ライフサイエンスコーパス: leucyl

1 PMNs stimulated with N-formyl-1-methionyl-1-leucyl-1-phenylalamine (FMLP) or permeabilized PMNs stim

2 tic agents, including N-formyl-1-methionyl-1-leucyl-1-phenylalanine (FMLP).

3 N/OFQ displaced [leucyl-(3)H]N/OFQ binding with pK(i) and slope values of

4 s, we have examined the effects of N/OFQ on [leucyl-(3)H]N/OFQ(1-17)OH ([leucyl-(3)H]N/OFQ) binding i

5 cts of N/OFQ on [leucyl-(3)H]N/OFQ(1-17)OH ([leucyl-(3)H]N/OFQ) binding in the presence and absence o

6 Optimal activity was observed against L-leucyl-7-amido-4-methylcoumarin (k(cat)/K(m) approximate

7 N-[N-(L-3-trans-carboxyoxirane-2-carbonyl)-L-leucyl]-agmatine, a cysteine protease inhibitor.

8 peptide surfactant, poly(sodium undecanoyl-l-leucyl-alaninate), poly(l-SULA), is investigated as a ne

9 -[N-[(l-3-trans-carboxyoxirane-2-carbonyl)-l-leucyl]amino]-4-guanidinobutane (E-64), an inhibitor of

10 , which can be unambiguously assigned to the leucyl aminopeptidase (LAP) structural family.

11 Intronless genes encoding a leucyl aminopeptidase (lap) were cloned from Leishmania

12 mpounds on X-Pro dipeptidase (prolidase) and leucyl aminopeptidase are also presented.

13 most restricted substrate specificity of any leucyl aminopeptidase described to date.

14 d 60-kDa proteins that displayed homology to leucyl aminopeptidases from Gram-negative bacteria, plan

15 O-QIC {L-threonine,(3R)-N-acetyl-3-hydroxy-L-leucyl-(aR)-a-hydroxybenzenepropanoyl-2,3- idehydro-N-me

16 -succinyl-beta-alanyl-L-isoleucyl-L-alanyl-L-leucyl-Dox (sAIAL-Dox).

17 [N-succinyl-beta-alanyl-L-leucyl-L-alanyl-L-leucyl-Dox (sALAL-Dox)] has been shown to have an improv

18 This proteolytic cleavage generates leucyl-Dox, which is capable of entering cells and gener

19 gen (PSA) to liberate the active cytotoxin L-leucyl-doxorubicin.

20 In the present study, L-prolyl-L-leucyl-glycinamide (1) peptidomimetics 3a-3d and 4a-4d w

21 primary target of the compound morpholinurea-leucyl-homophenyl-vinyl sulfone phenyl (LHVS), which was

22 with the calpain inhibitor N-[N-(N-acetyl-l-leucyl)-l-leucyl]-l-norleucine (ALLN) restores endoplasm

23 he small molecule inhibitor N-[N-(N-acetyl-L-leucyl)-L-leucyl]-L-norleucine (ALLN).

24 including 6-OHDA and MG-132 (carbobenzoxy-L-leucyl- L-leucyl-L-leucinal), whereas RNA interference (

25 nyl-L-phenylalanyl-L-leucyl-L-phenylalanyl-L-leucyl-L- phenylalanine did not inhibit basal GTPgammaS

26 (Dox), CPI-0004Na [N-succinyl-beta-alanyl-L-leucyl-L-alanyl-L-leucyl-Dox (sALAL-Dox)] has been shown

27 ; (f) L-isoleucyl-L-leucine dipeptide; (g) L-leucyl-L-isoleucine dipeptide.

28 he amino acid L-isoleucine and the peptide L-leucyl-L-isoleucine showed greater efficiency in translo

29 roteasome inhibitor carbobenzoxyl-l-leucyl-l-leucyl-l-leucinal (MG-132) and the anthracycline idarubi

30 Carbobenzoxy-L-leucyl-L-leucyl-L-leucinal (MG-132), a proteasome inhibitor, indu

31 norvalinal (MG-115), carbobenzoxy-L-leucyl-L-leucyl-L-leucinal (MG-132), or lactacystin induced NF-ka

32 Carbobenzoxy-L-leucyl-L-leucyl-L-leucinal (MG-132, a proteasome inhibitor, which

33 oteasome inhibitors [carbobenzoxy-L-leucyl-L-leucyl-L-leucinal (MG132), MG115 (carbobenzoxy-L-leucyl-

34 oteolysis inhibitor carbobenzoxy- L-leucyl-L-leucyl-L-leucinal (MG132).

35 me inhibitor MG-132 (carbobenzoxy-L-leucyl-L-leucyl-L-leucinal) prevented decreases in the size of th

36 6-OHDA and MG-132 (carbobenzoxy-L-leucyl- L-leucyl-L-leucinal), whereas RNA interference (RNAi)-medi

37 3-propanediyl)bis[(phenylmethoxy)carbonyl]-l-leucyl-l-leucinamide ketone inhibits formation of N-term

38 estabilized using the lysosomotropic agent L-leucyl-L-leucine methyl ester (Leu-Leu-OMe).

39 e permeabilization by lysosomotropic agent l-leucyl-l-leucine methyl ester that allows cytosolic rele

40 hermolysin of N-(4-methoxyphenylazoformyl)-L-leucyl-L-leucine plus some congeneric peptides provides

41 ith the proteasome inhibitor carbobenzoxyl-l-leucyl-l-leucyl-l-leucinal (MG-132) and the anthracyclin

42 Carbobenzoxy-L-leucyl-L-leucyl-L-leucinal (MG-132), a proteasome inhibi

43 leucyl-L-norvalinal (MG-115), carbobenzoxy-L-leucyl-L-leucyl-L-leucinal (MG-132), or lactacystin indu

44 Carbobenzoxy-L-leucyl-L-leucyl-L-leucinal (MG-132, a proteasome inhibit

45 ltiple proteasome inhibitors [carbobenzoxy-L-leucyl-L-leucyl-L-leucinal (MG132), MG115 (carbobenzoxy-

46 asomal proteolysis inhibitor carbobenzoxy- L-leucyl-L-leucyl-L-leucinal (MG132).

47 proteasome inhibitor MG-132 (carbobenzoxy-L-leucyl-L-leucyl-L-leucinal) prevented decreases in the s

48 ycosylated TCRalpha is blocked by N-acetyl-L-leucyl-L-leucyl-L-norleucinal (ALLN) and lactacystin, im

49 inhibitors, the peptide aldehyde N-acetyl-L-leucyl-L-leucyl-L-norleucinal (LLnL) and the highly spec

50 N-acetyl-L-leucyl-L-leucyl-L-norleucinal (LLnL), which reversibly i

51 easome inhibitors lactacystin and N-acetyl-L-leucyl-L-leucyl-L-norleucinal (LLnL).

52 showed that proteasome inhibitors N-acetyl-L-leucyl-L-leucyl-L-norleucinal and lactacystin but not ly

53 ell specificity in the ability of N-acetyl-L-leucyl-L-leucyl-L-norleucine (LLnL) or doxorubicin to au

54 lective proteasome inhibitors carbobenzoxy-L-leucyl-L-leucyl-L-norvalinal (MG-115), carbobenzoxy-L-le

55 yl-L-leucinal (MG132), MG115 (carbobenzoxy-L-leucyl-L-leucyl-L-norvalinal), and clasto-lactacystin-be

56 complex between subtilisin Carlsberg and Z-L-leucyl-L-leucyl-L-phenylalanyltrifluoromethyl ketone (Z-

57 d using the fluorescent peptide N-succinyl-L-leucyl-L-leucyl-L-valyl-L-tyrosine-7-amido-4- methylcoum

58 permeable fluorescent substrate N-succinyl-L-leucyl-L-leucyl-L-valyl-L-tyrosine-7-amido-4-methylcouma

59 A), or the protease inhibitor carbobenzoxy-L-leucyl-L-leucyl-leucinal (MG-132).

60 L-leucyl-L-leucyl-norleucinal and N-acetyl-L-leucyl-L-leucyl-methional.

61 bited by the tripeptide aldehydes N-acetyl-L-leucyl-L-leucyl-norleucinal and N-acetyl-L-leucyl-L-leuc

62 d TCRalpha is blocked by N-acetyl-L-leucyl-L-leucyl-L-norleucinal (ALLN) and lactacystin, implicating

63 rs, the peptide aldehyde N-acetyl-L-leucyl-L-leucyl-L-norleucinal (LLnL) and the highly specific inhi

64 N-acetyl-L-leucyl-L-leucyl-L-norleucinal (LLnL), which reversibly inhibits t

65 hibitors lactacystin and N-acetyl-L-leucyl-L-leucyl-L-norleucinal (LLnL).

66 at proteasome inhibitors N-acetyl-L-leucyl-L-leucyl-L-norleucinal and lactacystin but not lysosome in

67 ficity in the ability of N-acetyl-L-leucyl-L-leucyl-L-norleucine (LLnL) or doxorubicin to augment rAA

68 roteasome inhibitors carbobenzoxy-L-leucyl-L-leucyl-L-norvalinal (MG-115), carbobenzoxy-L-leucyl-L-le

69 inal (MG132), MG115 (carbobenzoxy-L-leucyl-L-leucyl-L-norvalinal), and clasto-lactacystin-beta-lacton

70 tween Ser 195 of chymotrypsin and N-acetyl-L-leucyl-L-phenylalanal (AcLF-CHO) has also been determine

71 esence and absence of N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP) (1 muM) stimulation.

72 1gamma2 reconstituted N-formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP)-stimulated guanosine 5'-O-

73 ntify the effects of (N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP)-stimulation on its mechani

74 a healthy donor with N-formyl-L-methionyl-L-leucyl-L-phenylalanine could also cause them to sediment

75 potent inhibitors of N-formyl-l-methionyl-l-leucyl-l-phenylalanine-induced migration of human neutro

76 s of Ser 195 in chymotrypsin with N-acetyl-L-leucyl-L-phenylalanyl trifluoromethyl ketone (AcLF-CF3)

77 agonist, N-t-butoxycarbonyl-L-phenylalanyl-L-leucyl-L-phenylalanyl-L-leucyl-L- phenylalanine did not

78 etween subtilisin Carlsberg and Z-L-leucyl-L-leucyl-L-phenylalanyltrifluoromethyl ketone (Z-LLF-CF3)

79 he fluorescent peptide N-succinyl-L-leucyl-L-leucyl-L-valyl-L-tyrosine-7-amido-4- methylcoumarin or t

80 fluorescent substrate N-succinyl-L-leucyl-L-leucyl-L-valyl-L-tyrosine-7-amido-4-methylcouma rin, as

81 calpain inhibitor N-[N-(N-acetyl-l-leucyl)-l-leucyl]-l-norleucine (ALLN) restores endoplasmic spreadi

82 olecule inhibitor N-[N-(N-acetyl-L-leucyl)-L-leucyl]-L-norleucine (ALLN).

83 elective calpain inhibitor benzyloxycarbonyl-leucyl-leucinal (5 micromol/L) prevented the up-regulati

84 e protease inhibitor carbobenzoxy-L-leucyl-L-leucyl-leucinal (MG-132).

85 factor (e.g. the dipeptide benzyloxycarbonyl-leucyl-leucine in vitro) to form the active ClpP1P2 tetr

86 specific proteasome inhibitor carbobenzoxy-l-leucyl-leucyl-l-leucinal (MG132).

87 yl-norleucinal (LLN), or the more potent CBZ-leucyl-leucyl-leucinal (MG132) suppressed proteolysis in

88 he presence of lactacystin and carboxybenzyl-leucyl-leucyl-leucinal, two inhibitors for proteasomal p

89 proteasome-specific inhibitors carboxybenzyl-leucyl-leucyl-leucine vinyl sulfone (Z-L3VS) and lactacy

90 The peptide vinyl sulfone, carboxybenzyl-leucyl-leucyl-leucine vinyl sulfone (Z-L3VS) covalently

91 teasome inhibitor studies with carboxybenzyl-leucyl-leucyl-leucine vinyl sulfone suggest an HCMV-asso

92 The calpain inhibitor, N-acetyl-leucyl-leucyl-methional, or the proteosome inhibitor, St

93 G132 (a 26S proteasomal inhibitor), N-acetyl-leucyl-leucyl-norleucinal (a calpain inhibitor), z-VAD-f

94 The calpain inhibitor N-acetyl-leucyl-leucyl-norleucinal (ALLN) has been reported to ha

95 ished by inhibition of calpain with N-acetyl-leucyl-leucyl-norleucinal (ALLN) or Calpeptin.

96 Compared with bortezomib, MG-132, N-acetyl-leucyl-leucyl-norleucinal (ALLN), and lactacystin, salin

97 by the cysteine protease inhibitor N-acetyl-leucyl-leucyl-norleucinal (ALLN).

98 ehyde inhibitors of the proteasome, N-acetyl-leucyl-leucyl-norleucinal (LLN), or the more potent CBZ-

99 de bond cleavage was obtained using N-acetyl-leucyl-leucyl-norleucinal (LLnL).

100 ncubation with calpain inhibitor I (N-acetyl-leucyl-leucyl-norleucinal [aLLN]), an active-site inhibi

101 ed with two proteolytic inhibitors, N-acetyl-leucyl-leucyl-norleucinal and lactacystin, the latter re

102 Calpain inhibitor N-acetyl-leucyl-leucyl-norleucinal blocked FAK cleavage, cell adh

103 hich was reversible by the calpain inhibitor leucyl-leucyl-norleucinal but not by the serine protease

104 This maturation is inhibited by N-acetyl-leucyl-leucyl-norleucinal but not lactacystin, indicatin

105 he peptide aldehydes (MG132, MG115, N-acetyl-leucyl-leucyl-norleucinal) and lactacystin, inhibited th

106 E-64 or the calpain inhibitor ALLN (N-acetyl-leucyl-leucyl-norleucinal).

107 N-Acetyl-leucyl-leucyl-norleucinal, a cysteine protease inhibitor

108 by the proteasome inhibitors MG132, N-acetyl-leucyl-leucyl-norleucinal, and lactacystin.

109 liminated by the protease inhibitor N-acetyl-leucyl-leucyl-norleucinal, consistent with rapid co- or

110 g apoB to be rapidly degraded by an N-acetyl-leucyl-leucyl-norleucinal-inhibitable process.

111 y abrogated by proteasome inhibitor N-acetyl-leucyl-leucyl-norleucinal.

112 uine (100 microM), but resistant to N-acetyl-leucyl-leucyl-norleucinal.

113 d HepG2 cells with brefeldin A plus N-acetyl-leucyl-leucyl-norleucinal.

114 teasome inhibitors, lactacystin and N-acetyl-leucyl-leucyl-norlucinal, caused a rapid and near-comple

115 lymphoblasts in culture to benzyloxycarbonyl-leucyl-leucyl-phenylalaninal (Z-LLF-CHO), a cell-permeab

116 oteasome inhibition with either carbobenzoxy-leucyl-leucyl-phenylalaninal or lactacystin led to a los

117 The amino acid editing site for leucyl- (LeuRS) and isoleucyl- (IleRS) tRNA synthetases

118 L-leucyl-norleucinal and N-acetyl-L-leucyl-L-leucyl-methional.

119 yl-1-oxo-2-[(1-oxopropyl)amino]pentyl]oxy]-L-leucyl-N,O-dimethyl-,(7-->1)-lac tone (9CI)}, a novel in

120 nd kappa-receptors were labelled with [(3)H] leucyl-nociceptin (0.4 nM), [(3)H] DAMGO (4 nM), [(3)H]

121 An approximately 50% decrease in [(3)H] leucyl-nociceptin binding was seen in heterozygous ORL1

122 the tripeptide aldehydes N-acetyl-L-leucyl-L-leucyl-norleucinal and N-acetyl-L-leucyl-L-leucyl-methio

123 t a 60-min chase in the presence of N-acetyl-leucyl-norleucinal, more than 90% of microsomes were iso

124 iols of the general structure N-mercaptoacyl-leucyl-p-nitroanilide (1a-c) were synthesized and found

125 nalogue, (S)-2-O-(H-phosphonoxy)-L-caproyl-L-leucyl-p-nitroanilide (PCLNA), have been determined.

126 cterial chemotactic peptide formyl-methionyl-leucyl-phenylalamine (fMLF), is activated by peptide dom

127 s significantly increased N-formyl-methionyl-leucyl phenylalanine (fMLF)-stimulated superoxide releas

128 Formyl methionyl leucyl phenylalanine (fMLP) stimulates neutrophils to ad

129 ly 10-fold in response to N-formyl methionyl leucyl phenylalanine (fMLP).

130 ses upon stimulation with N-formyl methionyl leucyl phenylalanine and CC chemokine ligand (CCL) 3 (ne

131 ty in cells stimulated with formyl-methionyl-leucyl phenylalanine plus dihydrocytochalasin B.

132 Mbeta2 integrin following N-formyl-methionyl-leucyl phenylalanine stimulation.

133 eness upon stimulation with formyl-methionyl-leucyl phenylalanine was found to identify sputum eosino

134 y the chemoattractant fMLF (formyl methionyl leucyl phenylalanine) was observed by RICM (reflection i

135 surface of unactivated and formyl methionyl leucyl phenylalanine-activated PMN as determined by indi

136 and after stimulation with formyl-methionyl-leucyl-phenylalanine (100 nM).

137 non-fluorescent peptide ligand CHO-methionyl-leucyl-phenylalanine (CHO-MLF).

138 the plasma membrane upon N-formyl-methionyl-leucyl-phenylalanine (fMLF) stimulation and colocalizes

139 licited by phorbol ester or formyl-methionyl-leucyl-phenylalanine (fMLF) was unaffected.

140 nd ex vivo perfusion with n-formyl-methionyl-leucyl-phenylalanine (fMLP) (10(-)(7) M).

141 PMN chemotactic responses to formylmethionyl-leucyl-phenylalanine (fMLP) and IL-8 were dose-dependent

142 neutrophils, which binds to formyl-methionyl-leucyl-phenylalanine (fMLP) and plays a role in neutroph

143 and elastase) exposed to N-formyl-methionyl-leucyl-phenylalanine (fMLP) and/or multivalent immune co

144 state 13-alpha-acetate or N-formyl methionyl-leucyl-phenylalanine (fMLP) for stimulus.

145 cells were exposed to an N-formyl-methionyl-leucyl-phenylalanine (FMLP) gradient whose source was pe

146 chemoattractant signal of N-formyl-methionyl-leucyl-phenylalanine (FMLP) in the absence of a spatial

147 his paradigm, we injected N-formyl-methionyl-leucyl-phenylalanine (FMLP) intradermally in guinea pigs

148 e primary chemoattractant N--formylmethionyl-leucyl-phenylalanine (fMLP) is mediated by leukotriene B

149 Microinjection of formyl-methionyl-leucyl-phenylalanine (fMLP) or macrophage inflammatory p

150 n secondary activation by N-formyl-methionyl-leucyl-phenylalanine (FMLP) or phorbol myristate acetate

151 ed human neutrophils with N-formyl-methionyl-leucyl-phenylalanine (fMLP) results in biphasic activati

152 The chemoattractant formyl-methionyl-leucyl-phenylalanine (fMLP) stimulated p38-MAPK-dependen

153 followed by treatment with formyl-methionyl-leucyl-phenylalanine (fMLP) stimulates cells in a physio

154 Formyl-methionyl-leucyl-phenylalanine (FMLP) stimulation (10(-7) M) resul

155 e assessed in response to N-formyl-methionyl-leucyl-phenylalanine (fMLP) stimulation.

156 rom cells with or without N-formylmethionine leucyl-phenylalanine (fMLP) stimulation.

157 lation of PMNs with 1 muM N-formyl-methionyl-leucyl-phenylalanine (fMLP) triggered earlier and more s

158 ing N-formylated peptide (N-formyl-methionyl-leucyl-phenylalanine (fMLP)), platelet activating factor

159 coincubated with 0.5 microM formyl-methionyl-leucyl-phenylalanine (fMLP), 1.3 microM 22:6OOH, or 5.0

160 lls permits absorption of N-formyl-methionyl-leucyl-phenylalanine (fMLP), as occurs in hPepT1 express

161 ) and then activated with N-formyl-methionyl-leucyl-phenylalanine (FMLP), C(2)-ceramide (10 microM) c

162 to the chemotactic peptide formyl-methionyl-leucyl-phenylalanine (FMLP), colony stimulating factor-1

163 dition of PMN stimulants, N-formyl-methionyl-leucyl-phenylalanine (FMLP), or phorbol myristate acetat

164 neutrophils were exposed to formyl-methionyl-leucyl-phenylalanine (fMLP), PKCbetaII was rapidly phosp

165 actic bacterial peptide, N-formyl- methionyl-leucyl-phenylalanine (fMLP), was able to specifically at

166 CNS, and also reduces the N-formyl-methionyl-leucyl-phenylalanine (fMLP)-induced neutrophil respirato

167 examine the mechanism of N-formyl-methionyl-leucyl-phenylalanine (fMLP)-mediated formation of CysLT.

168 ion of FPRwt reconstituted N-formylmethionyl-leucyl-phenylalanine (FMLP)-stimulated extracellular sig

169 Our results show that formyl-methionyl-leucyl-phenylalanine (fMLP)-stimulated respiratory burst

170 polysaccharide (LPS)- and N-formyl-methionyl-leucyl-phenylalanine (FMLP)-stimulated U937 adhesion to

171 d their chemotaxis toward N-formyl-methionyl-leucyl-phenylalanine (FMLP).

172 bacterial chemoattractant, formyl-methionyl-leucyl-phenylalanine (fMLP).

173 ted upon stimulation with N-formyl-methionyl-leucyl-phenylalanine (fMLP).

174 with LPS, RPMI alone, and N formyl-methionyl-leucyl-phenylalanine (FMLP).

175 lammatory stimuli such as N-formyl-methionyl-leucyl-phenylalanine (fMLP).

176 multaneously treated with N-formyl-methionyl-leucyl-phenylalanine and IgE plus polyvalent antigen.

177 ogically relevant agents, N-formyl-methionyl-leucyl-phenylalanine and leukotriene B4, by approximatel

178 CAM-1, and stimulation with formyl-methionyl-leucyl-phenylalanine boosted capture efficiency through

179 ammatory process induced by formyl-methionyl-leucyl-phenylalanine exposure.

180 atelet-activating factor or formyl-methionyl-leucyl-phenylalanine induced beta(2)-integrin-dependent

181 ine before stimulation with formyl methionyl-leucyl-phenylalanine inhibited A3 receptor expression an

182 cells were stimulated by N-formyl-methionyl-leucyl-phenylalanine or opsonized zymosan.

183 without the high-affinity N-formylmethionyl-leucyl-phenylalanine receptor antagonist N-tert-butoxyca

184 were assayed in vitro for N-formyl-methionyl-leucyl-phenylalanine receptor binding and superoxide pro

185 mannose receptor, and the N-formyl-methionyl-leucyl-phenylalanine receptor) did not have demonstrated

186 d doubling of the number of formyl-methionyl-leucyl-phenylalanine receptors on the cells.

187 generation before and after formyl-methionyl-leucyl-phenylalanine stimulation was significantly reduc

188 e-colony-stimulating factor/formyl-methionyl-leucyl-phenylalanine stimuli, which can induce eicosanoi

189 ha (TNF-alpha) as well as N-formyl-methionyl-leucyl-phenylalanine treatment leads to increased phosph

190 retains coupling between N-formyl-methionyl-leucyl-phenylalanine tripeptide (FMLP) receptor stimulat

191 e, opsonized zymosan, and N-formyl-methionyl-leucyl-phenylalanine) induce p22(phox) phosphorylation i

192 otype N-formylpeptide fMLF (formyl-methionyl-leucyl-phenylalanine) were both absent in FPR-/- mice.

193 We found that N-formyl-methionyl-leucyl-phenylalanine, an FPR agonist peptide, rapidly in

194 tants interleukin 8, C5a, N-formyl-methionyl-leucyl-phenylalanine, and interleukin 15, adhesion molec

195 ads, Staphylococcus aureus, formyl-methionyl-leucyl-phenylalanine, and zymosan were reduced by approx

196 or necrosis factor (TNF) or formyl-methionyl-leucyl-phenylalanine, as described for human PMNs.

197 neutrophil stimulation with formyl-methionyl-leucyl-phenylalanine, FcgammaR cross-linking, or phospha

198 nse to multiple agonists (N-formyl-methionyl-leucyl-phenylalanine, interleukin-8, and C5a).

199 ntact cells stimulated with formyl-methionyl-leucyl-phenylalanine, intermediate filament assembly is

200 s activated to secrete with formyl-methionyl-leucyl-phenylalanine, intermediate filaments are phospho

201 h configuration with PMA, N-formyl-methionyl-leucyl-phenylalanine, or anti-IgE greatly enhanced proto

202 bol myristate acetate (PMA), formylmethionyl-leucyl-phenylalanine, or Escherichia coli.

203 stimulated with anti-IgE, N-formyl-methionyl-leucyl-phenylalanine, or phorbol 12-myristate 13-acetate

204 hil activation induced by N-formyl-methionyl-leucyl-phenylalanine, phorbol 12-myristate 13-acetate, o

205 od extension induced with N-formyl-methionyl-leucyl-phenylalanine, platelet activating factor, and le

206 on and O(2)(-) responses to formyl-methionyl-leucyl-phenylalanine, reflecting the same cellular pheno

207 by neutrophils, induced by N-formylmethionyl-leucyl-phenylalanine, was strongly inhibited by inhibito

208 also seen in response to N-formyl-methionyl-leucyl-phenylalanine, zymosan-activated serum, or macrop

209 activity and adhesiveness of formylmethionyl-leucyl-phenylalanine- and arachidonic acid-stimulated ne

210 bolish the TNF-alpha- and N-formyl-methionyl-leucyl-phenylalanine-induced activation of acetyltransfe

211 Since the kinetics of formyl-methionyl-leucyl-phenylalanine-induced F-actin response were highl

212 quantitative analysis of N-formyl-methionyl-leucyl-phenylalanine-induced increase in binding of (35)

213 icient in spontaneous and N-formyl-methionyl-leucyl-phenylalanine-induced polarization, 0.5 microM pe

214 peptide receptor agonist (N-formyl-methionyl-leucyl-phenylalanine-lysine; N-For-MLFK) were compared w

215 phils under conditions of N-formyl-methionyl-leucyl-phenylalanine-mediated cPLA(2)alpha activation.

216 ation, and TNFalpha-primed, formyl-methionyl-leucyl-phenylalanine-stimulated respiratory burst.

217 rachidonate production in N-formyl-methionyl-leucyl-phenylalanine-stimulated U937 cells.

218 onic saline-treatment after formyl methionyl-leucyl-phenylalanine-stimulation augmented A3 receptor e

219 myristate acetate (PMA) and formyl-methionyl-leucyl-phenylalanine.

220 ence of the chemoattractant formyl-methionyl-leucyl-phenylalanine.

221 tase after stimulation with formyl-methionyl-leucyl-phenylalanine.

222 er muscle in response to N-formyl- methionyl-leucyl-phenylalanine.

223 ants, such as the peptide N-formyl-methionyl-leucyl-phenylalanine.

224 ation of Erk and adhesion by formylmethionyl-leucyl-phenylalanineand arachidonic acid.

225 alanyl-lysine-fluorescein and N-formyl-valyl-leucyl-phenylalanyl-lysine-fluorescein to the N-formyl p

226 the fluorescent peptide ligand CHO-norleucyl-leucyl-phenylalanyl-norleucyl-tyrosyl-lysine-fluorescein

227 Binding kinetics of N-formyl-methionyl-leucyl-phenylalanyl-phenylalanyl-lysine-fluorescein and

228 The leucyl/phenylalanyl-tRNA-protein transferase (L/F-transf

229 tate acetate (PMA)- but not formyl methionyl-leucyl-proline (fMLP)-induced respiratory burst activity

230 BP12 binds the IP3R at residues 1400-1401, a leucyl-prolyl dipeptide epitope that structurally resemb

231 nnel activity via interaction with conserved leucyl-prolyl dipeptides located near the cytoplasmic mo

232 ring to mimic the isobutyl side chain of the leucyl residue of PLG would increase the dopamine recept

233 htly held at a single amino acid position (a leucyl residue) that is buried in a deep pocket lined wi

234 Both the Escherichia coli tyrosyl- and leucyl-RS/tRNA(CUA) pairs were shown to be orthogonal in

235 by downregulating TOR signalling via LARS-1/leucyl-transfer RNA synthase.

236 rom Methanobacterium thermoautotrophicum and leucyl tRNA derived from Halobacterium sp. NRC-1 as an o

237 carboxy-terminal domain (Cterm) of human mt-leucyl tRNA synthetase rescues the pathologic phenotype

238 85% of RNAP III transcription activity using leucyl-tRNA as a template.

239 sma KIC enrichment most accurately predicted leucyl-tRNA enrichment, whereas plasma Leu enrichment wa

240 convenient and reliable surrogate measure of leucyl-tRNA in liver.

241 gnment we have analyzed the Candida albicans leucyl-tRNA synthetase (CaLeuRS) gene (CaCDC60).

242 Human mitochondrial leucyl-tRNA synthetase (hs mt LeuRS) achieves high amino

243 er the overexpression of human mitochondrial leucyl-tRNA synthetase (LARS2) in the cytoplasmic hybrid

244 Escherichia coli leucyl-tRNA synthetase (LeuRS) aminoacylates up to six d

245 Yeast mitochondrial leucyl-tRNA synthetase (LeuRS) binds to the bI4 intron a

246 c and editing activities of Escherichia coli leucyl-tRNA synthetase (LeuRS) demonstrate that the enzy

247 Leucyl-tRNA synthetase (LeuRS) has been identified as a

248 Leucyl-tRNA synthetase (LeuRS) has evolved an editing fu

249 Mitochondrial leucyl-tRNA synthetase (LeuRS) in the yeast Saccharomyce

250 Leucyl-tRNA synthetase (LeuRS) is a class I enzyme, whic

251 Leucyl-tRNA synthetase (LeuRS) is an essential RNA splic

252 In one case, Mycoplasma mobile leucyl-tRNA synthetase (LeuRS) is uniquely missing its e

253 Leucyl-tRNA synthetase (LeuRS) misactivates non-leucine

254 Leucyl-tRNA synthetase (LeuRS) performs dual essential r

255 Leucyl-tRNA synthetase (LeuRS) relies on its editing fun

256 this biocontrol agent targets A. tumefaciens leucyl-tRNA synthetase (LeuRS), an essential enzyme for

257 In leucyl-tRNA synthetase (LeuRS), editing activities that

258 Leucyl-tRNA synthetase (LeuRS), isoleucyl-tRNA synthetas

259 Leucyl-tRNA synthetase (LeuRS), isoleucyl-tRNA synthetas

260 a unique tRNA-dependent mechanism to inhibit leucyl-tRNA synthetase (LeuRS), while the TM84-producer

261 thanogenesis, protein-modifying factors, and leucyl-tRNA synthetase (LeuRS).

262 synthetase (GluRS):tRNA(Glu) and an archaeal leucyl-tRNA synthetase (LeuRS):tRNA(Leu) complex.

263 lpha was found to form a stable complex with leucyl-tRNA synthetase (LeuRS; K(D) = 0.7 microM).

264 ulting from cancer-associated MTOR mutations.Leucyl-tRNA synthetase (LRS) is a leucine sensor of the

265 Leucyl-tRNA synthetase (LRS) is known to function as leu

266 The yeast mitochondrial leucyl-tRNA synthetase (ymLeuRS) performs dual essential

267 Binding of gold-labeled tRNA(Leu) places leucyl-tRNA synthetase and the bifunctional glutamyl-/pr

268 ein, different mutations in Escherichia coli leucyl-tRNA synthetase are combined to unmask the pretra

269 of onychomycosis, inhibits yeast cytoplasmic leucyl-tRNA synthetase by formation of a stable tRNA(Leu

270 he collective motion in Thermus thermophilus leucyl-tRNA synthetase by studying the low frequency nor

271 We present structures of leucyl-tRNA synthetase complexed with analogs of the dis

272 These mutations that altered or abolished leucyl-tRNA synthetase editing were introduced into comp

273 overcome this limitation, we have adapted a leucyl-tRNA synthetase from Methanobacterium thermoautot

274 n identified a mutation in the mitochondrial leucyl-tRNA synthetase gene (lrs-2) that impaired mitoch

275 ell, Bonfils et al. and Han et al. implicate leucyl-tRNA synthetase in this evolving story.

276 A point mutation in CP1 of class I leucyl-tRNA synthetase inactivates deacylase activity an

277 rving cells of leucine or treating them with leucyl-tRNA synthetase inhibitors did not elicit nuclear

278 ted that the transfer of human mitochondrial leucyl-tRNA synthetase into the cybrid cells carrying th

279 cid editing active site for Escherichia coli leucyl-tRNA synthetase resides within the CP1 domain tha

280 tational analysis within yeast mitochondrial leucyl-tRNA synthetase showed that the enzyme has mainta

281 ed conformational changes of T. thermophilus leucyl-tRNA synthetase upon substrate binding and analyz

282 red the refolding of the human mitochondrial leucyl-tRNA synthetase variant H324Q to that of wild typ

283 hreonine-rich region of the Escherichia coli leucyl-tRNA synthetase's CP1 domain that is hypothesized

284 4-Azaleucine, a competitive inhibitor of leucyl-tRNA synthetase, surprisingly triggered the heat

285 be aminoacylated by the human mitochondrial leucyl-tRNA synthetase, we examined the aminoacylation k

286 nate amino acids that can be misactivated by leucyl-tRNA synthetase.

287 he ser-tRNACAG and preventing binding of the leucyl-tRNA synthetase.

288 e mechanochemical motions in T. thermophilus leucyl-tRNA synthetase.

289 d mutations in LARS2, encoding mitochondrial leucyl-tRNA synthetase: homozygous c.1565C>A (p.Thr522As

290 erminal domain extension is required by most leucyl-tRNA synthetases (LeuRS) for aminoacylation.

291 cluding a complex between prolyl-(ProRS) and leucyl-tRNA synthetases (LeuRS) in Methanothermobacter t

292 Aminoacylation and editing by leucyl-tRNA synthetases (LeuRS) require migration of the

293 Leucyl-tRNA synthetases (LeuRSs) have an essential role

294 Mycoplasma leucyl-tRNA synthetases (LeuRSs) have been identified in

295 ing pocket within the editing active site of leucyl-tRNA synthetases (LeuRSs).

296 Leucyl-tRNA synthetases have a hydrolytic active site th

297 is activated by methionyl-, isoleucyl-, and leucyl-tRNA synthetases in vivo.

298 editing of mischarged tRNA similar to other leucyl-tRNA synthetases.

299 lytic turnover, thus inhibiting synthesis of leucyl-tRNA(Leu) and consequentially blocking protein sy

300 y a constitutive protein complex composed of leucyl-tRNA-synthetase and folliculin, which regulates m

301 f E. coli TruA in complex with two different leucyl tRNAs in conjunction with functional assays and c