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

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

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

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

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

7 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

8 -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

9 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

10 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)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

94 -1028 and Asn-1029 from domain A, as well as Leu-938, Ala-978, and Leu-981 from domain B) near subsit

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

96 3, named CP), but with an innovative Ile-Asp-Leu tail (IDL) that dramatically increased the inhibitor

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

161 1 regulator under AA-starved conditions, how Leu regulates autophagy is poorly understood.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

226 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

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

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

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

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

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

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

235 374, Pro-375, and Leu-378 with ZapD residues Leu-74, Trp-77, Leu-91, and Leu-174.

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

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

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

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

240 69, Ile-72, Tyr-76), and C-terminal segment (Leu-81, Glu-84) are critical for in vivo Fe-S cluster bi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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