ライフサイエンスコーパス: Ala

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

2 of the delta-aminolevulinate synthase gene (Alas).

3 in the binding tunnel had been replaced with Ala.

4 ing follow-up exams showed regression of the ALA.

5 e most tightly controlled enzyme upstream of ALA.

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

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

8 ove the therapeutic efficacy of MRgFUS and 5-ALA.

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

10 iants of PEPT2 have different affinities for ALA.

11 lpX and provide it with a grip for acting on ALAS.

12 uired for mtClpX to gate cofactor binding to ALAS.

13 10.3 mum The improvements obtained with both Ala(101) and Leu(106) have implications regarding glypho

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

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

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

17 acids (PUFAs) such as alpha-linolenic acid (ALA, 18:3Delta(9) (cis) (,12) (cis) (,15) (cis) ) have h

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

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

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

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

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

23 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),

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

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

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

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

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

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

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

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

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

33 Unexpectedly, we found that ALA activation promotes RIS depolarization.

34 f PVD somatosensory neurons independently of ALA activity.

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

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

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

38 The restoration of mitochondrial function by ALA/ALC was accompanied by a reversal of arborization de

39 sed by Alpha Lipoic Acid/Acetyl-L-Carnitine (ALA/ALC) but not by other chemicals previously identifie

40 However, ALA alone also exhibited no bactericidal activity and di

41 5-ALA alone and FUS alone did not improve survival.

42 umor growth response for animals receiving 5-ALA alone, FUS alone, 5-ALA + FUS and a sham control gro

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

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

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

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

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

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

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

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

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

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

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

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

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

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

57 3,5-Di-I-Tyr-Ala and N-Br-Tyr-Ala were detected in treated water but

58 Notably, ALA and PBG concentrations in the cerebral spinal fluid

59 plasma, but not in the CNS, indicating that ALA and PBG do not readily cross the blood-brain barrier

60 T1/T2 mice were administered phenobarbital, ALA and PBG markedly accumulated in their liver and plas

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

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

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

64 ripeptide stems lacking the terminal d-ala-d-ala and reduced peptidoglycan cross-linking, prompting u

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

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

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

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

69 LET is a complex of human alpha-lactalbumin (ALA) and oleic acid and kills several Gram-positive bact

70 ed plasma and urinary 5-aminolevulinic acid (ALA) and porphobilinogen (PBG), profound early-onset ata

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

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

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

74 of flax (Linum usitatissimum) is enriched in ALA, and this plant has many lipid biosynthetic enzymes

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

76 s and an Ala306-Phe307-Arg308 motif of human ALAD are important for [Fe(4)S(4)] cluster acquisition a

77 Aminophospholipid ATPases (ALAs) are lipid flippases involved in transporting speci

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

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

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

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

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

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

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

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

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

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

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

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

90 PVD 1 degrees dendrites mimic ALA axon guidance defects in loss-of-function mutants fo

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

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

93 Both HAMLET and ALA bound directly to each glycolytic enzyme in solution

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

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

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

97 w UV active derivative of alpha-lipoic acid (ALA) by its esterification with 4-methoxybenzyl alcohol

98 iosynthesis, 5-aminolevulinic acid synthase (ALAS), by promoting cofactor incorporation.

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

100 ve transcranial MRgFUS in conjunction with 5-ALA can produce an inhibitory effect on rat brain tumor

101 5'-aminolevulinate synthase (ALAS) catalyzes the first step in heme biosynthesis, gen

102 Members of the third ALA cluster are at least partially interchangeable, as t

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

104 many lipid biosynthetic enzymes that prefer ALA-containing substrates.

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

106 with tripeptide stems lacking the terminal d-ala-d-ala and reduced peptidoglycan cross-linking, promp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

128 n murine tumors within 2 hours of systemic 5-ALA delivery.

129 ALA-dependent drowsiness, rather than RIS-dependent slee

130 plemented diets increased the egg content in ALA, DHA, RmA, as well as alpha-ESA or PunA.

131 7, and -5 fatty acids, alpha-linolenic acid (ALA), docosahexaenoic acid (DHA), rumenic acid (RmA), an

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

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

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

135 tly increased the omega-3 PUFA, particularly ALA, EPA, DPA, and DHA of broiler chicken meat due to th

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

137 activity in whole cells after HAMLET but not ALA exposure.

138 l patients received 5-aminolevulinic acid (5-ALA) fluorescence guidance surgery and postoperative tem

139 to evaluate the efficacy and safety of oral ALA for the treatment of geographic atrophy (GA).

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

141 animals receiving 5-ALA alone, FUS alone, 5-ALA + FUS and a sham control group were evaluated with M

142 urvival were significantly improved in the 5-ALA + FUS group with 32 degrees C or 37 degrees C as the

143 p, and 26 participants (36 eyes) were in the ALA group.

144 2) mm and 0.31 (0.02) mm for the placebo and ALA groups, respectively (difference, 0.04 mm; 95% confi

145 4) mm and 0.32 (0.05) mm for the placebo and ALA groups, respectively (difference, 0.05 mm; 95% CI, -

146 of 36) and 14% (5 of 36) in the placebo and ALA groups, respectively (P = 0.54).

147 rious AEs (P = 0.28) between the placebo and ALA groups.

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

149 Results do not support ALA having beneficial effects on GA or BCVA.

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

151 the obtained compound for quantification of ALA in food items was examined using HPLC-UV and GC-MS s

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

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

154 It was found that it is possible to assay ALA in the ester form in the concentration ranges: 5.10(

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

156 ocedure was applied for the determination of ALA in the food samples.

157 t NSCLC models fluoresce after exposure to 5-ALA in vitro.

158 abidopsis (Arabidopsis thaliana) contains 12 ALAs in five phylogenetic clusters, including four in cl

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

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

161 10-minute or 20-minute aminolevulinic acid (ALA) incubation times, after pretreatment with a microne

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

163 gave the same phenotype of aminolevulinate (ALA)-inducible uroporphyria as found in Leishmania subge

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

165 ALA intake was not associated with advanced AMD in eithe

166 lipids did not affect the conversion rate of ALA into DHA.

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

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

169 Our results suggest that ALA is a drowsiness neuron with two separable functions:

170 ProXp-ala is another editing domain that clears Ala-tRNAPro in

171 The enzymatic activity of human ALAD is greatly reduced upon loss of its Fe-S cluster, w

172 Alpha lipoic acid (ALA) is a nutraceutical and potent antioxidant that has

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

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

175 Amoebic liver abscess (ALA) is the most common extraintestinal manifestation of

176 Synthesis of 5-aminolevulinic acid (ALA) is the rate-limiting step in tetrapyrrole biosynthe

177 requires the sleep-promoting neurons RIS and ALA, it is not accompanied by decreased arousability, an

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

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

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

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

182 Elevated serum-PC EPA and ALA levels at the time of STEMI were associated with a l

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

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

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

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

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

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

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

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

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

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

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

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

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

196 in Caenorhabditis elegans, the axons of the ALA neuron control guidance and extension of the 1 degre

197 Activation of EGFR signaling in the ALA neuron has previously been suggested to promote slee

198 indirect mechanism through activation of the ALA neuron that acts upstream of the sleep-active RIS ne

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

200 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.

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

202 5G variants in which Tyr-15 is replaced with Ala or Gly, respectively, are monomeric.

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

204 icipants were randomized to 1200 mg daily of ALA or placebo.

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

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

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

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

209 Whereas ALA plays a strong role in surviving cellular stress, su

210 tuple mutants confirmed the crucial roles of ALA proteins in regulating plant development as well as

211 As ALAD provides an early Fe-S-dependent checkpoint in the

212 red the association of alpha-linolenic acid (ALA, proxy for vegetable omega-3 intake) with all-cause

213 of PVD 1 degrees dendrites and maintain the ALA-PVD axon-dendritic fascicle, respectively.

214 ectron system confined to a modulation-doped AlAs quantum well.

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

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

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

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

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

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

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

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

223 ent clones were obtained and were invariably ALA-responsive, albeit to different extent for uroporphy

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

240 patial datasets, store files and link to the ALA spatial portal, improve graphics and provide the nov

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

242 ccumulation of heme, induced by feeding with ALA, stimulates Clp-protease-dependent degradation of Ar

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

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

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

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

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

248 Although an Ala substitution locally destabilized hydrogen bonding a

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

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

251 9A, containing a threonine (Thr) to alanine (Ala) substitution at amino acid 79, failed to induce the

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

253 Ala substitutions for aromatic residues at the alphaM4-a

254 Even Ala substitutions for coevolved pairs of residues at the

255 Ala substitutions for most alphaM4 residues, including t

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

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

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

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

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

261 orphyrin IX (PPIX)/5-aminiolevulinic acid (5-ALA) system.

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

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

264 ubtilis RQC complexes representing different Ala tail synthesis steps.

265 Ala tailing thus follows mechanistic principles surprisi

266 fied sequence and structural features within ALAS that position mtClpX and provide it with a grip for

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

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

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

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

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

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

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

274 Ala-tRNAPro is specifically hydrolyzed by the editing do

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

276 obust proofreading activity of ThrRS towards Ala-tRNAThr.

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

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

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

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

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

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

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

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

285 Observation of ALAS undergoing remodeling by mtClpX revealed that unfol

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

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

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

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

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

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

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

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

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

295 Serum-PC ALA was inversely related to all-cause mortality (HR: 0.

296 5-aminolevulinic acid (5-ALA) was injected at a dose of 60 mg/kg six hours before

297 3,5-Di-I-Tyr-Ala and N-Br-Tyr-Ala were detected in treated water but not in the corres

298 that human aminolevulinic acid dehydratase (ALAD), which catalyzes the second step of heme biosynthe

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

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

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

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