ライフサイエンスコーパス: Leu

1 ated, with Val(1)-Val(2), Ile(1)-Ala(2), and Leu(1)-Val(2) variants exhibiting ProT(QQQ) affinity and

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

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

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

5 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.

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

7 improvements obtained with both Ala(101) and Leu(106) have implications regarding glyphosate-tolerant

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

9 nserved residues in the Nef dimer interface (Leu(112), Tyr(115), and Phe(121)) and demonstrated atten

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

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

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

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

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

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

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

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

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

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

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

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

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

23 Leu(137) of HY5 is found to be important for the HY5-BIN

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

30 rotease trypsin due to replacement of the P1 Leu(15) in the reactive loop with Arg(15).

31 unusual inhibitory properties are due to (a) Leu(15) in the reactive site loop P1 position that sits

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

33 f class D SBLs (i.e. Trp(105), Val(120), and Leu(158), using OXA-48 numbering) impact on the relative

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

35 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

36 -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

37 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

38 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)

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

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

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

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

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

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

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

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

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

48 c peptide arising from cleavage at Gly(2196)-Leu(2197) We noted that this scissile bond is in the lin

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

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

51 hereas replacing Pro-29 together with either Leu-25 or Val-17 of TM4SF20 with the corresponding resid

52 Because Val-17, Gly-22, Leu-25, Asn-26, and Pro-29 are predicted to reside along

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

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

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

56 ey for ceramide binding and that Arg(258) or Leu(293) residues are involved in the myosin IIA interac

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

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

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

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

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

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

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

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

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

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

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

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

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

70 Thus, replacement of either Leu-395 or Phe-396 with Ala led to inactivation of MGAT4

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

72 Site-directed mutagenesis revealed that Leu(46) and Phe(123) were involved in NADH binding, wher

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

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

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

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

77 te dependent enzymes, l-Ile 4-hydroxylase, l-Leu 5-hydroxylase and polyoxin dihydroxylase, are previo

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

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

80 Finally, we defined Leu-601 in NBD2 as crucial for Hsp104 hexamerization.

81 xposed cluster included residues adjacent to Leu(63) in the loop connecting helices 1 and 2.

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

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

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

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

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

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

88 localization of PC7 and its Ala variants of Leu-725 and Glu-719 and Glu-721 revealed that Leu-725 en

89 eu-725 and Glu-719 and Glu-721 revealed that Leu-725 enhances PC7 localization to early endosomes and

90 dues in the CT, namely Glu-719, Glu-721, and Leu-725, that are part of a novel motif, EXEXXXL(725), c

91 acid-long amphipathic helix (residues Gln-62-Leu-73) that together confer cholesterol responsiveness.

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

93 ntedanib co-crystal structure disclosed that Leu-730 in RET engages in hydrophobic interactions with

94 374, Pro-375, and Leu-378 with ZapD residues Leu-74, Trp-77, Leu-91, and Leu-174.

95 Interestingly, a short sequence of FtsN (Leu(75)-Gln(93), known as (E)FtsN) was shown to be essen

96 h and Ile(36) patch, respectively, including Leu(8), which is part of the two patches).

97 er the potency nor efficacy of Pro(8)-OT and Leu(8)-OT differed with respect to G(q) signaling.

98 he mOTR, Pro(8)-OT was more efficacious than Leu(8)-OT in measures of G(q) activation, with both pept

99 In both mOTR- and hOTR-expressing cells, Leu(8)-OT was more potent and modestly more efficacious

100 nserved with leucine in the eighth position (Leu(8)-OT).

101 In mOTR cells, Leu(8)-OT-induced hyperpolarization was modestly inhibit

102 Both Leu(8)-OXT and Pro(8)-OXT produce a less efficacious res

103 ) signaling responses of AVP, Pro(8)-OXT and Leu(8)-OXT at human, macaque, and marmoset AVPR1a.

104 cts than the consensus mammalian OXT ligand (Leu(8)-OXT).

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

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

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

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

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

110 69, Ile-72, Tyr-76), and C-terminal segment (Leu-81, Glu-84) are critical for in vivo Fe-S cluster bi

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

112 ling and survival, whereas overexpression of Leu-89 NCS1 variants decreased Ca(2+) signaling and surv

113 We also identified Leu-89, a residue in the hydrophobic pocket of NCS1, as

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

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

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

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

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

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

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

121 -1028 and Asn-1029 from domain A, as well as Leu-938, Ala-978, and Leu-981 from domain B) near subsit

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

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 nesis studies suggest that Ile-A10, Ser-A12, Leu-A13, and Glu-A17 also belong to insulin's site 2.

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

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

127 least two-base substitutions, in contrast to Leu and Arg, of which codons are mutually exchangeable b

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

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

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

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

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

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

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

135 h amino acid in PSLFQ to Ala identified both Leu and Phe as independently essential for MGAT4D-L acti

136 than in CTL (-22% +/- 4%; P < 0.01) in both LEU and PLA.

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

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

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

140 isrupt hydrolytic editing of mischarged tRNA(Leu) and to result in variation within the proteome of t

141 peptides were rich in Glu, Asp, Lys, Gly and Leu, and also exhibited diverse bioactivities, among the

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

143 Phe, Leu, and Met are favored residues, each with a cleavage

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

145 ensive (13)C-methyl relaxation study of Ile, Leu, and Val (ILV) residues of PTP1B, which, because of

146 itions are, in general, more rigid than Ile, Leu, and Val methyl probes in protein side chains.

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

150 Very hydrophobic segments (e.g., 16 Leu) are stably incorporated into the inner membrane, re

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

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

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

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

155 that the hexapeptide H(2)N-(CH(2))(4)-CO-Pro-Leu-Arg-Phe-Gly-Ala-NH-CH(2)-Fc is the optimal probe for

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

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

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

159 ived from the hexapeptide acetyl-Arg-Tyr-Arg-Leu-Arg-Tyr-NH(2) (1), reported to be a Y(4)R partial ag

160 ncation of 1 resulted in a tetrapeptide (Arg-Leu-Arg-Tyr-NH(2)), being a Y(4)R partial agonist with u

161 g the 20 amino acids, three of them-leucine (Leu), arginine (Arg), and serine (Ser)-are encoded by si

162 it capitalizes on a highly conserved Asp-Ser-Leu-Asp amino acid sequence in ACPs to which acyl groups

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

164 Treatment of TCam-2 cells with the peptide Leu-Asp-Phe-Ile (LDFI), a full leptin-receptor antagonis

165 acid changes, an Arg in place of the native Leu at L185-positioned over one face of H(B) and only ~4

166 ACE prefers to cleave substrates with Phe or Leu at the C-terminal P2' position and Gly in the P6 pos

167 The mis-incorporation of Nva for leucine (Leu) causes heterogeneity and in some cases even toxicit

168 Leu co-ingestion with daily meals enhances integrated My

169 Interestingly, in Leu deprivation conditions, the dominant effects on auto

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

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

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

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

174 The opioid receptor agonist, leu-enkephalin, was predicted to have antisurvival effec

175 hypothalamic levels of the endogenous opioid Leu-enkephalin, which is derived from the KOR agonist pr

176 m Gly residue was proved by the synthesis of Leu-enkephalin.

177 In extent, the substrate Leu-FC can effectively monitor cisplatin induced overexp

178 The substrate Leu-FC empowered sensor displayed broad dynamic range wi

179 y hydrolyze the Leu residue of the substrate Leu-FC to eliminate the unmasked electrochemical reporte

180 On top of this, the probe Leu-FC was employed in real-time active profiling of cel

181 ubstrate leucine-benzyl ferrocene carbamate (Leu-FC) for selective profiling of LAP activity in live

182 tase that accurately charges leucine to tRNA(Leu) for protein translation.

183 XAT contains a canonical Gly-Asp-Ser-Leu (GDSL) motif and is encoded by a member of the GDSL

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

185 tution assays revealing that the p7 residue (Leu/Gln) is critical for specific epitope recognition by

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

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

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

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

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

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

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

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

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

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

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

197 Remarkably, replacement of Leu in 1 and in derivatives of 1 by Trp turned Y(4)R ago

198 the recognition of motifs based on Tyr or di-Leu in their cytoplasmic tails.

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

200 biting a DFG-out and an unprecedented DFG-in/Leu-in conformation.

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

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

203 While leucine (Leu) is a critical mTORC1 regulator under AA-starved con

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

205 r, which recognises a C-terminal Lys-Asp-Glu-Leu (KDEL) sequence.

206 cognition of a carboxyl-terminal Lys-Asp-Glu-Leu (KDEL) signal by the KDEL receptor.

207 fied two volatile cyclic dipeptides, cyclo(L-Leu-L-Pro) and cyclo(L-Pro-L-Pro), from the complex mixt

208 blend, compared to the controls, the cyclo(L-Leu-L-Pro) blend, or a combined blend with both cyclic d

209 ro-L-Pro) and a modulating effect of cyclo(L-Leu-L-Pro) that may depend on the relative concentration

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

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

212 resence of the pulcherrimin precursors cyclo(Leu-Leu) and pulcherriminic acid and identified new prec

213 ent pulcherrimin, from cyclodileucine (cyclo(Leu-Leu)) as a precursor, and exhibits strong antifungal

214 nalysis of Spo7, we identified a hydrophobic Leu-Leu-Ile (LLI) sequence comprising residues 54-56 as

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

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

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

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

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

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

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

222 te and a C-terminal swinging arm, with a Cys-Leu-Met-Cys sequence suggested to act as a shuttle dithi

223 that the loss of the C-terminal Tyr-Ala-Met-Leu motif is responsible for P0 mislocalization, as its

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

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

226 uced transmission and the subsequent Pro(323)Leu mutation in the RNA-dependent RNA polymerase led to

227 b immobilization, with thrice-daily leucine (LEU; n = 8) or placebo (PLA; n = 8) supplementation (15

228 that in most cell types, including neurons, Leu negatively regulates autophagosome biogenesis via it

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

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

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

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

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

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

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

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

237 the de novo biosynthesis of fatty acids and Leu; peroxisome-localized ACN1 enables the incorporation

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

239 hemotaxis towards chemoattractant formyl Met-Leu-Phe (fMLP) coupled with their decreased polarization

240 ia coli and the chemoattractant N-formyl-Met-Leu-Phe (fMLP)-coated beads.

241 reased neutrophil chemotaxis to a formyl-Met-Leu-Phe gradient.

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

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

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

245 In budding yeast, CDK substrates with Leu/Pro-rich (LP) docking motifs are recognized by Cln1/

246 1 regulator under AA-starved conditions, how Leu regulates autophagy is poorly understood.

247 Thus, in most cell types we examined, Leu regulates autophagy via the impact of its metabolite

248 practice, LAP instantaneously hydrolyze the Leu residue of the substrate Leu-FC to eliminate the unm

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

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

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

252 oducing Trp(85) or Phe(29) to replace Cys or Leu, respectively, disrupts packing in the hydrophobic c

253 MD simulations, substitution of Arg259 with Leu resulted in the loss of morphine, 4-methylumbellifer

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

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

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

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

258 Here, we show that specific PM-located Leu-rich-repeat receptor-like-kinases, Qian Shou kinase

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

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

261 Most substrates contain a C-terminal Ser-Lys-Leu (SKL) sequence that is recognized by the receptor Pe

262 oCLU is translated from a non-canonical CUG (Leu) start site in Exon 3, a site that coincides with an

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

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

265 change at nucleotide 1965 producing a Val-to-Leu substitution at position 330 of the viral envelope (

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

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

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

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

270 LAT1 features a canonical Leu T-fold and exhibits an unusual loop structure on tra

271 3, named CP), but with an innovative Ile-Asp-Leu tail (IDL) that dramatically increased the inhibitor

272 the hexapeptide VEALYL (Val-Glu-Ala-Leu-Tyr-Leu), the B-chain residue 12-17 segment of insulin that

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

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

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

276 TR2-L129Q receptor, with the substitution of Leu to Gln at position 129 (3.43).

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

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

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

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

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

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

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

284 o acids were composed of Val, Pro, Tyr, Met, Leu, Trp, Phe, Lys and Glu.

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

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

287 ation of the hexapeptide VEALYL (Val-Glu-Ala-Leu-Tyr-Leu), the B-chain residue 12-17 segment of insul

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

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

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

291 easing heteroplasmy levels of the mtDNA tRNA(Leu(UUR)) nucleotide (nt) 3243A > G mutation result succ

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

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

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

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

296 ed and subjected to a d-amino acid scan, and Leu was replaced by different amino acids.

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

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 nteract with TGACG-motif binding (TGA) basic Leu zipper (bZIP) transcription factors for recruitment

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