ライフサイエンスコーパス: alanyl

1 evis oocytes conferred a 48-fold increase in alanyl-[14C]phenylalanine uptake relative to water injec

2 idehydro-N-methylalanyl-L-alanyl-N-methyl-L-alanyl-(3R)-3-[[(2S,3R)-3-hydroxy-4- methyl-1-oxo-2-[(1-

3 D-Alanyl-ACP in the presence of LTA was not hydrolyzed.

4 catalyzed the hydrolysis of the mischarged D-alanyl-ACP.

5 d has thioesterase activity for mischarged D-alanyl-acyl carrier proteins (ACPs).

6 elevated acylation velocities with seryl and alanyl-adenylates.

7 hed peptides that most frequently carried an alanyl-alanine substituent on the epsilon amino group of

8 vity and can cleave the substrate N-succinyl-alanyl-alanyl-prolyl-phenylalanine-p-nitroanilide (SAAPF

9 l endopeptidase as well as N-acetylmuramyl-L-alanyl amidase activity.

10 sequence homology to known N-acetylmuramyl-L-alanyl amidases; however, their precise cleavage sites o

11 A series of water-soluble L-lysyl- and L-alanyl-amide prodrugs of the lipophilic antitumor 2-(4-a

12 d evaluated for their ability to detect beta-alanyl aminopeptidase activity in bacteria known to hydr

13 gh overall yield and were selective for beta-alanyl aminopeptidase activity in bacteria, producing a

14 Protocols that use microsomal alanyl aminopeptidase as a discovery-enabling agent are

15 Seven crystal structures of alanyl aminopeptidase from Neisseria meningitides (the e

16 Here, enzymatic digestion using microsomal alanyl aminopeptidase is combined with MS characterizati

17 The midgut-specific anopheline alanyl aminopeptidase N (AnAPN1) is highly conserved acr

18 Here we identify membrane alanyl aminopeptidase N (APN) as a receptor for pea enat

19 mycin-sensitive aminopeptidase (PSA, cytosol alanyl aminopeptidase).

20 t such hydrogen bonding may explain both the alanyl and amide I/III markers of PH75 capsid subunits a

21 pts of four specificities (valyl, methionyl, alanyl, and phenylalanyl) from higher plants or Escheric

22 It also acted at lower rates on beta-alanyl-arginine and gamma-aminobutyryl-arginine but virt

23 es to histidyl-tRNA synthetase (HisRS) or to alanyl-, asparaginyl-, glycyl-, isoleucyl-, or threonyl-

24 cause benzyloxycarbonyl-valyl-aspartyl-valyl-alanyl-aspartic acid fluoromethyl ketone (Z-VDVAD-FMK) t

25 RGD in the pro-toxin was changed to arginyl-alanyl-aspartic or to arginyl-glycyl-glutamic, were expr

26 otent antiapoptotic agent carbobenzoxy-valyl-alanyl-aspartyl(beta-methyl ester)-fluoromethyl ketone (

27 the pancaspase inhibitor carbobenzoxyl-valyl-alanyl-aspartyl-[O-methyl]-fluoromethylketone before the

28 to other cell wall subunits, in which the D-alanyl at position four was amide linked to the pentagly

29 Several possibilities exist for the alanyl beta-cation equivalent, including direct activati

30 ine involve the reaction of cysteine with an alanyl beta-cation equivalent.

31 city in glial expression of ebony, an N-beta-alanyl-biogenic amine synthase, and show that Ebony acti

32 circadian rhythm in Drosophila Ebony (N-beta-alanyl-biogenic amine synthetase) abundance can be visua

33 odification of the beta-position of the beta-alanyl carboxylate group of 29 had only a modest effect

34 dification at the alpha-position of the beta-alanyl carboxylate group resulted in the identification

35 -D-alanyl carrier protein ligase (Dcl) and D-alanyl carrier protein (Dcp), respectively.

36 carrier protein ligase (AMP) (Dcl) and the D-alanyl carrier protein (Dcp).

37 rrier protein ligase (Dcl) and the 8.9-kDa D-alanyl carrier protein (Dcp).

38 -positive organisms requires the D-alanine-D-alanyl carrier protein ligase (AMP) (Dcl) and the D-alan

39 D-alanine into LTA requires the D-alanine:D-alanyl carrier protein ligase (AMP-forming) (Dcl) and th

40 dltA and dltC encode the D-alanine-D-alanyl carrier protein ligase (Dcl) and D-alanyl carrier

41 cillus casei requires the 56-kDa D-alanine-D-alanyl carrier protein ligase (Dcl) and the 8.9-kDa D-al

42 cement of the dltA gene encoding d-alanine-d-alanyl carrier protein ligase in an invasive serotype M1

43 This DNA encoded D-alanine-D-alanyl carrier protein ligase that was expressed in Esch

44 incorporated into acyl carrier protein and D-alanyl carrier protein, the prosthetic groups of which a

45 s 7 with N-trifluoroacetyl-protected D- or L-alanyl chloride, followed by ketone reduction and N-depr

46 l-gamma-D-glutamyl-meso-2,6-diaminopimelyl-D-alanyl-D-alan ine as substrate, mutation of Asp155, Phe1

47 The VanX protein is a D-alanyl-D-alanine (D-Ala-D-Ala) dipeptidase essential for

48 The zinc-containing D-alanyl-D-alanine (D-Ala-D-Ala) dipeptidase VanX has been

49 tion of peptidoglycan precursors ending in D-alanyl-D-alanine (D-Ala-D-Ala) in glycopeptide-resistant

50 to encode amino acid racemases however, a D-alanyl-D-alanine (D-Ala-D-Ala) ligase homologue (Ddl) is

51 bacterial cell wall through binding to the D-alanyl-D-alanine (D-Ala-D-Ala) terminal peptide of the p

52 ctam antibiotics, are believed to catalyze d-alanyl-d-alanine carboxypeptidase and transpeptidase rea

53 c hedgehog and the Zn(2+)-dependent N-acyl-D-alanyl-D-alanine carboxypeptidase of S. albus G.

54 ctive site of the bifunctional serine type D-alanyl-D-alanine carboxypeptidase/transpeptidase (EC ) f

55 exchange was detected over temperature for D-alanyl-D-alanine carboxypeptidases (dac1 and dac2), DEAD

56 The crystal structures of VanX, the VanX:D-alanyl-D-alanine complex, the VanX:D-alanine complex, an

57 VanX is a zinc-dependent D-alanyl-D-alanine dipeptidase that is a critical componen

58 bination of this motif with the C-terminal D-alanyl-D-alanine moiety required of a DD-peptidase subst

59 hibit DD-peptidases because they mimic the D-alanyl-D-alanine motif of the peptidoglycan substrate of

60 tages of peptidoglycan synthesis, that the d-alanyl-d-alanine of the stem peptide and the lipid II N-

61 e thiols were reacted with either acryloyl-D-alanyl-D-alanine or haloalkanoyl-D-alanyl-D-alanines.

62 hibit this reaction because they mimic the D-alanyl-D-alanine peptide precursors of cell-wall structu

63 lanyl-D-iso-glutaminyl-meso-diaminopimelyl-D-alanyl-D-alanine peptides, with the exception of the pep

64 eptidases, because of their resemblance to D-alanyl-D-alanine peptides.

65 in peptidoglycan synthesis) by binding to D-alanyl-D-alanine stem termini in Gram-positive bacteria.

66 atalyze hydrolysis and aminolysis of small D-alanyl-D-alanine terminating peptides, especially those

67 iently catalyze acyl transfer reactions of D-alanyl-D-alanine terminating peptides.

68 The bacterial D-alanyl-D-alanine transpeptidases (DD-peptidases) are the

69 ntibiotics act through their inhibition of D-alanyl-D-alanine transpeptidases (DD-peptidases) that ca

70 Nevertheless, the bacterial D-alanyl-D-alanine transpeptidases (DD-peptidases), the ki

71 the final step of biosynthesis by specific D-alanyl-D-alanine(DD)-peptidases/transpeptidases.

72 ch as glycyl-L-alpha-amino-epsilon-pimelyl-D-alanyl-D-alanine, 1, contain the glycyl-L-alpha-amino-ep

73 tide, glycyl-l-alpha-amino-epsilon-pimelyl-d-alanyl-d-alanine, 1, is a very specific and reactive car

74 rate, glycyl-l-alpha-amino-epsilon-pimelyl-d-alanyl-d-alanine, has been described that is much more s

75 alent complex, vancomycin/diacetyl-L-lysyl-D-alanyl-D-alanine, obtained from ESI and from nanoelectro

76 anine-D-glutamate-meso-diaminopimelic acid-D-alanyl-D-alanine, whereas those isolated from lipid II f

77 The D-alanyl-D-alanine-adding enzyme encoded by the murF gene

78 gh site-directed mutagenesis of the murein D-alanyl-D-alanine-adding enzyme from Escherichia coli (mu

79 ormed on three virulent PAI proteins (Fic; D-alanyl-D-alanine-carboxypeptidase; transposase) dated th

80 catalyzes the hydrolysis and aminolysis of d-alanyl-d-alanine-terminating peptides by specific amines

81 valent complex vancomycin/diacetyl-L-lysyl-D-alanyl-D-alanine.

82 rate, glycyl-L-alpha-amino-epsilon-pimelyl-D-alanyl-D-alanine.

83 cryloyl-D-alanyl-D-alanine or haloalkanoyl-D-alanyl-D-alanines.

84 sotropic, and anisotropic Raman spectra of L-alanyl-D-alanyl-L-alanine, acetyl-L-alanyl-L-alanine, L-

85 a holin-like protein (ChiW) and a putative l-alanyl-d-glutamate endopeptidase (ChiX), and subsequent

86 ylococcus aureus MurE UDP-N-acetylmuramoyl-L-alanyl-D-glutamate:meso-2,6-diaminopimelate ligase (MurE

87 inal domain resembles UDP-N-acetylmuramoyl-L-alanyl-D-glutamate:meso-diaminopimelate ligase (MurE), y

88 Mycobacterial peptidoglycan contains L-alanyl-D-iso-glutaminyl-meso-diaminopimelyl-D-alanyl-D-a

89 ding protein for apoptotic N-acetylmuramyl-L-alanyl-D-isoglutamine (L,D-MDP) or peptidoglycan in RK(1

90 eoisomeric configuration of the dipeptide (L-alanyl-D-isoglutamine) moiety.

91 nist, N-acetylglucosaminyl-N-acetylmuramyl-l-alanyl-d-isoglutamyl-meso-diaminopimelic acid (GM-triDAP

92 tidoglycan chain precursors terminating in D-alanyl-D-lactate (D-Ala-D-lactate) rather than D-Ala-D-A

93 s and is distinct from previous models for d-alanyl-d-lactate ligase mechanistic studies.

94 The structure of d-alanyl-d-lactate ligase provides a revised interpretatio

95 The peptides N-(phenylacetyl)-D-alanyl-D-phenylalanine and N-(phenylacetyl)glycyl-D-phen

96 strate, 3-(N-glycyl-l-cysteinyl)-propanoyl-d-alanyl-d-thiolactate, that the enzyme hydrolyzes and ami

97 d-Alanyl:d-lactate (d-Ala:d-Lac) and d-alanyl:d-serine lig

98 d-Alanyl:d-lactate (d-Ala:d-Lac) and d-alanyl:d-serine ligases are key enzymes in vancomycin re

99 o this reaction inhibited the formation of D-alanyl-Dcp and stimulated the hydrolysis of D-alanyl-Dcp

100 In previous results it was shown that D-alanyl-Dcp donates its ester residue to membrane-associa

101 us, may determine the donor specificity of D-alanyl-Dcp in the D-alanylation of membrane-associated D

102 l-Dcp was functionally identical to native D-alanyl-Dcp in the incorporation of D-alanine into lipote

103 It was discovered that incubation of D-alanyl-Dcp in the presence of LTA resulted in the time-d

104 Dcp with D-alanine and that the resulting D-alanyl-Dcp is translocated to the primary site of D-alan

105 e and concentration-dependent formation of D-alanyl-Dcp was found.

106 The recombinant D-alanyl-Dcp was functionally identical to native D-alanyl

107 lanyl-Dcp and stimulated the hydrolysis of D-alanyl-Dcp.

108 ard the palladated pincer complexes with the alanyl derivative being the strongest overall, demonstra

109 tion of Ala-PG and a novel alanylated lipid, Alanyl-diacylglycerol (Ala-DAG).

110 Mass spectrometry analysis of aspartyl-alanyl diketopiperazine (DA-DKP) content of HSA and perc

111 disclose their cooperative activity in beta-alanyl-dopamine formation.

112 a mechanism for the transacylation of the D-alanyl ester residues between LTA and wall teichoic acid

113 ngle insertion in dltA exhibited a loss of D-alanyl esters in lipoteichoic acid (LTA) and a loss of i

114 - 1,6 - anhydro - N - acetylmuramyl - (L) - alanyl - gamma - (D) - glutamyl - meso - diaminopimelyl

115 A cephalosporin analogue, 7beta-[N-Acetyl-L-alanyl-gamma-D-glutamyl-L-lysine]-3-acetoxymethyl-3-ceph

116 Using N-acetylmuramyl-L-alanyl-gamma-D-glutamyl-meso-2,6-diaminopimelyl-D-alanyl

117 es, i.e., recycles, its murein tripeptide, L-alanyl-gamma-D-glutamyl-meso-diaminopimelate, to form ne

118 uptake of the cell wall murein tripeptide L-alanyl-gamma-D-glutamyl-meso-diaminopimelate.

119 pimelic acid bond in the murein tripeptide L-alanyl-gamma-D-glutamyl-meso-diaminopimelic acid, was de

120 placed by the cell wall murein tripeptide, L-alanyl-gamma-D-glutamyl-mesodiaminopimelate.

121 he GLN group (n = 75) received PN containing alanyl-GLN dipeptide (0.5 g/kg/d), proportionally replac

122 ng a perioperative supplement of intravenous alanyl-glutamine (0.5 g . kg(-1) . d(-1)).

123 g/ml) in medium with or without glutamine or alanyl-glutamine (3 to 100 mM).

124 -competence of PD fluid supplementation with alanyl-glutamine (AlaGln) in 6 patients in an open-label

125 Alanyl-glutamine (AQ) is a highly soluble dipeptide deri

126 taining unmethylated CpG motif (CpG-ODN) and alanyl-glutamine in vivo and in vitro.

127 Addition of alanyl-glutamine increased O-GlcNAcylation and partly co

128 Glutamine and alanyl-glutamine inhibited the apoptosis of T84 cells by

129 ast, increasing O-GlcNAc levels by PUGNAc or alanyl-glutamine led to significantly improved cell surv

130 ls and evaluate the effects of glutamine and alanyl-glutamine on TxA-induced apoptosis in vitro and d

131 Both glutamine and alanyl-glutamine reduced TxA-induced ileal mucosal disru

132 Alanyl-glutamine showed similar benefits.

133 Glutamine or alanyl-glutamine significantly reduced TxA-induced apopt

134 and its stable and highly soluble derivative alanyl-glutamine, have been beneficial in models of inte

135 ated the protective effects of glutamine and alanyl-glutamine.

136 an N-acetylmuramoyl-L-alanine amidase and D-alanyl-glycine endopeptidase.

137 onic model dipeptides, L-alanyl-L-alanine, L-alanyl-glycine, glycyl-L-alanine, and glycyl-glycine, in

138 e and mechanisms of LTA modifications with D-alanyl, glycosyl, and phosphocholine residues will be di

139 ce, phi11(Delta181-381), revealed that the D-alanyl-glycyl endopeptidase activity is contained within

140 Our results show that the phi11 enzyme has D-alanyl-glycyl endopeptidase as well as N-acetylmuramyl-L

141 The N-terminal L-alanyl group is needed for cellular import but not for i

142 ates beta-alanine to histamine, forming beta-alanyl-histamine or carcinine.

143 Carcinine (beta-alanyl-histamine) is a natural imidazole-containing pept

144 ndent ligase responsible for carnosine (beta-alanyl-histidine) and homocarnosine (gamma-aminobutyryl-

145 g lost its amino terminal dipeptide aspartyl alanyl (HSA-DA) were correlated.

146 methyl]-4-methylpentanoyl)-L-3-(tert-bu tyl)-alanyl-l -alanine, 2-aminoethyl amide), which has previo

147 Acetyl-L-alanyl-L-alanine exhibits a structure which is very simi

148 That d-alanyl-l-alanine shows little activity as an acceptor su

149 )- methyl]-4-methylpentano)-L-3-(tert-butyl)-alanyl-L-alanine, 2-aminoethyl amide, which blocks leuko

150 and anisotropic Raman spectra of L-alanyl-D-alanyl-L-alanine, acetyl-L-alanyl-L-alanine, L-vanyl-L-v

151 ies of four zwitterionic model dipeptides, L-alanyl-L-alanine, L-alanyl-glycine, glycyl-L-alanine, an

152 tra of L-alanyl-D-alanyl-L-alanine, acetyl-L-alanyl-L-alanine, L-vanyl-L-vanyl-L-valine, L-seryl-L-se

153 e synthetic substrate N-t-butyloxycarbonyl-L-alanyl-L-alanyl-L-aspartyl (Boc-Ala-Ala-Asp) thiobenzyl

154 ic substrate N-t-butyloxycarbonyl-L-alanyl-L-alanyl-L-aspartyl (Boc-Ala-Ala-Asp) thiobenzyl ester wit

155 unable to use the dipeptide carnosine (beta-alanyl-L-histidine) as a sole carbon or nitrogen source

156 g precursor of the dipeptide carnosine (beta-alanyl-l-histidine) in muscle.

157 The endogenous dipeptide carnosine (beta-alanyl-L-histidine), at 0.1-10 mM, provokes sustained co

158 , a methylated derivative of carnosine (beta-alanyl-L-histidine), is an abundant constituent of verte

159 +) and the natural dipeptide carnosine (beta-alanyl-L-histidine).

160 ted peptide prodrugs such as N-succinyl-beta-alanyl-L-isoleucyl-L-alanyl-L-leucyl-Dox (sAIAL-Dox).

161 nzoxy-L-isoleucyl-gamma-t-butyl-L-glutamyl-L-alanyl-L-leucinal (PSI), to rodents.

162 such as N-succinyl-beta-alanyl-L-isoleucyl-L-alanyl-L-leucyl-Dox (sAIAL-Dox).

163 PI-0004Na [N-succinyl-beta-alanyl-L-leucyl-L-alanyl-L-leucyl-Dox (sALAL-Dox)] has been shown to have

164 xorubicin (Dox), CPI-0004Na [N-succinyl-beta-alanyl-L-leucyl-L-alanyl-L-leucyl-Dox (sALAL-Dox)] has b

165 l --> gas exchange of Xe in self-assembled L-alanyl-L-valine (AV) nanotubes was facilitated by contin

166 oxycarbonyl-isoleucyl-glutamyl(O-tert-butyl)-alanyl-leucinal (PSI), could be a source of Ag-specific

167 tion of D-alanine into membrane-associated D-alanyl-lipoteichoic acid in Lactobacillus casei requires

168 n the D-alanylation of membrane-associated D-alanyl-lipoteichoic acid.

169 Thus, it is hypothesized that D-alanyl LTA may provide binding sites for the putative 10

170 Dcp was incubated with membrane-associated D-alanyl LTA, a time and concentration-dependent formation

171 ates on some "classic dipeptides" like alpha-alanyl-lysine and alpha-lysyl-lysine.

172 lotting showed coelution of PM20D2 with beta-alanyl-lysine dipeptidase activity.

173 heart, and brain contained a cytosolic beta-alanyl-lysine dipeptidase activity.

174 Recombinant mouse PM20D2 hydrolyzed beta-alanyl-lysine, beta-alanyl-ornithine, gamma-aminobutyryl

175 he accumulation of abnormal dipeptides (beta-alanyl-lysine, beta-alanyl-ornithine, gamma-aminobutyryl

176 2 (MMP2), interleukin (IL)-6, insulin (INS), alanyl (membrane) aminopeptidase (ANPEP), and IL-10 were

177 GC1 enzyme, also has space available for a D-alanyl methyl group because of an extended omega loop.

178 Molecular modeling showed that the D-alanyl methyl group fits snugly into the space originall

179 Accommodation of the penultimate D-alanyl methyl group is therefore necessary for efficient

180 of a H-bonding interaction between the 2'-O-alanyl moiety and the N-3 atom of the adenine nucleobase

181 f the glycyl-l-alpha-amino-epsilon-pimelyl-d-alanyl moiety to amines.

182 Anserine (beta-alanyl-N(Pi)-methyl-L-histidine), a methylated derivativ

183 phenylcarbamoyl-(S)-prolyl-(S)-3-(2-naphthyl)alanyl-N-benz yl- N-methylamide, SDZ NKT 343), a highly

184 zenepropanoyl-2,3- idehydro-N-methylalanyl-L-alanyl-N-methyl-L-alanyl-(3R)-3-[[(2S,3R)-3-hydroxy-4- m

185 bnormal dipeptides (beta-alanyl-lysine, beta-alanyl-ornithine, gamma-aminobutyryl-lysine), thus favor

186 e PM20D2 hydrolyzed beta-alanyl-lysine, beta-alanyl-ornithine, gamma-aminobutyryl-lysine, and gamma-a

187 The ester 4-((tosyl-l-alanyl)oxy)phenyl tosyl-l-alaninate (TAPTA) was synthesi

188 apable of hydrolyzing the substrate N-acetyl-alanyl-p-nitroanilide.

189 O-[N-(2,7-difluoro-4'-fluoresceincarbonyl)-L-alanyl]paclitaxel, a fluorescent paclitaxel derivative,

190 rcuit for the appropriate tuning of cellular alanyl-PG concentrations.

191 Consequently, PA0919 was termed alanyl-PG hydrolase.

192 say in the presence of radioactively labeled alanyl-PG then revealed hydrolysis of the aminoacyl link

193 9 indicated significantly enlarged levels of alanyl-PG.

194 ol (PG) catalyzed by Ala-tRNA(Ala)-dependent alanyl-phosphatidylglycerol synthase (A-PGS) or by Lys-t

195 s, such as histidyl (Jo-1), threonyl (PL-7), alanyl (PL-12), glycyl (EJ), and isoleucyl (OJ), are clo

196 The phenylalanyl-glycyl-glycyl-alanyl-prolyl (FG-GAP) domain plays an important role in

197 , which provides a general method to prepare alanyl proteins from their cysteinyl forms, can be used

198 f HPr is replaced with an unphosphorylatable alanyl residue are resistant to carbon catabolite repres

199 either a central pyridyl glycyl or a pyridyl alanyl residue between two terminally protected glycines

200 PacB catalyzes the transfer of the alanyl residue from alanyl-tRNA to the N terminus of the

201 ATP-dependent addition of D-glutamate to an alanyl residue of the UDP-N-acetylmuramyl-L-alanine prec

202 rium leprae, in which glycine replaces the L-alanyl residue.

203 e of covalent FAD attachment (Cys-406) to an alanyl residue.

204 In addition, both the glycyl and alanyl residues of the GXXXG or GXXXA motifs form van de

205 aration of lysyl charges by intercalation of alanyl residues reduced assembly promoting potency for h

206 When alanyl residues replaced all TMD residues except Ser(16)

207 0)-O(eq)-glycyl-ryanodine < C(10)-O(eq)-beta-alanyl-ryanodol, implying an inverse relationship with t

208 0)-O(eq)-glycyl-ryanodine > C(10)-O(eq)-beta-alanyl-ryanodol.

209 se inhibitor N-(N-[3,5-difluorophenacetyl]-l-alanyl)-S-phenylglycine t-butyl ester (DAPT) or followin

210 se inhibitor N-(N-(3,5-difluorophenacetyl)-l-alanyl)-S-phenylglycine t-butyl ester, supporting the co

211 ase inhibitor N-[N-(3,5-Difluorophenacetyl-L-alanyl)-S-phenylglycine]-t-butyl ester, which blocks Not

212 se inhibitors N-[N-(3,5-difluorophenacetyl-L-alanyl)]-S-phenylglycine t-butyl ester and L-685,458.

213 ibitor, DAPT (N-[N-(3,5-difluorophenacetyl-l-alanyl)]-S-phenylglycine t-butyl ester), reduces the sur

214 ted whether N-[N-(3,5-difluorophenylacetyl-l-alanyl)]-S-phenylglycine t-butylester (DAPT), a specific

215 mma-secretase inhibitor difluorophenacetyl-l-alanyl-S-phenylglycine t-butyl ester (DAPT) or dimethyl

216 ng inhibitor N-[N-(3,5-difluorophenacetyl)-l-alanyl]-S-phenylglycine t-butyl ester (DAPT) significant

217 Similarly N-[N-(3,5-difluorophenacetyl)-l-alanyl]-S-phenylglycine t-butyl ester (DAPT), a chemical

218 istration of N-[N-(3,5-difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (DAPT), a gamma-se

219 e inhibitor, N-[N-(3,5-difluorophenacetyl)-1-alanyl]-S-phenylglycine t-butyl ester (DAPT), or Notch1

220 e inhibitor, N-[N-(3,5-Difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (DAPT), which sign

221 se inhibitor N-[N-(3,5-difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester failed to promote

222 ibitor (GSI) N-[N-(3,5-difluorophenacetyl)-l-alanyl]-S-phenylglycine-t-butylester (DAPT), at a dose t

223 ase inhibitorN-[N-(3,5-difluorophenacetyl)-l-alanyl]-S-phenylglycinet-butyl ester negated the up-regu

224 ch inhibitor N-[N-(3,5-difluorophenacetyl)-L-alanyl]-(S)-phenylglycine t-butyl ester (DAPT) preferent

225 we show that N-[N-(3,5-difluorophenacetyl)-L-alanyl]-(S)-phenylglycine t-butyl ester, a potent gamma-

226 hat different rotameric states of the indole alanyl side-chain are responsible for the observed fluor

227 Alanyl-substituted and N-terminal truncated analogues id

228 tures, none of the single, double, or triple alanyl substitutions at arginyl residues significantly d

229 readily hydrolyzes and aminolyzes acyclic D-alanyl substrates than glycyl analogues, in contrast to

230 owever, no enhancement of activity against D-alanyl substrates with respect to glycyl was observed.

231 lycyl substrates but not for more specific d-alanyl substrates; hydroxy acids actually behave, more g

232 cysteinyl-sulfamoyl-, prolyl-sulfamoyl-, and alanyl-sulfamoyl-adenylates.

233 the presence of thiol probably proceeds via alanyl thioester, which is produced by rearrangement of

234 d in the time-dependent hydrolysis of this D-alanyl thioester.

235 A complex of alanyl-tmRNA (which functions as a tRNA and mRNA), SmpB

236 Biallelic mutations in the alanyl-transfer (t)RNA synthetase 2 (AARS2) gene were fo

237 tase autoantibody (anti-Jo-1) and 1 had anti-alanyl-transfer RNA synthetase autoantibody (anti-PL-12)

238 Ps in the coding regions of two human mRNAs: alanyl tRNA synthetase and replication protein A, 70-kDa

239 s that bacterial GlyRS is closely related to alanyl tRNA synthetase, which led us to define a new sub

240 e relatively easily altered to be charged by alanyl tRNA synthetase.

241 al neuropathy, demonstrating that defects of alanyl-tRNA charging can result in a wide spectrum of di

242 identified mutations in the nuclear-encoded alanyl-tRNA synthetase (AARS) in these two unrelated fam

243 ntly recognized by A. gossypii mitochondrial alanyl-tRNA synthetase (AgAlaRS).

244 tion of alanine-specific tRNA (tRNA(Ala)) by alanyl-tRNA synthetase (AlaRS) gave rise to the concept

245 Here we show that the class II alanyl-tRNA synthetase (AlaRS) has a specialized interna

246 Throughout evolution, tRNA(Ala) selection by alanyl-tRNA synthetase (AlaRS) has depended predominantl

247 Transfer of alanine from Escherichia coli alanyl-tRNA synthetase (AlaRS) to RNA minihelices that m

248 machinery provides MurM, quality control by alanyl-tRNA synthetase (AlaRS) was investigated.

249 ) that are associated with aminoacylation by alanyl-tRNA synthetase (AlaRS) were investigated in vivo

250 ypomorphic mutation in the editing domain of alanyl-tRNA synthetase (AlaRS), resulted in accumulation

251 major determinants for recognition by Dm mt alanyl-tRNA synthetase (AlaRS).

252 Paradoxically, although alanyl-tRNA synthetase activates glycine as well as alan

253 es of an active fragment of Aquifex aeolicus alanyl-tRNA synthetase complexed, separately, with Mg2+-

254 minihelix) lacked determinants for editing, alanyl-tRNA synthetase effectively cleared a mischarged

255 Alanyl-tRNA synthetase efficiently aminoacylates tRNAAla

256 Data on alanyl-tRNA synthetase from an early eukaryote and other

257 ssense mutation in the editing domain of the alanyl-tRNA synthetase gene that compromises the proofre

258 d, a small defect in the editing activity of alanyl-tRNA synthetase is causally linked to neurodegene

259 he AlaXp redundancy of the editing domain of alanyl-tRNA synthetase is thought to reflect an unusual

260 y was within 1-2 kcal.mol(-1) of a truncated alanyl-tRNA synthetase that has aminoacylation activity

261 Here we identify a two-helix pair in alanyl-tRNA synthetase that is required for RNA microhel

262 he transfer of alanine from Escherichia coli alanyl-tRNA synthetase to a cognate RNA minihelix involv

263 e contacts between tRNA and Escherichia coli alanyl-tRNA synthetase, an enzyme previously shown to in

264 ponents, such as the alpha-subunit of phenyl-alanyl-tRNA synthetase, and several metabolic enzymes.

265 Here we show that the editing site of alanyl-tRNA synthetase, as an artificial recombinant fra

266 te that prevents aminoacylation by the dicot alanyl-tRNA synthetase, indicating that features identif

267 When applied to Escherichia coli alanyl-tRNA synthetase, the assay allowed accurate measu

268 d by a strain harboring an editing-defective alanyl-tRNA synthetase, was rescued by an AlaXp-encoding

269 agenesis of the homologous editing pocket of alanyl-tRNA synthetase, where even a mild defect in edit

270 , we examined a fragment of Escherichia coli alanyl-tRNA synthetase, which catalyzes aminoacyl adenyl

271 Similarly, autonomous alanyl-tRNA synthetase-editing domain homologues (AlaX p

272 for clearance of errors of aminoacylation by alanyl-tRNA synthetase.

273 We report that CDC64 encodes Ala1p, an alanyl-tRNA synthetase.

274 (G3.U70) marks a tRNA for aminoacylation by alanyl-tRNA synthetase.

275 not to be a substrate for (re)activation by alanyl-tRNA synthetase.Application of the optimized syst

276 sing from confusion of serine for alanine by alanyl-tRNA synthetases (AlaRSs) has profound functional

277 evented in part by the editing activities of alanyl-tRNA synthetases (AlaRSs), which remove serine fr

278 rative aminoacylation and editing domains of alanyl-tRNA synthetases (AlaRSs).

279 n bacterial and eukaryotic threonyl- and all alanyl-tRNA synthetases is missing from archaebacterial

280 G. lamblia's archaeal-type prolyl- and alanyl-tRNA synthetases refine our understanding of the

281 nine, is activated by both human prolyl- and alanyl-tRNA synthetases.

282 ome-encoded homolog of the editing domain of alanyl-tRNA synthetases.

283 yzes the transfer of the alanyl residue from alanyl-tRNA to the N terminus of the tetrapeptide interm

284 on in mutants forming substantial amounts of alanyl-tRNAAla.

285 ate quality of the molecule for formation of alanyl-tRNAAla.

286 ay that could significantly amplify cellular alanyl-tRNAAla.

287 uent cross coupling of the aryl iodide to an alanyl zinc reagent (in the presence of a Pd(0) catalyst