ライフサイエンスコーパス: Leu

1 Leu co-ingestion with daily meals enhances integrated My

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

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

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

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

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

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

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

9 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

10 -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

11 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

12 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)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

43 lagen alpha chains sequentially, at Gly(775)-Leu(776) in collagen II.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

95 Ile-Pro-Ile-Gln-Tyr, Tyr-Pro-Tyr-Tyr and Leu-Pro-Tyr-Pro-Tyr were substrate-, Leu-Pro-Leu-Pro-Leu

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

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

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

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

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

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

102 -1028 and Asn-1029 from domain A, as well as Leu-938, Ala-978, and Leu-981 from domain B) near subsit

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

104 3, named CP), but with an innovative Ile-Asp-Leu tail (IDL) that dramatically increased the inhibitor

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

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

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

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

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

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

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

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

113 Additionally, the relationship between Leu/Ile and GDR was magnified in T2DM males.

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

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

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

117 ions formed on ionization being protected by Leu, Tyr and Phe residues.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

157 d leucine curve was greatest for the W6+High-Leu group compared with the W6 and W6+Low-Leu groups (P

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

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

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

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

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

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

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

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

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

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

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

169 NMR data for the methyl side chains on Ile, Leu, and Val residues showed changes in conformational e

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

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

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

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

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

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

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

177 of HO-2 reveals specific residues, including Leu-201, near the heme face of HO-2 that are affected by

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

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

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

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

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

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

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

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

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

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

188 gh-Leu group compared with the W6 and W6+Low-Leu groups (P < 0.001).

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

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

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

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

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

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

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

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

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

198 The enantiomeric phosphonic acid analogs of Leu and hPhe, which correspond to the P1 amino acid resi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

221 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

222 -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

223 Tyr-Pro-Tyr were substrate-, Leu-Pro-Leu-Pro-Leu and CasH were prodrug- while WPH and LFH were true D

224 ptides (Ile-Pro-Ile-Gln-Tyr, Leu-Pro-Leu-Pro-Leu, Tyr-Pro-Tyr-Tyr, Leu-Pro-Tyr-Pro-Tyr and Ile-Pro-Il

225 Leu-Pro-Tyr-Pro-Tyr were substrate-, Leu-Pro-Leu-Pro-Leu and CasH were prodrug- while WPH and LFH wer

226 hetic peptides (Ile-Pro-Ile-Gln-Tyr, Leu-Pro-Leu-Pro-Leu, Tyr-Pro-Tyr-Tyr, Leu-Pro-Tyr-Pro-Tyr and Il

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

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

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

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

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

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

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

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

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

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

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

238 374, Pro-375, and Leu-378 with ZapD residues Leu-74, Trp-77, Leu-91, and Leu-174.

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

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

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

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

243 69, Ile-72, Tyr-76), and C-terminal segment (Leu-81, Glu-84) are critical for in vivo Fe-S cluster bi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

259 Tyr and Leu-Pro-Tyr-Pro-Tyr were substrate-, Leu-Pro-Leu-Pro-Leu and CasH were prodrug- while WPH and

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

285 ved synthetic peptides (Ile-Pro-Ile-Gln-Tyr, Leu-Pro-Leu-Pro-Leu, Tyr-Pro-Tyr-Tyr, Leu-Pro-Tyr-Pro-Ty

286 n-Tyr, Leu-Pro-Leu-Pro-Leu, Tyr-Pro-Tyr-Tyr, Leu-Pro-Tyr-Pro-Tyr and Ile-Pro-Ile) and a casein (CasH)

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

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

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

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

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

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

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

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

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

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

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

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

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

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