ライフサイエンスコーパス: Leu

1 ino acid mixture enriched with leucine (BCAA/LEU).

2 oholic cirrhosis is acutely reversed by BCAA/LEU.

3 terminal side of Ala, Glu, Gly, Ser, Lys and Leu.

4 treatment in the rested (pooled mean +/- SD: Leu, 1.57% +/- 0.11%/d; placebo, 1.48% +/- 0.08%/d; main

5 treatment: P < 0.001) and REX (pooled mean: Leu, 1.87% +/- 0.09%/d; placebo, 1.71 +/- 0.10%/d; main

6 lean mass loss after 7 d (CON compared with LEU: -1.5 +/- 0.3 and -0.8 +/- 0.3 kg; group x time inte

7 n, P < 0.05) but not 14 d (CON compared with LEU: -1.5 +/- 0.3 and -1.0 +/- 0.3 kg) of bed rest.

8 motif of secretin (sec), Phe(6), Thr(7), and Leu(10), and cysteines incorporated into the extracellul

9 pes degradation and is cleaved N-terminal to Leu-104 to yield a fragment that is no longer tethered t

10 c residues Phe-1012, Val-1025, Tyr-1089, and Leu-1092).

11 e GRP78 primary amino acid sequence (Leu(98)-Leu(115)).

12 Interchanging Leu-119 for Pro-119 at the tip of the beta4-beta5 loop i

13 sition 12 or 14 of GWALP23 (replacing either Leu(12) or Leu(14)) and incorporated specific [(2)H]Ala

14 of amino acid sequences outside the Lys(87)-Leu(122) central portion of the molecule either failed t

15 tion of the cyclase localizes to the Lys(87)-Leu(122) region.

16 ity, its flanking residues (132 to 140), and Leu-122, a pore-gating residue.

17 lize an open state regulated by pore residue Leu-122.

18 Another similar pair is Leu-126 in RF1 and Asp-143 in RF2, which are also conser

19 We also demonstrated that Leu-127 and Leu-135 are important residues for disruptio

20 Using alanine scanning, we demonstrated that Leu-127 and Leu-135 are the key residues for NSs-induced

21 By replacement of the C-terminal Leu(13)-Met(14)-NH2 dipeptide of SB3 by Sta(13)-Leu(14)-

22 We also demonstrated that Leu-127 and Leu-135 are important residues for disruption of the mit

23 e scanning, we demonstrated that Leu-127 and Leu-135 are the key residues for NSs-induced apoptosis.

24 r 14 of GWALP23 (replacing either Leu(12) or Leu(14)) and incorporated specific [(2)H]Ala labels with

25 (13)-Met(14)-NH2 dipeptide of SB3 by Sta(13)-Leu(14)-NH2, the novel GRPR antagonist NeoBOMB1 was gene

26 , P < 0.05) and endurance (CON compared with LEU: -14% +/- 3% and -2% +/- 4%; group x time interactio

27 on was due to an additional cleavage site at Leu-148 in the autolysis loop and the lack of the conser

28 mutations of CTRC cleavage sites Leu-81 and Leu-148, autolytic cleavage site Arg-122, and restoratio

29 contiguous conserved amino acids Pro-148 and Leu-149 in the GHSR1a intracellular second loop generate

30 to cysteine proteases, the importance of the Leu(15) in anchoring the inhibitor into the S2 active si

31 Substitution of the unusual P1 Leu(15) within the exposed reactive loop of FhKT1 for th

32 ct, whereas a selective agonist, [Ala(11), d-Leu(15)]OXB, reproduced it.

33 is of the N-Cap amphipathic helix identified Leu-15, Ile-18, and Ile-19 as residues critical for the

34 Asp(69)) and loop C (Val(141), His(151), and Leu(154)).

35 a highly solvent-exposed apoA-I loop domain (Leu(159)-Leu(170)) in nascent HDL, the so-called "solar

36 33)-NHEt), and 85 ([Gly(2),Nle(10),D-Phe(11),Leu(16)]hGLP-2-(1-33)-NH-((CH2)2O)4-(CH2)2-CONH2) displa

37 -2-(1-33)-OH), 73 ([Gly(2),Nle(10),D-Phe(11),Leu(16)]hGLP-2-(1-33)-NH2), 81 ([Gly(2),Nle(10),D-Phe(11

38 2-(1-33)-NH2), 81 ([Gly(2),Nle(10),D-Phe(11),Leu(16)]hGLP-2-(1-33)-NHEt), and 85 ([Gly(2),Nle(10),D-P

39 2-(1-30)-NH2), 72 ([Gly(2),Nle(10),D-Phe(11),Leu(16)]hGLP-2-(1-33)-OH), 73 ([Gly(2),Nle(10),D-Phe(11)

40 ynamics of the hydrophobic regions probed at Leu-17, Leu-34, Val-36, and Met-35 side chains were foun

41 solvent-exposed apoA-I loop domain (Leu(159)-Leu(170)) in nascent HDL, the so-called "solar flare" (S

42 as well as deletion of Arg-172, Ser-173, or Leu-174 all caused a decrease in Ca(2+) binding affinity

43 of an extra Gly residue between Ser-173 and Leu-174 as well as deletion of Arg-172, Ser-173, or Leu-

44 changes solvent accessibility of Thr-171 and Leu-174 that affects the domain interface.

45 th ZapD residues Leu-74, Trp-77, Leu-91, and Leu-174.

46 ultiple amino acid residues, but Gly-171 and Leu-175 of P2 were more critical.

47 tation Ser(45) --> His, Thr(46) --> Arg, and Leu(186) --> Tyr replaces porcine with E. coli type side

48 in a hydrophobic pocket on Galphai1 (Val-34, Leu-194, Phe-196, Phe-336, Thr-340, Ile-343, and Ile-344

49 peptide Gramicidin S cyclo(d-Phe-Pro-Val-Orn-Leu-)2 (GS).

50 Alanine substitutions at HO-2 residues Leu-201 and Lys-169 cause a respective 3- and 22-fold in

51 s in Ca(2+)-bound CaBP4 (Phe(137), Glu(168), Leu(207), Phe(214), Met(251), Phe(264), and Leu(268)) ma

52 from RasGRP1/3 (Thr(7), Tyr(8), Gly(19), and Leu(21), respectively) conferred potent binding affinity

53 F interface, where, in contrast to Phe(231), Leu(231) lacks interactions stabilizing the ERCC1-XPF co

54 pens through coordinated motions of residues Leu(25), Tyr(108), and Phe(253) The resulting water chan

55 Leu(207), Phe(214), Met(251), Phe(264), and Leu(268)) make contacts with the IQ motif in Cav1.4, and

56 We found here that Leu-27 is buried in the dimer and that the L27A mutation

57 Leu-27 is evolutionarily well conserved even though it i

58 contiguous amino acid residues, Arg(286) and Leu(287).

59 , five residues (Gln(45)-TMD1, Asn(90)-TMD2, Leu(290)-TMD7, Ser(407)-TMD11 and Asn(411)-TMD11) in the

60 -MSH as a template, we developed a peptide, [Leu(3), Leu(7), Phe(8)]-gamma-MSH-NH2 (compound 5), whic

61 [Leu(3), Leu(7), Phe(8)]-gamma-MSH-NH2 is ideal for induc

62 Moreover, proximity between Leu-32 in mambalgin-1 and Phe-350 in rASIC1a was propose

63 ore precisely in the face containing Phe-27, Leu-32, and Leu-34 residues.

64 n and on the contact between the Phe(19) and Leu(34) regions, making them potentially sensitive targe

65 R shows that the contact between Phe(19) and Leu(34) residues, observed in full-length Abeta and Abet

66 y in the face containing Phe-27, Leu-32, and Leu-34 residues.

67 these patches is formed by residues Ser-33, Leu-34, Ala-66, Lys-68, Ile-69, Leu-70, Ser-71, and Glu-

68 of the hydrophobic regions probed at Leu-17, Leu-34, Val-36, and Met-35 side chains were found to be

69 age, which occurred equally well at Thr(345)-Leu(346) and Asn(347)-Leu(348), was abolished by the pre

70 ually well at Thr(345)-Leu(346) and Asn(347)-Leu(348), was abolished by the presence of Asn(347) glyc

71 e hot spot residues (Galphas/Galphaq-Gln-384/Leu-349, Gln-390/Glu-355, and Glu-392/Asn-357) that cont

72 agonist trigger likely pulled away from its Leu(356) target on TM7.

73 The residues of Trp-354, Arg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that are import

74 between FtsZ residues Ile-374, Pro-375, and Leu-378 with ZapD residues Leu-74, Trp-77, Leu-91, and L

75 We suggest that a surface of GRK2, including Leu(4), Val(7), Leu(8), Val(11), and Ser(12), directly i

76 Leu(406) is located >10 A from the central inhibitor bin

77 al interaction of ATP with Lys-378, Glu-428, Leu-430, and Phe-633 residues.

78 R-ABL TKIs interacted with Met(33) (TM1) and Leu(442) (TM11) residues of hENT1.

79 ch of rFII allowed for the identification of Leu(480) and Gln(481) as the two essential amino acids r

80 in the amino acid sequence Ser(478)-Val(479)-Leu(480)-Gln(481)-Val(482).

81 dence demonstrating that amino acid sequence Leu(480)-Gln(481): 1) is crucial for proper recognition

82 man alpha-thrombin with amino acids Ser(478)/Leu(480)/Gln(481) deleted).

83 tif, triple alanine substitution of residues Leu(496), Leu(500), and Trp(503), which are thought to m

84 on, our data strongly suggest that the motif Leu(496)-Leu(500)-Trp(503) within the beta1a C-terminal

85 e alanine substitution of residues Leu(496), Leu(500), and Trp(503), which are thought to mediate dir

86 ata strongly suggest that the motif Leu(496)-Leu(500)-Trp(503) within the beta1a C-terminal tail play

87 Mutant alpha subunits containing Leu-58(E7) autoxidize approximately 8 times and lose hem

88 abTRP Ia, Ala(1)-Pro(2)-Ser(3)-Gly(4)-Phe(5)-Leu(6)-Gly(7)-Met(8)-Arg(9)-NH2).

89 nging to putative helix 1 (Phe-40), helix 3 (Leu-63, Arg-68, Gln-69, Ile-72, Tyr-76), and C-terminal

90 interacting with IFN-beta residues Phe(63), Leu(64), Glu(77), Thr(78), Val(81), and Arg(82) that und

91 Mutating SM residues Phe-35/Ser-37/Leu-65/Ile-69 into alanine, based on the key residues in

92 ectron transfer proceeds via the leucine 69 (Leu(69)) and valine 68 (Val(68)) residues.

93 a template, we developed a peptide, [Leu(3), Leu(7), Phe(8)]-gamma-MSH-NH2 (compound 5), which is 16-

94 [Leu(3), Leu(7), Phe(8)]-gamma-MSH-NH2 is ideal for inducing shor

95 dues Ser-33, Leu-34, Ala-66, Lys-68, Ile-69, Leu-70, Ser-71, and Glu-72.

96 te-directed mutagenesis showed that Glu-713, Leu-716, and Lys-645, all of which interact with the ade

97 dentify a 12-residue region (residues Gln-62-Leu-73), required for SM cholesterol-mediated turnover.

98 374, Pro-375, and Leu-378 with ZapD residues Leu-74, Trp-77, Leu-91, and Leu-174.

99 a surface of GRK2, including Leu(4), Val(7), Leu(8), Val(11), and Ser(12), directly interacts with re

100 Here, we demonstrate that, compared with the Leu(8)OXT found in most placental mammals, the Cebidae P

101 on with the AVPR1a, Pro(8)OXT and the common Leu(8)OXT yielded similar signaling profiles, being equa

102 he hydrophobic patch of ubiquitin comprising Leu-8 and Ile-44 is important for E6AP-mediated ubiquiti

103 cognition, which likely involves Gln(41) and Leu(81) as DNA lesion sensors.

104 imultaneous mutations of CTRC cleavage sites Leu-81 and Leu-148, autolytic cleavage site Arg-122, and

105 trypsinogen where single mutations of either Leu-81 or Arg-122 resulted in almost complete resistance

106 le peptide bond was not dependent on CTRC or Leu-81, as re-synthesis was also accomplished by other p

107 69, Ile-72, Tyr-76), and C-terminal segment (Leu-81, Glu-84) are critical for in vivo Fe-S cluster bi

108 for JAK3(L857P) was observed for homologous Leu(857) mutations of JAK1 and JAK2 and for JAK3(L875H).

109 Well-known BR ligands, BK, [des-Arg(10), Leu(9)]-kallidin (DALKD), and HOE140 showed different bi

110 Several specific PON1 residues (Leu-9, Tyr-185, and Tyr-293) were identified through cov

111 mutagenesis of the identified PON1 residues (Leu-9, Tyr-185, and Tyr-293), coupled with functional st

112 d of bed-rest inactivity (CON compared with LEU: -9% +/- 2% and +1% +/- 3%; group x time interaction

113 tion mapping identified the cleavage site as Leu(90)/Val(91) in the 95-amino acid ADRA1D NT domain, s

114 d Leu-378 with ZapD residues Leu-74, Trp-77, Leu-91, and Leu-174.

115 ependent on a single autoinhibitory residue (Leu-919) upstream of the C-terminal cytoplasmic domain i

116 Second, Leu-938 mutants (except L938F) and Asp-1028 mutants show

117 -1028 and Asn-1029 from domain A, as well as Leu-938, Ala-978, and Leu-981 from domain B) near subsit

118 Thus, residue Leu(940) in domain B is crucial for linkage and reaction

119 Residue Leu(940) in domain B of GTF180, the glucansucrase of the

120 Herein, we show that mutations in Leu(940) of wild-type GTF180-DeltaN all caused an increa

121 on of the GRP78 primary amino acid sequence (Leu(98)-Leu(115)).

122 Third, mutation of Leu-981 and Asn-1029 significantly affected the transgly

123 m domain A, as well as Leu-938, Ala-978, and Leu-981 from domain B) near subsite +1 that may be criti

124 approximately 280% more than placebo and EAA-Leu after exercise.

125 molecular recognition of the tripeptide Tyr-Leu-Ala by the synthetic receptor cucurbit[8]uril (Q8) i

126 ith the straightforward incorporation of Tyr-Leu-Ala into recombinant proteins should make this syste

127 the minimal active sequence of pep5, whereas Leu-Ala substitutions totally abolished pep5 cell death

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

129 Three novel DPP-IV inhibitory peptides, Ile-Leu-Ala-Pro, Leu-Leu-Ala-Pro and Met-Ala-Gly-Val-Asp-His

130 lacebo-treated patients, as measured by FACT-Leu and EQ-5D, during maintenance treatment.

131 nzyme revealed that BCAT6 transaminates Val, Leu and Ile as well as the corresponding 2-oxo acids but

132 rometry (MS) for de novo protein sequencing, Leu and Ile have been generally considered to be indisti

133 sion mass spectrometer, to reliably identify Leu and Ile residues in proteins and peptides.

134 amino acid sequences, including identity of Leu and Ile residues, can be accurately obtained solely

135 reduced by supplementation of LNAAs, such as Leu and Ile, with a strong affinity for the LNAA transpo

136 eu homeostasis, where AHAS affects total Val+Leu and IPMS controls partitioning between these amino a

137 bstantial reduction in content of JA-Ile, JA-Leu and JA-Val in florets.

138 ed all three six-fold code amino acids (Arg, Leu and Ser) and significantly higher counts of Di-amino

139 aurane as well as kaurene are produced since Leu and Tyr in the P. patens kaurene synthase active sit

140 hese critical functions, S. aureus represses Leu and Val synthesis, instead preferring to acquire the

141 , and not BcaP, is required for transporting Leu and Val to be used for iso-BCFA synthesis.

142 ells (MCF-7) decreases the induction of tRNA(Leu) and 5S rRNA genes by alcohol, whereas reduction of

143 ination of isobaric residues (Xle): leucine (Leu) and isoleucine (Ile).

144 ely) but not conserved in E. coli OtsA (His, Leu, and Asp, respectively), providing a rationale for t

145 residues of the SRT were replaced with Ala, Leu, and Gly, trans-activation activities of the modifie

146 . suis is auxotrophic for Arg, Gln/Glu, His, Leu, and Trp in chemically defined medium.

147 easurements of the methyl groups of the Ile, Leu, and Val residues at two static magnetic fields.

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

149 Met to Leu apoA-I variants were used to establish the predomina

150 ched-chain amino acids (BCAAs) Ile, Val, and Leu are essential nutrients that humans and other animal

151 utions (Trp --> Pro, Gly --> Ser and Arg --> Leu) are responsible for the evolution of HTG's unique s

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

153 efined by their conserved N-terminal Arg-Xaa-Leu-Arg (RxLR) motif.

154 binds to host macrophages with its ELR (Glu-Leu-Arg) peptide motif.

155 l liberate 5 and cathepsin K cleavage of the Leu-Arg-PABA element will liberate alendronic acid.

156 yl-argininyl-para-aminophenylmeth ylalcohol (Leu-Arg-PABA).

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

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

159 two fragments from Glp-His-Trp-Ser-Tyr-D-Ala-Leu-Arg-Pro-NHEt (LHRHa) to Trp-Ser-Tyr-D-Ala-Leu-Arg-Pr

160 en milk bioactive peptides, Ile-Asn-Tyr-Trp, Leu-Asp-Gln-Trp, and Leu-Gln-Lys-Trp, and different bile

161 In electrophysiological studies, Leu at the 9'-position in the M2 membrane-spanning segme

162 Leu co-ingestion with daily meals enhances integrated My

163 Leu transamination and higher intracellular Leu concentrations than the cells from wild type (WT) mi

164 eter can provide sufficient evidence for Ile/Leu discrimination.

165 ions employing MS(3) (ETD-HCD) for rapid Ile/Leu distinction.

166 ion-phase- and gas-phase deuterium uptake of Leu-Enkephalin and Glu-Fibrinopeptide B, confirmed that

167 he endogenous peptide opioid receptor ligand Leu-enkephalin as a model compound.

168 and/or efficacy of the orthosteric agonists leu-enkephalin, SNC80 and TAN67, as measured by receptor

169 Insertion of (one at a time) Glu, Leu, Gln, or Cys at positions R295, R141, and R363, or L

170 tides, Ile-Asn-Tyr-Trp, Leu-Asp-Gln-Trp, and Leu-Gln-Lys-Trp, and different bile salts in the submice

171 with the highest sensitivity and selectivity Leu-Gly-Arg-Met-Gly-Leu-Pro-Gly-Lys was selected to cons

172 with a C-terminal Gly, H-Asn-Phe-Gly-Ala-Ile-Leu-Gly-NH2) and acyl carrier protein (65-74) fragment (

173 -Flp-(Gly-Pro-Hyp)4-Gly-Lys(Mca)-Thr-Gly-Pro-Leu-Gly-Pro-Pro-Gly-Lys(Dnp)- Ser-(Gly-Pro-Hyp)4-NH2] ha

174 y 30% +/- 9% (CON group) and by 10% +/- 10% (LEU group) (main effect for time, P < 0.05), but no diff

175 knee extensor peak torque (CON compared with LEU group: -15% +/- 2% and -7% +/- 3%; group x time inte

176 according to AA was: Trp > norleucine > Phe, Leu > Ile > His >3,4-dihydroxyphenylalanine, Arg > Val >

177 cat/Km), we show that ClpP1P2 prefers Met >> Leu > Phe > Ala in the X1 position, basic residues or Tr

178 n binding domain: (i) a previously reported (Leu --> Pro) stabilizing mutant (FnIII9'10), (ii) an Arg

179 The hierarchy Leu>Met>Ile>Val at the C-terminal position was determine

180 AHAS and IPMS AHAS and IPMS regulate Val and Leu homeostasis, where AHAS affects total Val+Leu and IP

181 The branched-chain amino acids (BCAAs) Leu, Ile, and Val are among nine essential amino acids t

182 Branched-chained amino acids (BCAAs) (Leu, Ile, and Val) and their catabolites, propionylcarni

183 , this integrated, online LC-MS approach for Leu/Ile assignment can be applied to de novo sequencing

184 The merits and limitations of this Leu/Ile discrimination approach are evaluated.

185 guidelines we unambiguously identified every Leu/Ile residue in peptides containing up to five Leu/Il

186 demonstrated, for the first time, that every Leu/Ile residue in the variable regions of a monoclonal

187 le residue in peptides containing up to five Leu/Ile residues and molecular masses up to 3000 Da.

188 Positioning of incorrect Leu/Ile residues in variable domains, especially in CDRs

189 In contrast, Leu/Ile was negatively associated with GDR in nonobese a

190 ssociation), followed by leucine/isoleucine (Leu/Ile) (negative association).

191 rms highly stable dimers/oligomers through a Leu/Ile/Phe-rich domain.

192 ites, which suggests a strong preference for Leu in the P1' position.

193 beta1c subunits preferentially bind Asp and Leu in their S1 pockets, while Glu and large hydrophobic

194 a-DOTA-dPEG2-Lys-Arg-Pro-Hyp-Gly-Cha-Ser-Pro-Leu) in B1R-positive (B1R+) HEK293T::hB1R tumor xenograf

195 The ADAMTSL5 autoantigen possessed a P7-Leu instead of the P7-Arg residue, but nevertheless was

196 whereas that of its sequence isomer Tyr-Ala-Leu is 34 muM.

197 Leu is a known activator of the mammalian target of rapa

198 ion of D-methionine (D-Met) and D-leucine (D-Leu) is presented.

199 Golgi and returned to the ER by Lys-Asp-Glu-Leu (KDEL) receptors, which bind to an eponymous tetrape

200 pha/alpha-pseudodipeptide, depsipeptide (Boc-Leu-Lac-OEt).

201 A conserved Ile Leu Leu sequence within the CWB2 repeats is essential fo

202 olution of 3.07 A and with benzyloxycarbonyl-Leu-Leu (Z-LL) bound at 2.9 A.

203 DPP-IV inhibitory peptides, Ile-Leu-Ala-Pro, Leu-Leu-Ala-Pro and Met-Ala-Gly-Val-Asp-His-Ile, with IC

204 Leu-Leu-Met (LLM)-domain B-GATAs are a subfamily of the

205 phore nigericin, or the lysosomotropic agent Leu-Leu-O-methyl ester.

206 thways or the lysosome-destabilizing agonist Leu-Leu-O-methyl ester.

207 EAAs with leucine, EAAs without leucine (EAA-Leu), leucine alone, or flavored water (placebo; control

208 This includes a Leu-Lys-Ile-Pro sequence (residues 125-128 of AKAP79) th

209 Seven synthetases, Ala-, Arg-, Asp-, Asn-, Leu-, Lys- and TyrRS, appear to associate with ES7.

210 ides subsp. cremoris (20%) whilst 25% CFS of Leu. mes. subsp. cremoris and Lc. lactis subsp. lactis s

211 jugating jasmonic acid (JA) to at least Ile, Leu, Met, Phe, Trp and Val and both osjar1 alleles had s

212 tabolism and highlight the important role of Leu metabolism in T cells.

213 y selective PACE4 inhibitor known as a Multi-Leu (ML) peptide.

214 ameters, planar sheets formed by the Arg(18)-Leu mutant (R18L-CA), and R18L-CA spheres with 20-100 nm

215 erization between the wild-type and the poly-Leu mutant are suggested to be responsible for the repor

216 terface was found for a fusion-inactive poly-Leu mutant.

217 patient and her father had a His-58(E7) --> Leu mutation in alpha1.

218 t MJ9, Pip-d-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH(2) (Pip, 4-amino-1-carboxymethyl-piperidine), was

219 piperidine-D-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2 ((68)Ga-RM2) is a synthetic bombesin receptor an

220 piperidine-d-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2 ((68)Ga-RM2) is a synthetic bombesin receptor an

221 piperidine-d-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2 (RM2, 1; DOTA:1,4,7,10-tetraazacyclododecane-1,4

222 betaAla-[H-D-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2], and NODA-MPAA is 2-[4-(carboxymethyl)-7-{[4-(c

223 betaAla-[H-D-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2], JMV4168 is DOTA-betaAla-betaAla-[H-D-Phe-Gln-T

224 diglycolic acid-DPhe-Gln-Trp-Ala-Val-Gly-His-Leu-NHEt), showing excellent tumor localizing efficacy i

225 thylpiperidine-d-Phe-Gln-Trp-Ala-Val-Gly-His-Leu-OCH3 (ARBA05, 3) analogues are labeled with (111)In

226 mong the small peptides 2-31, (H)Gly-Gly-Phe-Leu(OMe) (30) reduced prostaglandin production of COX-2

227 nd length (i.e. Ala, Arg, Cys, His, Glu, and Leu) on transporter stability and function.

228 controls (P < 0.05) but increased with BCAA/LEU only in controls (P < 0.001).

229 ase, beta-ketosulfonamides derived from Val, Leu or Ile gave the expected beta-keto-alpha,alpha-diflu

230 hydrophobic character; (3) ISDs tend to have Leu or Ile residues at their core; (4) ISDs are approxim

231 atients with cirrhosis was reduced with BCAA/LEU (P = 0.01).

232 The guest residues were Thr, Ala, Leu, Phe, Tyr, and Trp.

233 ired chemotactic migration toward formyl-Met-Leu-Phe (fMLP) and stromal cell-derived factor 1alpha (S

234 rified recombinant protein, we show that the Leu-Phe substitution increases turnover rate of acetalde

235 lock the AnxA1 pathway (by using N-t-Boc-Met-Leu-Phe, a nonselective AnxA1 receptor antagonist, or by

236 the natural chemotactic peptide n-formyl-Met-Leu-Phe.

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

238 at least 9 sense codons coding for Ser, Arg, Leu, Pro, Thr, and Gly.

239 Val-Glu-Leu-Tyr-Pro, Ala-Phe-Val-Gly-Tyr-Val-Leu-Pro and Glu-Lys-Ser-Tyr-Glu-Leu-Pro.

240 th severe periodontitis (P2 and P3), cyclo (-leu-pro) and cyclo (-phe-pro) were significantly associa

241 associated with 2 novel metabolites-cyclo (-leu-pro) and cyclo (-phe-pro)-at 21 d of biofilm overgro

242 sitivity and selectivity Leu-Gly-Arg-Met-Gly-Leu-Pro-Gly-Lys was selected to construct calibration cu

243 -Gly-Tyr-Val-Leu-Pro and Glu-Lys-Ser-Tyr-Glu-Leu-Pro.

244 the Nt-acetylated Ac-MX-Rgs2 (X = Arg, Gln, Leu) proteins are specific substrates of the mammalian A

245 example of the substitution of a stabilizing Leu residue in a coiled-coil hydrophobic core position d

246 Slo2 channels contain two conserved Leu residues in each of the four S6 segments that line t

247 ggests that hydrophobic interactions between Leu residues in the upper region of the S6 segments cont

248 e in hydrophobic gating, replacement of both Leu residues with the isosteric but polar residue Asn (L

249 reased the amounts of adaptive his, met, and leu revertants produced by the B. subtilis YB955 parenta

250 Human patients expressing Met-Leu-Rgs2 (ML-Rgs2) or Met-Arg-Rgs2 (MR-Rgs2) are hyperte

251 Our findings indicate that a Leu-rich region preceding the polyQ tract causes it to b

252 e chimeric proteins containing an N-terminal Leu-rich repeat (LRR) and a C-terminal extensin domain.

253 e resistance genes encode nucleotide binding Leu-rich repeat (NLR) proteins that trigger a rapid loca

254 Leu-rich repeat extensins (LRXs) are chimeric proteins c

255 es of immune deficiency (Imd), JAK/STAT, and Leu-rich repeat immune factors.

256 proximately 300 site-directed mutants by Ala/Leu scanning mutagenesis, the expression of each mutant

257 enantiomer pairs d/l-Ala, -Asp, -Glu, -His, -Leu, -Ser, -Val and the three achiral amino acids Gly, b

258 tion at the phoU gene that results in Ser200 Leu substitution and a constitutive expression of the Ph

259 e is only one amino acid N-terminal to a Val/Leu substitution associated with schizophrenia.

260 methylated analogue of sanguinamide A with a Leu substitution at position 2 that exhibits solvent-dep

261 kest-binding analogs contained Val, Ile, and Leu substitutions.

262 stable peptide sequence NLys-Lys-Pro-Tyr-Tle-Leu suitable for PET imaging.

263 ets while ingesting a placebo (days 0-2) and Leu supplement (5 g leucine/meal; days 3-5) with their 3

264 The BCAA/LEU supplement did not alter myostatin expression, but m

265 3, named CP), but with an innovative Ile-Asp-Leu tail (IDL) that dramatically increased the inhibitor

266 A loci (e.g., the nuclear tRNA(Gly) and tRNA(Leu), the mitochondrial tRNA(Val) and tRNA(Pro)) were st

267 we evaluated treatment of one tetra-peptide, Leu-Thr-Lys-Glu, in APBD patient cells.

268 A Leu to Ala amino acid substitution approximately 10 A fr

269 Here, we have identified a Leu to Glu mutation at position 406 (L406E) in the extra

270 ymous and involves an amino acid change from Leu to Ser.

271 After the addition of IDL (Ile-Asp-Leu) to the C terminus of CHR peptide WQ or MT-WQ, the c

272 ells from the BCATc(-/-) mouse exhibit lower Leu transamination and higher intracellular Leu concentr

273 Induction of BCATc correlates with increased Leu transamination, whereas T cells from the BCATc(-/-)

274 the WT pro-SP-C poly-Val and a designed poly-Leu transmembrane (TM) segment in the endoplasmic reticu

275 Leucinemia was higher with Leu treatment than with placebo treatment (P < 0.001).

276 th treatments (P = 0.39) but was higher with Leu treatment than with placebo treatment in the rested

277 egrated rate of MyoPS during the placebo and Leu treatments in the rested and REX legs.

278 ral REX was performed during the placebo and Leu treatments.

279 transcription termination occurs within the leu-tRNA gene and is mediated by the DNA binding protein

280 sition (ligand 3: H-Dmt-d-Ala-Gly-NMePhe-Pro-Leu-Trp-NH-Bn(3',5'-(CF3)2)) displays binding as well as

281 tion (ligand 5: H-Dmt-d-Ala-Gly-Phe(4-F)-Pro-Leu-Trp-NH-Bn(3',5'-(CF3)2)) exhibits balanced binding a

282 ds 3, 5, and 7 (H-Tyr-d-Ala-Gly-Phe(4-F)-Pro-Leu-Trp-NH-Bn(3',5'-(CF3)2)) showed that their stability

283 ysis of a polar mixture composed of Leu-Val, Leu-Tyr, Gly-Tyr, and Ala-Tyr dissolved in DMSO-d6/GL (8

284 Lineweaver-Burk plots suggest that Val-Glu-Leu-Tyr-Pro acts as a non-competitive inhibitor against

285 revealed that oral administration of Val-Glu-Leu-Tyr-Pro can decrease systolic blood pressure signifi

286 These results suggest that the Val-Glu-Leu-Tyr-Pro would be a beneficial ingredient for nutrace

287 t potent peptides were identified as Val-Glu-Leu-Tyr-Pro, Ala-Phe-Val-Gly-Tyr-Val-Leu-Pro and Glu-Lys

288 if is dependent on stretches of rare codons, Leu(UUA)-Gly(GGU)-Val(GUA).

289 affinity wild-type and mutant human mt-tRNA(Leu(UUR)) and mt-tRNA(Lys), and stabilize mutant mt-tRNA

290 ither with the m.3243A>G mutation in mt-tRNA(Leu(UUR)) or with mutations in the mt-tRNA(Ile), both of

291 d mt-tRNA(Lys), and stabilize mutant mt-tRNA(Leu(UUR)).

292 the analysis of a polar mixture composed of Leu-Val, Leu-Tyr, Gly-Tyr, and Ala-Tyr dissolved in DMSO

293 ions was similar to that in water, while Fru-Leu was reduced up to 47% in the emulsions.

294 The clinical mutation (Leu) was found to markedly impair multiple biochemical a

295 lalanine (Fru-Phe) and fructose-leucine (Fru-Leu) was monitored by mass spectrometry.

296 D-Met and D-Leu were successfully detected becoming this proof-of-th

297 n this way, a group I intron located in tRNA(Leu), which has been used extensively for phylogenetic s

298 n is facilitated by the misacylation of tRNA(Leu) with methionine by the methionyl-tRNA synthetase (M

299 wing the enzyme to conditionally charge tRNA(Leu) with methionine.

300 NE3 and possibly cooperates with homeodomain Leu zipper IV transcription factors.