ライフサイエンスコーパス: Ala

1 Ala and Glu mutations of the FG loop KHR residues showed

2 Ala variants of His(1092) and His(1098) also elicit larg

3 Ala-DAG formation in Corynebacterium glutamicum is depen

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

5 atches is formed by residues Ser-33, Leu-34, Ala-66, Lys-68, Ile-69, Leu-70, Ser-71, and Glu-72.

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

7 sition 241 in both CELA3A ( approximately 4% Ala(241) alleles) and CELA3B ( approximately 2% Gly(241)

8 es which possess two extra residues (Ile 41 &Ala 42) that the non-pathological strain (Abeta40) lacks

9 gion of APOB bound RAD21 but not RAD21 p.622 Ala>Thr; expression of wild-type RAD21 in HEK293 cells r

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

11 Asn-1029 from domain A, as well as Leu-938, Ala-978, and Leu-981 from domain B) near subsite +1 that

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

13 ectification depends on a single amino acid (Ala(254)) at the inner pore mouth of the channels and is

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

15 ion of glycine with eight other amino acids (Ala, Asp, Glu, His, Lys, Pro, Thr and Val), incorporatin

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

17 nd alanine [Ala]) and combined AAs (Tyr-Ala, Ala-Tyr, Tyr-Tyr-Tyr, Ala-Ala-Ala), and found that HAcAm

18 AAs (Tyr-Ala, Ala-Tyr, Tyr-Tyr-Tyr, Ala-Ala-Ala), and found that HAcAm formation from the chlorinati

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

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

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

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

23 s from free AAs (tyrosine [Tyr] and alanine [Ala]) and combined AAs (Tyr-Ala, Ala-Tyr, Tyr-Tyr-Tyr, A

24 lopathy susceptibility 2 gene linked to AMD, Ala(69)-->Ser, did not improve the statistical model.

25 the prevention of telomere shortening among Ala carriers.

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

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

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

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

30 The Asp-102 and Ala-285 variants are more stable than wild-type rhodanes

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

32 7 impact sodium binding, whereas Arg-257 and Ala-260 may participate in interactions leading to closu

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

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

35 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

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

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

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

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

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

41 most potent scaffold, c[Pro-Arg-Phe-Phe-Asn-Ala-Phe-DPro], comprised the hexa-peptide beta-hairpin l

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

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

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

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

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

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

48 In particular, the mu-agonist c[beta-Ala-d-Pro-Phe-Trp] 9 was shown to elicit potent antinoci

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

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

51 lipid phosphatidylglycerol (PG) catalyzed by Ala-tRNA(Ala)-dependent alanyl-phosphatidylglycerol synt

52 yclic hexapeptide with replacement of Cys by Ala.

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

54 ion channels, GLIC and ELIC, was examined by Ala scanning mutagenesis, deletion mutations, and mutant

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

56 tive Gs but not Gq signaling was observed by Ala substitution of four out of the six core polar resid

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

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

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

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

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

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

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

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

65 This reshaping removes the role of C-Ala in prokaryotes for docking tRNA and instead repurpos

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

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

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

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

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

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

72 d-Ala-d-Ala catalyzes the aggregation of a d-Ala-d-Ala-containing small peptide derivative in water.

73 hat beta-lactam antibiotics mimic the acyl-D-Ala-D-Ala moiety of the stem and, thus, are recognized b

74 teins, PBPs) have evolved to bind the acyl-D-Ala-D-Ala segment of the stem peptide of the nascent pep

75 jection of the mu-opioid receptor agonist [D-Ala(2), NMe-Phe(4), Gly-ol(5)]-enkephalin produces parad

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 r interaction between vancomycin and d-Ala-d-Ala catalyzes the aggregation of a d-Ala-d-Ala-containin

79 ta-lactam antibiotics mimic the acyl-D-Ala-D-Ala moiety of the stem and, thus, are recognized by the

80 tapeptide revealed that the terminal D-Ala-D-Ala motif of the repressor forms the primary contacts wi

81 roMurNAc-tripeptide (which lacks the D-Ala-D-Ala motif).

82 PBPs) have evolved to bind the acyl-D-Ala-D-Ala segment of the stem peptide of the nascent peptidogl

83 Mutation of d-Ala-d-Ala to l-Ala-l-Ala or removal of the aromatic group in t

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

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

86 d-Ala catalyzes the aggregation of a d-Ala-d-Ala-containing small peptide derivative in water.

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

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

89 ncomycin analogues designed for dual D-Ala-D-Ala/D-Ala-D-Lac binding.

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

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

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

93 in analogues designed for dual D-Ala-D-Ala/D-Ala-D-Lac binding.

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

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

96 eceptor interaction between vancomycin and d-Ala-d-Ala catalyzes the aggregation of a d-Ala-d-Ala-con

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

98 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-

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

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

101 F) at the fourth position (ligand 5: H-Dmt-d-Ala-Gly-Phe(4-F)-Pro-Leu-Trp-NH-Bn(3',5'-(CF3)2)) exhibi

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

103 ied vancomycin analogues designed for dual D-Ala-D-Ala/D-Ala-D-Lac binding.

104 Favorable candidates for d-Ala substitution can be identified using a rapid algorit

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

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

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

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

112 Mutation of d-Ala-d-Ala to l-Ala-l-Ala or removal of the aromatic grou

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 Attempts to alter the mu-selectivity of [D-Ala(2),N-MePhe(4),Gly-ol(5)]enkephalin (DAMGO)-related g

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

117 Ac-pentapeptide revealed that the terminal D-Ala-D-Ala motif of the repressor forms the primary conta

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

119 -anhydroMurNAc-tripeptide (which lacks the D-Ala-D-Ala motif).

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

121 NpnJA reduces dehydroalanine to D-Ala using NAPDH as cosubstrate.

122 We critically examine the effect of Gly-to-d-Ala substitutions on protein stability using experimenta

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

124 rat plasma with ligands 3, 5, and 7 (H-Tyr-d-Ala-Gly-Phe(4-F)-Pro-Leu-Trp-NH-Bn(3',5'-(CF3)2)) showed

125 la-Leu-Arg-Pro-NHEt (LHRHa) to Trp-Ser-Tyr-D-Ala-Leu-Arg-Pro-NHEt (fragment 1) and Ser-Tyr-D-Ala-Leu-

126 -Leu-Arg-Pro-NHEt (fragment 1) and Ser-Tyr-D-Ala-Leu-Arg-Pro-NHEt (fragment 2).

127 nto two fragments from Glp-His-Trp-Ser-Tyr-D-Ala-Leu-Arg-Pro-NHEt (LHRHa) to Trp-Ser-Tyr-D-Ala-Leu-Ar

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

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

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

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

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

133 Two peptides AEERYP and DEDTQAMP (Ala-Glu-Glu-Arg-Tyr-Pro and Asp-Glu-Asp-Thr-Gln-Ala-Met-

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

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

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

137 tified a homozygous mutation (p.622, encodes Ala>Thr) in RAD21 in patients from a consanguineous fami

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

139 De novo biosynthesis was shown for Ala, Asp, Ser, and Thr at high rates and for Gly, Lys, P

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

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

142 -Glu-Glu-Arg-Tyr-Pro and Asp-Glu-Asp-Thr-Gln-Ala-Met-Pro) showed the highest ORAC values.

143 pha-aminobutyric acid > Gln, Thr, Ser > Glu, Ala, Gly, Asn, Asp.

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

145 Here, we have identified the DEAD (Asp-Glu-Ala-Asp) box RNA helicase 24 (DDX24) as a novel regulato

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

147 These reactions build up H2N-Pro-Gly-Ala-CONHL and H2N-Cys-His-Asp-CONHL (where L = organic s

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

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

150 sidues or Trp in the X2 position, and Pro >> Ala > Trp in the X3 position.

151 show that ClpP1P2 prefers Met >> Leu > Phe > Ala in the X1 position, basic residues or Trp in the X2

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

153 Adar1(E861A), where E861A denotes Glu(861)-->Ala(861)).

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

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

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

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

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

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

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

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

162 haeroides and a mutant that mimics the human Ala(147)-->Thr(147) polymorphism associated with psychia

163 and a tachykinin-related peptide (CabTRP Ia, Ala(1)-Pro(2)-Ser(3)-Gly(4)-Phe(5)-Leu(6)-Gly(7)-Met(8)-

164 s at gp120 positions 23, 45, 47, and 70 (Ile-Ala-Lys-Asn [I-A-K-N]) emerged as signatures of mucosal

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

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

167 Interestingly, Ala carriers showed lower telomere shortening after 5 ye

168 ence of muropeptides cross-linked by (1-3) l-Ala-d-(meso)-diaminopimelate cross-links.

169 Mutation of d-Ala-d-Ala to l-Ala-l-Ala or removal of the aromatic group in the derivative r

170 t peptide sequence (i.e., PhCO-(R)-Oxo-Azn-L-Ala-Aib-L-AlaNHMe) and a stable 310-helix conformation w

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

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

173 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-

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

175 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

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

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

178 Mutation of d-Ala-d-Ala to l-Ala-l-Ala or removal of the aromatic group in the deriva

179 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

180 ecular recognition of the tripeptide Tyr-Leu-Ala by the synthetic receptor cucurbit[8]uril (Q8) in aq

181 the straightforward incorporation of Tyr-Leu-Ala into recombinant proteins should make this system at

182 For the peptide Tyr-Leu-Ala, the equilibrium dissociation constant value is 7.2

183 cid composition had high proportions of Lys, Ala and Glu.

184 well as in knock-in mice expressing a mutant Ala(286)-CaMKIIalpha that cannot autophosphorylate to be

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

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

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

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

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

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

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

192 Moreover, the His(nuc)Ala mutant was catalytically active in vitro, albeit at

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

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

195 ty of an aaPGS homolog, whereas formation of Ala-PG requires the same enzyme acting in concert with a

196 First, mutants of Ala-978 (to Leu, Pro, Phe, or Tyr) and Asp-1028 (to Tyr

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

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

199 Substitution of Ala for Phe at position 5 conferred 300-fold selectivity

200 Substitution of Ala for Thr at position 136 of apocarotenoid oxygenase,

201 s the ability to cleave at the C-terminal of Ala, Leu, Arg and His residues.

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

203 ivative along with an l-peptide in which one Ala has been replaced by a beta-amino acid residue.

204 ith nonphosphorylatable residues like Phe or Ala significantly affected autophosphorylation on select

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

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

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

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

209 200-residue polypeptide tag comprising Pro, Ala, and Ser (PAS200) and by fusion with an albumin-bind

210 ides were identified as Val-Glu-Leu-Tyr-Pro, Ala-Phe-Val-Gly-Tyr-Val-Leu-Pro and Glu-Lys-Ser-Tyr-Glu-

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

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

213 The gene variant Pro/Ala (rs1801282) in the PPARgamma2 has been associated wi

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

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

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

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

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

219 age- and sex-matched control subject (seven Ala/Ala and two Ala/Thr, five males and four females in

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

221 t hairpin loop 2 are replaced by the smaller Ala and Thr, respectively.

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

223 ging of nascent chains with carboxy-terminal Ala and Thr extensions ("CAT tails").

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

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

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

227 aim was to study the association between the Ala allele and changes in TL in high cardiovascular risk

228 ning was detected to a greater extent in the Ala carriers compared with the Pro/Pro subjects (P for i

229 milarly, vascular endothelial cells with the Ala/Ala genotype had higher intracellular cadmium concen

230 ntration and lower cell viability than their Ala/Thr counterpart following cadmium exposure.

231 A conserved late domain motif, Pro-Thr-Ala-Pro (PTAP), located in the p6 region of Gag (p6(Gag)

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

233 1 to Asp in the double E loop and Gln-329 to Ala in the canonical THW loop enables the enzyme to prod

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

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

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

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

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

239 Mutation of Glu-87 to Ala or Gly rendered the protein constitutively active as

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

241 abilizing mutant (FnIII9'10), (ii) an Arg to Ala synergy site mutation (FnIII9(R)-->(A)10), (iii) a t

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

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

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

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

246 e shown that due to the site-specific Lys to Ala mutations of PIP5K at Lys-244 and Lys-490, it is una

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

248 ished when all Phe residues were modified to Ala.

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

250 45A mutant (in which Ser(845) was mutated to Ala) mice were tested in a water maze after chronic nalt

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

252 pk1(11A)), in which 11 sites were mutated to Ala, was hyperactive, causing increased inward transport

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

254 A His(nuc) to Ala mutant protein is reportedly inactive, whereas the a

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

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

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

258 t, expression of occludin mutated at S490 to Ala, completely inhibited angiogenesis in cell culture m

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

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

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

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

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

264 Metal rescue of Asp-to-Ala mutations identified two aspartates important for en

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

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

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

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

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

270 sphatidylglycerol (PG) catalyzed by Ala-tRNA(Ala)-dependent alanyl-phosphatidylglycerol synthase (A-P

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

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

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

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

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

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

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

278 tched control subject (seven Ala/Ala and two Ala/Thr, five males and four females in each group; medi

279 combined AAs (Tyr-Ala, Ala-Tyr, Tyr-Tyr-Tyr, Ala-Ala-Ala), and found that HAcAm formation from the ch

280 yr] and alanine [Ala]) and combined AAs (Tyr-Ala, Ala-Tyr, Tyr-Tyr-Tyr, Ala-Ala-Ala), and found that

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

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

283 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

284 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

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

286 nM, whereas that of its sequence isomer Tyr-Ala-Leu is 34 muM.

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

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

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

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

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

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

293 ly, substitution of Thr-553 and Ser-555 with Ala promoted PIPKIgamma90 ubiquitination but enhanced th

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

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

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

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

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

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

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