ライフサイエンスコーパス: Phe

1 Phe accumulation had multifaceted intercompartmental eff

2 Phe has been proposed to bind, in addition to the cataly

3 Phe is the substrate for the PAH active site, but also a

4 Phe residues in Delta-somatostatin are hypothesised as i

5 Phe(79) interacts with His(85), and Phe(79) mutants show

6 yl-insulin when infused into the ileum, B(1)-Phe-cholyl-insulin did cause a long lasting hypoglycaemi

7 ese results were taken as evidence that B(1)-Phe-cholyl-insulin had been taken up by the ileal bile s

8 This would indicate that B(1)-Phe-cholyl-insulin is worthy of further investigation fo

9 B(29)-Lys-cholyl-insulin and B(1)-Phe-cholyl-insulin, both were biologically active as ind

10 e KYE28A, with Ala substitutions at Phe(11), Phe(19), Phe(23), and Tyr(25) was designed, which showed

11 Analogues 69 ([Gly(2),Nle(10),D-Thi(11),Phe(16)]hGLP-2-(1-30)-NH2), 72 ([Gly(2),Nle(10),D-Phe(11

12 ts of side chain residues His(57), Phe(189), Phe(191), and Phe(336); it also disturbs the rotation of

13 with Ala substitutions at Phe(11), Phe(19), Phe(23), and Tyr(25) was designed, which showed attenuat

14 ribosomes and others to incorporate beta(3)-Phe analogs into full length DHFR in vivo.

15 erized by a type II' beta-turn around Gly(3)-Phe(4) and a gamma-turn around Gly(2), providing spectro

16 port requires URAT1 residues Cys-32, Ser-35, Phe-365 and Ile-481.

17 arrangements of side chain residues His(57), Phe(189), Phe(191), and Phe(336); it also disturbs the r

18 site I and mimics the interactions of IL-6R Phe(229).

19 of HCDR3 valine ties into site I like IL-6R Phe(279), whereas a LCDR1 tyrosine side chain occupies a

20 having e.g. 4.8% Lys, 2.7% Met+Cys, and 7.7% Phe+Tyr.

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

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

23 The analog containing a Phe(3) was identified as not only exhibiting binding aff

24 s in the absence of Phe, is different from a Phe-stabilized allosterically activated PAH tetramer.

25 ggest gating was associated with shifts of a Phe residue between open and closed conformations plus a

26 enylketonuria treatment consists mainly of a Phe-restricted diet, which leads to suboptimal neurocogn

27 cylation of tRNA(Phe) with the more abundant Phe oxidation product o-Tyr is limited by kinetic discri

28 To achieve Phe hyperaccumulation in a plant system, we simultaneous

29 new aspects of the metabolism of amino acid Phe operative during the interaction between T. gondii a

30 that PAA is synthesized from the amino acid Phe, via phenylpyruvate.

31 clized analogues of the aromatic amino acids Phe, Tyr, Trp, and His within peptide medicinal chemistr

32 orrelate to ASP loop residues, an additional Phe to Ala substitution was synthesized and observed to

33 hile beta-ketosulfonamides derived from Ala, Phe, or hPhe gave the hydrates of the imino beta-keto-al

34 at the mMC4R, c[Pro-His-DPhe-Arg-Trp-Asn-Ala-Phe-DPro] and c[Pro-His-DPhe-Arg-Trp-Dap-Ala-DPro], and

35 rocyclic scaffold (c[Pro-Arg-Phe-Phe-Asn-Ala-Phe-DPro]) were explored with 14-compound and 8-compound

36 ve loop derivative c[Pro-Arg-Phe-Phe-Xxx-Ala-Phe-DPro], where Xxx was the native Asn of AGRP or a dia

37 e point where binding was abolished when all Phe residues were modified to Ala.

38 proximity between Leu-32 in mambalgin-1 and Phe-350 in rASIC1a was proposed from double mutant cycle

39 d motions of residues Leu(25), Tyr(108), and Phe(253) The resulting water channel enables the binding

40 Residues Thr-123 and Phe-382 in the catalytic domain form a latch-like intera

41 le antiparallel structures (with Asp(15) and Phe(19) aligned), are highly stable and ordered.

42 in residues His(57), Phe(189), Phe(191), and Phe(336); it also disturbs the rotation of the alpha5 he

43 s mimicking the interactions of Phe(229) and Phe(279) of IL-6R.

44 tions between a residue in M3 (Tyr(309)) and Phe(167), a residue adjacent to the Cys loop FPF motif,

45 the active site, particularly in Arg-316 and Phe-318, to achieve the correct geometry for catalysis.

46 parison with FeLOX suggests that Phe-332 and Phe-525 might contribute to the unique suprafacial hydro

47 e alpha5 helix between residues Gln(333) and Phe(334) (Ins4A).

48 Two of these residues, Ser-35 and Phe-365, are also important for urate transport kinetics

49 nd the pi-pi interaction between His(57) and Phe(189) In addition, the insertion mutant abolishes G p

50 s Tyr-37(I:07/1.39), Trp-86(II:20/2.60), and Phe-109(III:09/3.33) The small molecules and CCL3 approa

51 the respective alphaCT residues Phe(701) and Phe(705) The structure provides a platform for the furth

52 Phe(79) interacts with His(85), and Phe(79) mutants showed diminished affinity for shorter c

53 , the peptides Gly-Pro-Ala-Val, Val-Cys, and Phe-Phe have not been previously identified to have the

54 ined with beta values (difference in Glu and Phe delta(15)N in primary producers) for aquatic and ter

55 ic position were obtained using bird Glu and Phe delta(15)N values combined with beta values (differe

56 nalysis highlighted highly conserved Ile and Phe residues at the RfaH interdomain interface.

57 CKS-ED has further revealed that its Lys and Phe residues play an essential role in how MARCKS-ED det

58 ions between the last residue of post-M4 and Phe(170) of the conserved FPF sequence of the Cys loop,

59 a-naphthylamide, Arg beta-naphthylamide, and Phe beta-naphthylamide, as substrates of AcrB and as mod

60 tion of these amino acids with Gln, Phe, and Phe, respectively, leads to complete loss of activity.

61 similar in S. venezuelae OtsA (Asp, Ser, and Phe, respectively) but not conserved in E. coli OtsA (Hi

62 hanced aromatic sequons (Phe-X-Asn-X-Thr and Phe-X-X-Asn-X-Thr), which can be efficiently N-glycosyla

63 Using misacylated Pro-tRNAPhe and Phe-tRNAPro, we show that the imino acid proline and not

64 ion containing peptides rich in Arg, Tyr and Phe.

65 r for the aromatic side chains Trp, Tyr, and Phe as a function of depth in the membrane.

66 hment of the aromatic residues Trp, Tyr, and Phe in rcSso7d-based binders.

67 synthesized analogue, Ac-Arg-Ala-[d-Cys-Arg-Phe-His-Pen]-COOH (19), displayed subnanomolar affinity

68 plasma stable peptide, Ac-Arg-Ala-[d-Cys-Arg-Phe-Phe-Cys]-COOH (3).

69 y active, selective MOR antagonist, c[-d-Arg-Phe-Lys-Dmt-] (1) ("cyclodal"), with subnanomolar bindin

70 tor (MOR) agonist [Dmt(1)]DALDA (H-Dmt-d-Arg-Phe-Lys-NH2 (9; Dmt = 2',6'-dimethyltyrosine) resulted i

71 n cyclodal resulted in an analogue, c[-d-Arg-Phe-LysPsi[CH2NH]Dmt-] (8), with MOR agonist activity.

72 For both ASP and AGRP, the hypothesized Arg-Phe-Phe pharmacophores are on exposed beta-hairpin loops

73 eported AGRP macrocyclic scaffold (c[Pro-Arg-Phe-Phe-Asn-Ala-Phe-DPro]) were explored with 14-compoun

74 in the AGRP active loop derivative c[Pro-Arg-Phe-Phe-Xxx-Ala-Phe-DPro], where Xxx was the native Asn

75 or tripeptide DPhe-Arg-Trp replaced the Arg-Phe-Phe sequence in the AGRP active loop derivative c[Pr

76 ution of various planar (including aromatic (Phe, Trp, Tyr, and His)/amide (Asn and Gln)/Guanidine (A

77 etaF as well as several side chains, such as Phe-57, Tyr-60, and Ile-77, that change their orientatio

78 f intrinsically disordered proteins, such as Phe-Gly repeat domains, alters drastically when they are

79 binding motifs containing the signature Asp-Phe-Pro (DFP) tripeptide.

80 ing of the trypsinogen activation peptide at Phe-18 by CTRC inhibited autoactivation of anionic tryps

81 nt peptide KYE28A, with Ala substitutions at Phe(11), Phe(19), Phe(23), and Tyr(25) was designed, whi

82 Aromatic rings (Tyr(B16), Phe(B24), Phe(B25), 3-I-Tyr(B26), and their symmetry-rel

83 Aromatic rings (Tyr(B16), Phe(B24), Phe(B25), 3-I-Tyr(B26), and their symmetry-related mates

84 nction, but the stacking interaction between Phe(364) and Pro(357), which is absolutely conserved in

85 Fasting plasma amino acid profiles, blood Phe concentrations, food records, and neuropsychological

86 Brain Phe concentrations were most effectively reduced by supp

87 is for Trp, and the relative effect of brain Phe reduction is higher for serotonin than it is for dop

88 her with LNAAs that effectively reduce brain Phe concentrations.

89 ics simulation data suggested that the bulky Phe acts as a pawl that stabilizes the downward ratchet-

90 s obtained with MeJ application, followed by Phe+MeJ; while Phe treatment barely increased phenolic c

91 When Trp is replaced by Phe, protons can be transferred to H37 bidirectionally w

92 naturally occurring mixed kappa/mu-ligand c[Phe-d-Pro-Phe-Trp] 1 (CJ-15,208).

93 as replaced with Phe, generating mutant CaM, Phe(99)-CaM, or Phe(138)-CaM, respectively.

94 , N,N-di-Cl-Tyr-Gly, N-Cl-Phe-Gly, N,N-di-Cl-Phe-Gly, N-Cl-Tyr-Ala, and N,N-di-Cl-Tyr-Ala were identi

95 table in water over 10 days except N,N-di-Cl-Phe-Gly.

96 N-Cl-Tyr-Gly, N,N-di-Cl-Tyr-Gly, N-Cl-Phe-Gly, N,N-di-Cl-Phe-Gly, N-Cl-Tyr-Ala, and N,N-di-Cl-

97 N-Cl-Tyr-Gly, N,N-di-Cl-Tyr-Gly, N-Cl-Phe-Gly, N-Cl-Tyr-Ala, and N,N-di-Cl-Tyr-Ala along with

98 I)DPhe" motif with respect to the classical "Phe-Arg" melanocortin signaling motif, which results in

99 tivity when supplemented with o-Tyr, cognate Phe, or Ala, the latter of which is not a substrate for

100 the alphaI alpha1-helix contains a conserved Phe.

101 inding was dependent upon a highly conserved Phe residue (F65) that in human POT1 directly contacts t

102 II and more precisely in the face containing Phe-27, Leu-32, and Leu-34 residues.

103 rotensin II (UII, 1, H-Glu-Thr-Pro-Asp-c[Cys-Phe-Trp-Lys-Tyr-Cys]-Val-OH) fragment 4-11 were synthesi

104 obe of TPETH-2(CFTERD3) (where CFTERD is Cys-Phe-Thr-Glu-Arg-Asp) was developed for chymase detection

105 the N-terminal alpha-helix of mature VEGF-D (Phe(93)-Arg(108)) is critical for binding VEGFR-2 and VE

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

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

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

109 6)]hGLP-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

110 ies of astressin B analogues {cyclo(30-33)[D-Phe(12),Nle(21,38),C(alpha)MeLeu(27,40),Glu(30),Lys(33)]

111 studies, the protective effect of [Nle(4), D-Phe(7)]-alpha-melanocyte stimulating hormone (NDP-MSH),

112 tifs such as d-Pro-Gly, both the 2-Abz and d-Phe rings may be further functionalized.

113 ration of the nonselective CRF antagonist, D-Phe-CRF, dose-dependently improved working memory perfor

114 mer (optical antipode) of cyclodal, c[-Arg-d-Phe-d-Lys-d-Dmt-] (2), also turned out to be a selective

115 he structural formula of the native L3P as D-Phe-N-Methyl-L-Val-L-Ala-OMe attached in N-ter to a 20-c

116 nity of the decapeptide Gramicidin S cyclo(d-Phe-Pro-Val-Orn-Leu-)2 (GS).

117 ith the GRPr antagonists HZ219, DOTA-PEG4-[D-Phe(6), Sta(13)]-BN(6-14)NH2 (DOTA-AR), and DOTA-(4-amin

118 ]-BN(6-14)NH2), by reacting DOTA-Lys-PEG4-[D-Phe(6), Sta(13)]-BN(6-14)NH2 (HZ219) with IRDye 650 N-hy

119 tagonist, HZ220 (DOTA-Lys(IRDye 650)-PEG4-[D-Phe(6), Sta(13)]-BN(6-14)NH2), by reacting DOTA-Lys-PEG4

120 DOTA-(4-amino-1-carboxymethyl-piperidine)-[D-Phe(6), Sta(13)]-BN(6-14)NH2 (DOTA-RM2).

121 ed DOTA-4-amino-1-carboxymethyl-piperidine-D-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2 ((68)Ga-RM2) is

122 ed DOTA-4-amino-1-carboxymethyl-piperidine-d-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2 ((68)Ga-RM2) is

123 The d-Phe-2-Abz turn may serve as a tool for the synthesis of

124 idine A, (Tyrc A) was substituted with the d-Phe-2-aminobenzoic acid (2-Abz) motif in a synthetic ana

125 The d-Phe-Pro beta-turn of the cyclic beta-hairpin antimicrobi

126 The inhibitors carbobenzoxy (Z)-d-Phe-l-Phe-Gly (fusion inhibitor peptide [FIP]) and 4-nit

127 Other homologues, such as Z-d-Phe, are less effective but may act through the same mec

128 cades ago, the small hydrophobic peptide Z-d-Phe-l-Phe-Gly (FIP) was shown to block MeV infections an

129 e resistant to the inhibitory effects of Z-d-Phe-l-Phe-Gly.

130 Phe derivatives; however, how plants endure Phe accumulating conditions in the absence of an excreti

131 aration of the BM2 channel using fluorinated Phe-5.

132 Results showed that foliar Phe and MeJ treatments decreased the concentration of mo

133 t pH 6.5 and temperature of 40 degrees C for Phe-pNA as a substrate.

134 ies that a binding site exists in the RD for Phe, and that Phe binding results in dimerization of PAH

135 he N-terminal part of this alpha-helix, from Phe(93) to Thr(98), is required for binding VEGFR-3 but

136 ion of several amino acids than samples from Phe and MeJ applications.

137 The concentration of Fru-Phe in submicron emulsions was similar to that in water,

138 the formation of fructose-phenylalanine (Fru-Phe) and fructose-leucine (Fru-Leu) was monitored by mas

139 H group avoids a clash with the steric gate, Phe-18, but the distance between primer end and Palpha o

140 Substitution of these amino acids with Gln, Phe, and Phe, respectively, leads to complete loss of ac

141 cognizes the pan-opioid sequence Tyr-Gly-Gly-Phe at the N terminus of most endogenous opioid peptides

142 Among the small peptides 2-31, (H)Gly-Gly-Phe-Leu(OMe) (30) reduced prostaglandin production of CO

143 Here we show that the gp120 Phe 43 cavity modulates the propensity of Env to sample

144 tophan for serine 375 (S375H/W) in the gp120 Phe 43 cavity, where Phe 43 of CD4 contacts gp120, resul

145 ral amino acid substitutions (including His, Phe, Pro, Trp, and Tyr) support an enhanced viability du

146 not in ECs transfected with pcDNA3.1-myc-His-Phe(138)-CaM, the lysoPC-induced TRPC6-CaM dissociation

147 ransiently transfected with pcDNA3.1-myc-His-Phe(99)-CaM, but not in ECs transfected with pcDNA3.1-my

148 ransiently transfected with pcDNA3.1-myc-His-Phe(99)-CaM.

149 condensation reaction of the resulting HOOC-Phe-SWCNT with 1-(3-aminoethyl)-4,4'-bipyridinium bromin

150 a disease-associated PAH mutant impaired in Phe binding disrupts the monomer:dimer equilibrium of PA

151 = 0.136), despite a significant increase in Phe intake from GMP-MFs (88 +/- 6 mg Phe/d, P = 0.026).

152 o-crystallized with a catalytically inactive Phe substitution in the His-Asp catalytic dyad of CurJ-D

153 led to an 18-fold expansion of the internal Phe pool.

154 465A>T; p.Ile489Phe, converting Ile 489 into Phe.

155 l-Phe(D8) from the host cell completely replaces the l-Phe

156 lular tachyzoites were not able to consume l-Phe(D8) after 24 hours of infection.

157 ndii tachyzoites are capable of extracting l-Phe(D8) from host cells as soon as it invades the cell.

158 s l-phenylalanine-glycine), and [Mn(II) + (l-Phe-Gly - H) + M](+) complex ions are used to determine

159 -serine and M is a given monosaccharide), [l-Phe-Gly + M + H](+) (where l-Phe-Gly is l-phenylalanine-

160 Our results show a very rapid uptake of l-Phe(D8) by the intracellular growing parasite.

161 ago, the small hydrophobic peptide Z-d-Phe-l-Phe-Gly (FIP) was shown to block MeV infections and sync

162 The inhibitors carbobenzoxy (Z)-d-Phe-l-Phe-Gly (fusion inhibitor peptide [FIP]) and 4-nitro-2-p

163 stant to the inhibitory effects of Z-d-Phe-l-Phe-Gly.

164 curate quantifications of L-phenylalanine (L-Phe) in plasma and whole-blood newborns samples diagnose

165 from the host cell completely replaces the l-Phe within T. gondii tachyzoites 7-9 hours after infecti

166 saccharide), [l-Phe-Gly + M + H](+) (where l-Phe-Gly is l-phenylalanine-glycine), and [Mn(II) + (l-Ph

167 itor the incorporation of deuterium-labelled Phe into proteins in individual live tachyzoites.

168 chemotactic migration toward formyl-Met-Leu-Phe (fMLP) and stromal cell-derived factor 1alpha (SDF-1

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

170 ed recombinant protein, we show that the Leu-Phe substitution increases turnover rate of acetaldehyde

171 nvestigated the efficacy and safety of a low-Phe diet combined with GMP-MFs or AA-MFs providing the s

172 phenylalanine (Phe) concentration with a low-Phe diet.

173 random order for 3 wk each, their usual low-Phe diet combined with AA-MFs or GMP-MFs.

174 losteric regulation is necessary to maintain Phe below neurotoxic levels.

175 MeJ+Phe treatment did not affect must nitrogen content.

176 nylalanine (Phe) as a precursor feeding (MeJ+Phe) and its application individually on must amino acid

177 Musts obtained from MeJ+Phe showed higher concentration of several amino acids t

178 ease in Phe intake from GMP-MFs (88 +/- 6 mg Phe/d, P = 0.026).

179 we discovered a four-residue pi-clamp motif (Phe-Cys-Pro-Phe) for regio- and chemoselective arylation

180 Mutating Phe(364) to tryptophan resulted in a genetically stable

181 e to CD4 binding by helping shape the nearby Phe 43 cavity, which directly contacts CD4.

182 he mu-opioid receptor agonist [D-Ala(2), NMe-Phe(4), Gly-ol(5)]-enkephalin produces paradoxical behav

183 Brain non-Phe LNAAs could be restored on supplementation, but unba

184 tetramer, which dominates in the absence of Phe, is different from a Phe-stabilized allosterically a

185 Accumulation of Phe did not lead to an increase in flux toward phenylace

186 imarily intact protein and a small amount of Phe.

187 nt (residues 22-27) directing the binding of Phe(22) into a hydrophobic pocket on the GLP-1R.

188 Remarkably, we found that the side-chain of Phe 34 can influence the position of the coenzyme, indic

189 during infection, including the cleavage of Phe/Gly-containing nucleoporin proteins (Nups) within nu

190 Blood concentrations of Phe across time were not significantly different (AA-MFs

191 at catalyze the non-oxidative deamination of Phe to trans-cinnamic acid, the committed step for the m

192 n on graphene due to an even distribution of Phe residues and hydrophilic residues.

193 ) that contributes to sequestering excess of Phe in the vacuole.

194 enylketonuria, are mitigated by excretion of Phe derivatives; however, how plants endure Phe accumula

195 by NOE spectroscopy, shows the importance of Phe and Arg interactions in driving the phase separation

196 The diet restricts intake of Phe from natural proteins in combination with traditiona

197 of IL-6, thus mimicking the interactions of Phe(229) and Phe(279) of IL-6R.

198 ld increase in the rate of mistranslation of Phe codons as Tyr compared to wild type, the increase in

199 6, as was also observed for IL-6R mutants of Phe(279) In the second antibody, the side chain of HCDR3

200 the committed step for the major pathway of Phe metabolism.

201 of a distinct metabolically inactive pool of Phe, likely localized in the vacuole.

202 line of defense to maintain the position of Phe-18.

203 on are strongly dependent on the presence of Phe-237.

204 llowed an estimation of the exchange rate of Phe as 0.5-1.6 x 10(4) molecules/s.

205 We suggest an additional role of Phe in supplying nutrients to the young seedling.

206 Since only subsets of Phe/Gly motifs, particularly those within Nup62, Nup98,

207 ating the hypothesis that the ADT3 supply of Phe is required to control ROS concentration and distrib

208 Phe, generating mutant CaM, Phe(99)-CaM, or Phe(138)-CaM, respectively.

209 residue into any other residue except Tyr or Phe significantly weakens binding of the antibody to IL-

210 free KLK2 toward peptidic substrates with P2-Phe, the situation was reverted toward protein substrate

211 gnition by hPDI therefore, step-wise peptide Phe-to-Ala changes were progressively introduced and sho

212 ge of the aromatic amino acid phenylalanine (Phe) between human retinal pigment epithelial cell line

213 on of the aromatic amino acid phenylalanine (Phe) in animals, known as phenylketonuria, are mitigated

214 lifelong management of blood phenylalanine (Phe) concentration with a low-Phe diet.

215 jasmonate (MeJ) supported by phenylalanine (Phe) as a precursor feeding (MeJ+Phe) and its applicatio

216 he hydroxylation of dietary I-phenylalanine (Phe) to I-tyrosine.

217 Vine foliar applications of phenylalanine (Phe) or methyl jasmonate (MeJ) could improve the synthes

218 c activation by the substrate phenylalanine (Phe); the allosteric regulation is necessary to maintain

219 ce of a critical role for the phenylalanine (Phe) biosynthetic activity of AROGENATE DEHYDRATASE3 (AD

220 ted by precursor feeding with phenylalanine (Phe), in order to improve Garnacha grape phenolic conten

221 actors based upon the source (phenylalanine, Phe) and trophic (glutamic acid, Glu) AAs were 4.1 (musc

222 lalanine (Tyr-Ala), and phenylalanylglycine (Phe-Gly), reacted with sodium hypochlorite, and these re

223 AA-MFs decreased plasma Phe (-85 +/- 40 mumol/L, P = 0.044) with stable Phe inta

224 o significant mean +/- SE increase in plasma Phe (62 +/- 40 mumol/L, P = 0.136), despite a significan

225 sent in crude extract cleaved preferentially Phe-pNA.

226 We show that arrayed Asp-Pro-Phe (DPF) motifs within the early-arriving endocytic pio

227 d a four-residue pi-clamp motif (Phe-Cys-Pro-Phe) for regio- and chemoselective arylation of cysteine

228 show a four-amino-acid sequence (Phe-Cys-Pro-Phe), which we call the 'pi-clamp', that tunes the react

229 occurring mixed kappa/mu-ligand c[Phe-d-Pro-Phe-Trp] 1 (CJ-15,208).

230 particular, the mu-agonist c[beta-Ala-d-Pro-Phe-Trp] 9 was shown to elicit potent antinociception in

231 P, RDP with the loss of a phenyl group (RDP-[Phe]) and RDP oligomers were detected in plastics contai

232 ronics, TPHP meta-HO-TPHP, meta-HO-RDP, RDP-[Phe] and RDP oligomers were detected.

233 FtsZ CTD residue Phe-377 inserts into the ZapD pocket, anchoring the CTD

234 When the hydrophobic residue Phe is labeled, however, the spin-label depth is close t

235 yptophan binds similarly to hot spot residue Phe(279) Mutation of this HCDR3 Trp residue into any oth

236 identical to the respective alphaCT residues Phe(701) and Phe(705) The structure provides a platform

237 Tyr(274) interacting with IFN-beta residues Phe(63), Leu(64), Glu(77), Thr(78), Val(81), and Arg(82)

238 Site-directed mutagenesis disclosed residues Phe(241) and Ser(203) in MFAP4 as being crucial for type

239 pocket, comprising the hydrophobic residues Phe-1012, Val-1025, Tyr-1089, and Leu-1092).

240 have focused on OleTJE active site residues Phe(79), His(85), and Arg(245) to interrogate their role

241 Mutating SM residues Phe-35/Ser-37/Leu-65/Ile-69 into alanine, based on the k

242 nd two structures of a novel analogue MTM SA-Phe in complex with DNA.

243 MTM SA-Phe is bound to sites AGGG and GGGT on one DNA, and to A

244 ach residue in this motif of secretin (sec), Phe(6), Thr(7), and Leu(10), and cysteines incorporated

245 Here, we show a four-amino-acid sequence (Phe-Cys-Pro-Phe), which we call the 'pi-clamp', that tun

246 T) sequon and the enhanced aromatic sequons (Phe-X-Asn-X-Thr and Phe-X-X-Asn-X-Thr), which can be eff

247 of the fluorogenic substrate hydrodabcyl-Ser-Phe-EDANS by the proteases thermolysin and papain.

248 Fs = 497 +/- 34 mumol/L), suggesting similar Phe control.

249 (-85 +/- 40 mumol/L, P = 0.044) with stable Phe intake.

250 ding site exists in the RD for Phe, and that Phe binding results in dimerization of PAH-RD.

251 Results showed that Phe+MeJ treatment did not improve phenolic content to a

252 Comparison with FeLOX suggests that Phe-332 and Phe-525 might contribute to the unique supra

253 The Phe, Ala, and Dap/Asn residues were successively removed

254 del, we found that the residue volume at the Phe position in the alpha1-helix is critical for alphaLb

255 mal SAC reinforcement occurred when both the Phe- and D-box of BubR1(I) were disrupted.

256 Here we investigate the influence of the Phe 43 cavity on ADCC responses.

257 s focusing on two pathogenic variants of the Phe-53 residue, which maps to the well-characterized neg

258 alphaLbeta2 activation because trimming the Phe by small amino acid substitutions abolished alphaLbe

259 A functional role of this Phe is structurally unpredictable.

260 d in petunia flowers expression of all three Phe ammonia lyase (PAL) isoforms that catalyze the non-o

261 f interaction partners for Tyr(187) in TMIV (Phe(171)) and TMV (Trp(194)).

262 orresponding to the sequence from Asp(15) to Phe(19) of human calcitonin and reported as the minimal

263 extends seven helical turns, from Pro-405 to Phe-431, and is flanked by unstructured loops.

264 d aromaticity of the side group analogous to Phe-2 of ritonavir and demonstrated the leading role of

265 mutation of the XPA residue corresponding to Phe-262 in Rad14, previously reported as being critical

266 um), the reverse reaction, phenylpyruvate to Phe, is also demonstrated.

267 , for example, mutating all Tyr1 residues to Phe (Y1F) is lethal in vertebrates but a related mutant

268 Importantly, Tyr to Phe substitution renders the kinase inactive, jeopardizi

269 Two visible picks in the pH profile toward Phe-pNA, together with other results (IEF) suggest the p

270 vitro assays confirmed PhCAT2 can transport Phe, and decreased PhCAT2 expression in PAL-RNAi transge

271 d these modules would produce the tripeptide Phe-N-Methyl-Val-Ala with a lipid moiety, termed lipotri

272 lytic hydrolysis of mispaired aminoacyl-tRNA(Phe) species.

273 rain, increased levels of aminoacylated tRNA(Phe) led to continued synthesis of the PheL leader pepti

274 iting, cellular levels of aminoacylated tRNA(Phe) were elevated during amino acid stress, whereas in

275 diting lowered the amount of deacylated tRNA(Phe) in the cell.

276 emonstrate that only mt-tRNA(Val) or mt-tRNA(Phe) are found in the mitoribosomes of five different ma

277 by switching to the incorporation of mt-tRNA(Phe) to generate translationally competent machinery.

278 al) compared with the porcine use of mt-tRNA(Phe) We have explored this observation further.

279 binds 16S mt-rRNA, mt-tRNA(Met), and mt-tRNA(Phe), and we demonstrate that it is responsible for pseu

280 s cerevisiae that PheRS misacylation of tRNA(Phe) with the more abundant Phe oxidation product o-Tyr

281 erivative m-Tyr after its attachment to tRNA(Phe) We now show in Saccharomyces cerevisiae that PheRS

282 scherichia coli strain defective in Tyr-tRNA(Phe) editing was used.

283 with SVBP, exhibited robust and specific Tyr/Phe carboxypeptidase activity on microtubules.

284 re of hGLUTs, and two previously undescribed Phe amide-derived inhibitors.

285 CRF01_AE HIV-1 strains have an unusual Phe 43 cavity-filling His 375 residue, which increases t

286 The methodology involved preparation of V-Phe-SWCNT(-HRP)-anti-TGF conjugates by covalent linkage

287 covalent linkage of HRP and anti-TGF onto V-Phe-SWCNT hybrids.

288 The V-Phe-SWCNT hybrids were characterized by using different

289 TGF-beta1 with signal amplification using V-Phe-SWCNT(-HRP)-anti-TGF conjugates as carrier tags.

290 (S375H/W) in the gp120 Phe 43 cavity, where Phe 43 of CD4 contacts gp120, results in the spontaneous

291 model of PAH allosteric regulation, whereby Phe binds to PAH-RD and mediates the dimerization of reg

292 l and modeling studies, a mechanism by which Phe-237 exerts this influence is presented.

293 in flux toward phenylacetaldehyde, for which Phe is a direct precursor.

294 a mechanism for allosteric coupling in which Phe(151) is the central residue in a hydrophobic interac

295 MeJ application, followed by Phe+MeJ; while Phe treatment barely increased phenolic compounds.

296 crystal structure of human PAH-RD bound with Phe at 1.8 A resolution, revealing a homodimer of ACT fo

297 could be supported by precursor feeding with Phe, when both applied together.

298 ion, revealing a homodimer of ACT folds with Phe bound at the dimer interface.

299 Tyr(99) or Tyr(138) of CaM was replaced with Phe, generating mutant CaM, Phe(99)-CaM, or Phe(138)-CaM

300 By swapping Val (V63) with Phe, AtPOT1bOB1 gained the capacity to bind telomeric DN