 350mug of 5-ALA using coated microneedles led to about 3.2-fold high

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

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

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

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

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

279 ntaining azide and alkyne at its termini (N3-Ala-Val-NHCH2C identical withCH, 1) was synthesized.

280 bation experiments amended with tetrapeptide ala-val-phe-ala (AVFA), a fragment of RuBisCO.

281 in the RlmN reaction, in which a Cys(118)-->Ala variant of the protein is cross-linked to a tRNA(Glu

282 nor and recipient (DR) ALA-treated, in which ALA was administered both to the deceased donor and to t

283 Dietary intake of ALA was assessed with the use of a validated semiquantit

284 s ALA in mayonnaise samples.A high intake of ALA was associated with an increased risk of intermediat

285 ohort, whereas the adipose tissue content of ALA was determined with the use of gas chromatography in

286 incides with the same time period when trans ALA was found in food and participants' blood; this find

287 Higher adipose tissue ALA was inversely associated with insulin resistance in

288 .13; 95% CI: -0.24, -0.01) of adipose tissue ALA was inversely associated with the HOMA-IR.

289 long-chain n-3 PUFAs, alpha-linolenic acid (ALA) was inversely associated with T2D (HR per standard

290 nding by human C-Ala, but not by bacterial C-Ala, was demonstrated.

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

292 on (Ser to Glu) or dephosphorylation (Ser to Ala) were mutated.

293 recursor omega-3 PUFA, alpha-linolenic acid (ALA), whereas terrestrial insects contain much lower lev

294 854 women for analyses of dietary intake of ALA, whereas 1994 men and 770 women were included in the

295 dermal delivery of 5-aminolevulinic acid (5-ALA), which naturally gets converted by cells of the tis

296 ctivation of delta-aminolevulinate synthase (ALAS), which catalyzes the first step of heme synthesis.

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

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

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

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