ライフサイエンスコーパス: Tyr

1 Tyr and Trp residues served as donor and acceptor at the

2 Tyr phosphorylation in the P + 1 loop of PKD2 increases

3 Tyr(30), Tyr(64), and Tyr(86) in the N-terminal domain (

4 Tyr-Pro had the highest ACE inhibitory activity (ACE IC5

5 -DOTATOC, respectively) and [(177)Lu-DOTA(0),Tyr(3)]octreotate ((177)Lu-DOTATATE).

6 OTA(0),Tyr(3)]octreotide or [(177)Lu-DOTA(0),Tyr(3)]octreotide ((90)Y- or (177)Lu-DOTATOC, respective

7 abeled sstr agonists, such as [(90)Y-DOTA(0),Tyr(3)]octreotide or [(177)Lu-DOTA(0),Tyr(3)]octreotide

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

9 AM domain (DeltaSAM) or mutation of Tyr-113, Tyr-128, and Tyr-145 to phenylalanine (3Y3F).

10 us, SLP-76 has three key tyrosines (Tyr-113, Tyr-128, and Tyr-145, "3Y") as well as a sterile alpha m

11 re four phosphorylated sites (Tyr-4, Tyr-19, Tyr-20, and Tyr-205) in ARH1.

12 hat two distinct aromatic residues in ECL-2, Tyr(184) (Cys + 1) and Tyr(187) (Cys + 4), are crucial f

13 H-stimulated ERK phosphorylation on Thr(202)/Tyr(204) was PKA-dependent, but MEK(Ser(217)/Ser(221)) p

14 P3, DUSP6) inhibitors increased ERK(Thr(202)/Tyr(204)) phosphorylation in the absence of FSH to level

15 Mutating the equivalent residue, Tyr-280/Tyr-261, in Erk1/Erk2 significantly impaired Erk1/2's ca

16 nteract with the back face of beta-strand 3 (Tyr(286)is on the front face) and loop 2, forming a hors

17 ues form hydrogen bonds with ADP-RA; and (3) Tyr-211 is also less flexible in the phosphorylated stat

18 Tyr(30), Tyr(64), and Tyr(86) in the N-terminal domain (NTD) of b

19 Mutation of NPF6.4 Tyr-370 to His (Y370H) resulted in saturable high-affini

20 There are four phosphorylated sites (Tyr-4, Tyr-19, Tyr-20, and Tyr-205) in ARH1.

21 well as several side chains, such as Phe-57, Tyr-60, and Ile-77, that change their orientations to ac

22 with elevated phosphorylation (i.e. Tyr-579, Tyr-581, Tyr-1009, and Tyr-1021) have previously been sh

23 ated phosphorylation (i.e. Tyr-579, Tyr-581, Tyr-1009, and Tyr-1021) have previously been shown to in

24 Absence of IGF-1R or mutation of Tyr-60, Tyr-133, or Tyr-250 in PCNA abrogated its ubiquitination

25 Alanine substitution of Glu(68), Tyr(92), or Asn(139), which interact with arabinose and

26 (Val) controls affinity, whereas position 7 (Tyr) acts as an efficacy switch.

27 rresponding residues from RasGRP1/3 (Thr(7), Tyr(8), Gly(19), and Leu(21), respectively) conferred po

28 Substitution of Arg-72, Tyr-190, Arg-234, or Glu-282 reduced LigY activity over

29 Several specific PON1 residues (Leu-9, Tyr-185, and Tyr-293) were identified through covalent c

30 esis of the identified PON1 residues (Leu-9, Tyr-185, and Tyr-293), coupled with functional studies,

31 tetradentate siderophores using a His and a Tyr side chain to complete the Fe(III) coordination.

32 Conversion of this residue, which is a Tyr in LodA, to Tyr or Ala eliminates the cooperativity

33 l measurements show that the para-group of a Tyr residue near the ion conduction pathway has a critic

34 hydroquinone (H2Q), N-acetyl-tyrosine (N-Ac-Tyr) or guanosine-5'-monophosphate (GMP) was investigate

35 itory activity was found with the amino acid Tyr (DPP-IV IC50=75.15+/-0.84muM).

36 In addition, Tyr-92 was identified as a second line of defense to mai

37 Oxidation of Ala-Ala-Ala-Tyr-Arg (AAAYR) produces a mixture of cation radicals in

38 antly to the extent of chlorination at alpha-Tyr-24 in nonsmokers.

39 the factor of smoking, chlorination at alpha-Tyr-24, nitration at alpha-Tyr-42, and oxidation at the

40 rination at alpha-Tyr-24, nitration at alpha-Tyr-42, and oxidation at the three methionine residues a

41 Also, Tyr-insensitive BvADHalpha orthologs arose during the ev

42 ic residues in ECL-2, Tyr(184) (Cys + 1) and Tyr(187) (Cys + 4), are crucial for binding of the CC ch

43 lation (i.e. Tyr-579, Tyr-581, Tyr-1009, and Tyr-1021) have previously been shown to interact with Sr

44 These results indicate that Tyr-108 and Tyr-503 are responsible for the activation of substrates

45 eals that two tyrosine residues, Tyr-108 and Tyr-503, are positioned to facilitate this deprotonation

46 ltaSAM) or mutation of Tyr-113, Tyr-128, and Tyr-145 to phenylalanine (3Y3F).

47 s three key tyrosines (Tyr-113, Tyr-128, and Tyr-145, "3Y") as well as a sterile alpha motif (SAM) do

48 tion;i.e.GIV phosphorylation at Tyr-1764 and Tyr-1798 recruits and activates PI3K.

49 specific PON1 residues (Leu-9, Tyr-185, and Tyr-293) were identified through covalent cross-links wi

50 dentified PON1 residues (Leu-9, Tyr-185, and Tyr-293), coupled with functional studies, reveals their

51 phorylated sites (Tyr-4, Tyr-19, Tyr-20, and Tyr-205) in ARH1.

52 wo pore-lining tyrosine residues, Tyr-23 and Tyr-149 in sheep AQP0, to the corresponding residues in

53 stitutions at Phe(11), Phe(19), Phe(23), and Tyr(25) was designed, which showed attenuated antimicrob

54 is centered on IFNAR1 residues Tyr(240) and Tyr(274) binding the C and N termini of the B and C heli

55 face created by IFNAR1 residues Tyr(240) and Tyr(274) interacting with IFN-beta residues Phe(63), Leu

56 e analogs) identified Arg(64), Lys(269), and Tyr(309) as key catalytic residues of VioA.

57 -1 revealed two unique residues, Arg(30) and Tyr(51), as critical in conferring CD1c-restricted autor

58 active-site residues (Trp(52), Trp(396), and Tyr(393)).

59 ggests that pre-S1 loop residues His-402 and Tyr-403 play an important role in regulating the kinetic

60 ng interacts with IsdB residues Tyr(440) and Tyr(444) Previously, Tyr(440) was observed to coordinate

61 of thyroglobulin (TG) at residues Tyr(5) and Tyr(130), whereas thyroidal T3 production may originate

62 f two UNG2 phosphorylation sites (Thr(6) and Tyr(8)) located within its PCNA-interacting motif (PIP-b

63 We further noted that Ser-610 and Tyr-634 also contribute to the mitotic checkpoint signal

64 Tyr(30), Tyr(64), and Tyr(86) in the N-terminal domain (NTD) of beta-catenin.

65 and focal adhesion kinase (FAK) Ser(722) and Tyr(576).

66 xpression and phosphorylation at Ser-727 and Tyr-701.

67 he cSH2 core domain encompassing Tyr-771 and Tyr-783 to facilitate the binding/phosphorylation of the

68 FPheK reacted with adjacent Lys, Cys, and Tyr residues in thioredoxin in high yields.

69 both guanine nucleotide exchange factor and Tyr(P) GIV signaling as well as on their convergence poi

70 uence positions corresponding to the Ser and Tyr ligands are almost completely covariant among Group

71 rs permitted elimination of both Ser/Thr and Tyr phosphatases and implicated dual specificity phospha

72 composed of a dual specificity (Ser/Thr and Tyr) kinase domain tethered to a calmodulin-like domain

73 as required for expression of Dct, Tyrp1 and Tyr, genes that are regulated by SOX10 and MITF and for

74 of hybrid 13a (H-Dmt-d-Arg-Aba-beta-Ala-Arg-Tyr-Tyr-Arg-Ile-Lys-NH2) to mice resulted in potent and

75 the rate of mistranslation of Phe codons as Tyr compared to wild type, the increase in mistranslatio

76 ed with the most hydrophobic peptide Ile-Asn-Tyr-Trp.

77 show that catalysis depends on a Lys-Tyr-Asn-Tyr tetrad that emerged adjacent to a computationally de

78 dicted to bind the minimal FLAG peptide (Asp-Tyr-Lys-Asp) were grafted onto a single-chain variable f

79 the last 30 years has been cancer-associated Tyr and Ser/Thr kinases, over 85% of the kinome has been

80 The BALB/c albino phenotype-associated Tyr(c) tyrosinase mutation appeared to contribute to the

81 by the non-receptor tyrosine kinase c-Abl at Tyr-153 reportedly leads to caspase-9 activation.

82 Phosphorylation of CaM at Tyr(99) (pY99) enhances PI3Kalpha activation.

83 Blocking phosphorylation of CaM at Tyr(99) also reduced CaM association with the p85 subuni

84 romotes dephosphorylation of beta-catenin at Tyr 142 and enhances the interaction between alpha- and

85 er, prior phosphorylation of beta-catenin at Tyr(654) was essential for further phosphorylation of be

86 , we show that phosphorylation of beta-DG at Tyr(890) is a key stimulus for beta-DG nuclear transloca

87 contraction, and beta2-AR phosphorylation at Tyr(350) were assessed.

88 t that lysoPC induces CaM phosphorylation at Tyr(99) by a Src family kinase and that phosphorylated C

89 substrate for Src kinase phosphorylation at Tyr-144.

90 actor stimulation;i.e.GIV phosphorylation at Tyr-1764 and Tyr-1798 recruits and activates PI3K.

91 how that DrRecA undergoes phosphorylation at Tyr-77 and Thr-318 by a DNA damage-responsive serine thr

92 Src, but Src phosphorylates deltaKD-T507A at Tyr(334) (in the newly exposed deltaKD N terminus), and

93 t the distance and degree of contact between Tyr residues and Kme3 plays an important role in tuning

94 The difference in steric hindrance between Tyr/Trp(604) and the trifluoromethoxy moiety of NMS-P715

95 K1 is bound to active IGF1R and inhibited by Tyr and Ser83/Ser966 phosphorylation.

96 er plant ADHs that are strongly inhibited by Tyr, BvADHalpha exhibited relaxed sensitivity to Tyr.

97 DESI MS, when 0 V was applied to the EC cell Tyr ion signal was detected only at low pH (2).

98 y, N-Cl-Phe-Gly, N-Cl-Tyr-Ala, and N,N-di-Cl-Tyr-Ala along with their corresponding dipeptides were d

99 N-di-Cl-Phe-Gly, N-Cl-Tyr-Ala, and N,N-di-Cl-Tyr-Ala were identified as the major products based on a

100 N-Cl-Tyr-Gly, N,N-di-Cl-Tyr-Gly, N-Cl-Phe-Gly, N,N-di-Cl-Phe-Gly, N-Cl-Tyr-Ala,

101 N-Cl-Tyr-Gly, N,N-di-Cl-Tyr-Gly, N-Cl-Phe-Gly, N-Cl-Tyr-Ala, and N,N-di-Cl-Tyr-A

102 r-Gly, N,N-di-Cl-Tyr-Gly, N-Cl-Phe-Gly, N-Cl-Tyr-Ala, and N,N-di-Cl-Tyr-Ala along with their correspo

103 r-Gly, N-Cl-Phe-Gly, N,N-di-Cl-Phe-Gly, N-Cl-Tyr-Ala, and N,N-di-Cl-Tyr-Ala were identified as the ma

104 N-Cl-Tyr-Gly, N,N-di-Cl-Tyr-Gly, N-Cl-Phe-Gly, N,N-di-Cl-Phe-

105 N-Cl-Tyr-Gly, N,N-di-Cl-Tyr-Gly, N-Cl-Phe-Gly, N-Cl-Tyr-Ala,

106 an editing pathway that targets non-cognate Tyr-tRNAPhe.

107 ket') that normally accommodates a conserved Tyr-Ser-Tyr motif from TPX2, blocking the AURKA-TPX2 int

108 diated phosphorylation of a highly conserved Tyr residue in the P + 1 loop of protein kinase D2 (PKD2

109 analyses revealed that the highly conserved Tyr-86 residue in E. coli TrmD is essential to discrimin

110 n bond network includes a strictly conserved Tyr residue, and previously we explored the role of this

111 s lack one or both residues of the conserved Tyr-Ser dyad that has previously been implicated in KR-c

112 s a concerted reaction involving coordinated Tyr ring deprotonation where Cu(II) coordination enables

113 This loop contains a functionally critical Tyr at position 71.

114 I) coordination enables formation of the Cys-Tyr cross-link.

115 receptor antagonist desGly-NH2 , d(CH2 )5 [D-Tyr(2) ,Thr(4) ]OVT, the ionotropic glutamate receptor a

116 a-c[d-Cys-Aph(Hor)-d-Aph(Cbm)-Lys-Thr-Cys]-d-Tyr-NH2), an antagonist with selectivity for sstr subtyp

117 ues, including the C-terminal decarboxylated Tyr (VY*).

118 ctivity increased Ser(P)-IRS-2 and decreased Tyr(P)-IRS-2 leading to reduced M2 gene expression (CD20

119 en conformation induced MEK-ERK1/2-dependent Tyr-447 phosphorylation.

120 TULA-2 is capable of dephosphorylating Tyr(P)(346) with high efficiency, thus controlling the o

121 g mouse injected with 3 MBq of [(213)Bi-DOTA,Tyr(3)]octreotate, tumor uptake could be visualized with

122 Binding of (111)In-DOTA-Tyr(3)-octreotate (SSTR agonist) and (111)In-DOTA-JR11 (

123 e was significantly higher than (111)In-DOTA-Tyr(3)-octreotate binding (P < 0.001).

124 on studies after injection with (177)Lu-DOTA-Tyr(3)-octreotate or (177)Lu-DOTA-JR11.

125 hybrid labeled somatostatin analog Cy5-DTPA-Tyr(3)-octreotate (DTPA is diethylene triamine pentaacet

126 ity and internalization capacity of Cy5-DTPA-Tyr(3)-octreotate were assessed in vitro.

127 to 1.32% +/- 0.02% applied dose for Cy5-DTPA-Tyr(3)-octreotate.

128 finity and internalization rate for Cy5-DTPA-Tyr(3)-octreotate.

129 from 33.76% +/- 1.22% applied dose for DTPA-Tyr(3)-octreotate to 1.32% +/- 0.02% applied dose for Cy

130 )In-DTPA-Tyr(3)-octreotate and (111)In -DTPA-Tyr(3)-octreotate (6.93 +/- 2.08 and 5.16 +/- 1.27, resp

131 optical in vivo imaging of Cy5-(111)In -DTPA-Tyr(3)-octreotate were performed in NET-bearing mice and

132 ilar tumor uptake values of Cy5-(111)In-DTPA-Tyr(3)-octreotate and (111)In -DTPA-Tyr(3)-octreotate (6

133 ompared with the performance of (111)In-DTPA-Tyr(3)-octreotate.

134 residues with elevated phosphorylation (i.e. Tyr-579, Tyr-581, Tyr-1009, and Tyr-1021) have previousl

135 egion past the cSH2 core domain encompassing Tyr-771 and Tyr-783 to facilitate the binding/phosphoryl

136 LUF by the introduction of fluorotyrosine (F-Tyr) analogues that modulated the pKa and reduction pote

137 dentified an IL-2-JAK-independent SRC family Tyr-kinase-controlled signaling network that regulates a

138 Surprisingly, we observed no evidence for Tyr-153 phosphorylation of caspase-9 in vitro or in cell

139 aromatic cluster of interaction partners for Tyr(187) in TMIV (Phe(171)) and TMV (Trp(194)).

140 The requirement for Tyr supplementation is higher than it is for Trp, and th

141 the reactive deprotonated tyrosine, forming Tyr(*).

142 site for Cbl-b, with some contribution from Tyr-1009.

143 cle, we detect 3-NT and discriminate it from Tyr with Differential Pulse Voltammetry (DPV) as it is a

144 m Gram-positive bacteria lack C-terminal Gly-Tyr-Gly-Ile motifs, suggesting that they do not interact

145 re of a mu-opioid receptor ligand, analogs H-Tyr-c[D-Lys-Xxx-Tyr-Gly] were synthesized and their biol

146 However, Tyr-992 appeared to be almost uniquely required to obser

147 Hs-Tyr is localized in the nematode esophageal gland.

148 We describe Hs-Tyr as a novel nematode effector.

149 In our study, we identified a gene (Hs-Tyr) encoding a tyrosinase functional domain (PF00264).

150 Interestingly, Hs-Tyr in the plant promoted plant growth and changed the r

151 Additionally, the expression of Hs-Tyr in Arabidopsis caused changes in the homeostasis of

152 Silencing Hs-Tyr by RNA interference made the treated nematodes less

153 Ectopically expressing the Hs-Tyr effector in Arabidopsis increased plant susceptibili

154 hy was performed with (125)I-JR11 and (125)I-Tyr(3)-octreotide in cancers from prostate, breast, colo

155 n vitro with that of the sst2 agonist (125)I-Tyr(3)-octreotide in large varieties of non-NET and NET.

156 11 binds to many more sst2 sites than (125)I-Tyr(3)-octreotide.

157 petition binding experiments against [(125)I-Tyr(4)]BBN in GRPR-positive PC-3 cell membranes.

158 t most EGF-stimulated signaling but identify Tyr-992 and its binding partners as a unique node within

159 ation surrounding the C-terminal Glu-Pro-Ile-Tyr-Ala (EPIYA) motifs as well as the number of EPIYA mo

160 Importantly, Tyr to Phe substitution renders the kinase inactive, jeo

161 sis, an Escherichia coli strain defective in Tyr-tRNA(Phe) editing was used.

162 laxation of Tyr pathway regulation increased Tyr production and contributed to the evolution of betal

163 phenotype, because crossing the independent Tyr(c-2J) allele to Egr1(-/-) C57BL/6 mice also produced

164 f FAK, an upstream component of the integrin Tyr(P) signaling cascade, was diminished in GIV-depleted

165 served in the crystal structure of a 3-[iodo-Tyr(B26)]insulin analog (determined as an R6 zinc hexame

166 uantitative atomistic simulations of 3-[iodo-Tyr(B26)]insulin to predict its structural features, and

167 or O-O cleavage derive from the cross-linked Tyr residue present at the active site.

168 display very different degrees of P + 1 loop Tyr phosphorylation and we identify one of the molecular

169 ale proteomics studies identified P + 1 loop Tyr phosphorylation in more than 70 Ser/Thr kinases in m

170 plasma of UCP3 Tg mice (e.g., Asp, Glu, Lys, Tyr, Ser, Met) were significantly reduced after an EB; t

171 studies show that catalysis depends on a Lys-Tyr-Asn-Tyr tetrad that emerged adjacent to a computatio

172 ctive gamma-turn conformation of the Bip-Lys-Tyr tripeptide in Urocontrin ([Bip(4)]URP), which modula

173 a137-141 fragment of hemoglobin (Thr-Ser-Lys-Tyr-Arg), a small (653Da) and hydrophilic antimicrobial

174 esidues in the biologically relevant Trp-Lys-Tyr triad.

175 (UII, 1, H-Glu-Thr-Pro-Asp-c[Cys-Phe-Trp-Lys-Tyr-Cys]-Val-OH) fragment 4-11 were synthesized to explo

176 tein hydroxylated phenylalanine derivative m-Tyr after its attachment to tRNA(Phe) We now show in Sac

177 th Arg55 of cyclophilin A (Cyp A), and the m-Tyr residue was displaced into solvent.

178 and the hydroxyl group of the m-tyrosine (m-Tyr) residue as key contributors to compound potency.

179 -m-tyrosine-piperazic acid tripeptide (Val-m-Tyr-Pip) in the sanglifehrin core, stereocenters at C14

180 ition, interactions between a residue in M3 (Tyr(309)) and Phe(167), a residue adjacent to the Cys lo

181 ion, we show that the hydroxyl group on MftA Tyr-30 is required for MftC catalysis.

182 work, tyrosine-protected gold nanoparticles (Tyr-Au NPs) were fabricated by one-step reduction of Au(

183 this residue, but instead labeled the nearby Tyr(62) within this same binding pocket.

184 , 100 muL, 10 pmol total peptide +/- 40 nmol Tyr(4)-BBN: for in vivo GRPR blockade) in severe combine

185 , the in vivo functional significance of NO2-Tyr(166)-apoA-I, a specific post-translational modificat

186 limited by kinetic discrimination against o-Tyr-AMP in the transfer step followed by o-Tyr-AMP relea

187 o-Tyr-AMP in the transfer step followed by o-Tyr-AMP release from the synthetic active site.

188 th the more abundant Phe oxidation product o-Tyr is limited by kinetic discrimination against o-Tyr-A

189 tion of PheRS editing caused accumulation of Tyr-tRNAPhe (5%), but not deacylated tRNAPhe during amin

190 both analytes, confirming the aggregation of Tyr-Au NPs induced by spermine and spermidine, which res

191 stic surface plasmon resonance (SPR) band of Tyr-Au NPs was red-shifted to 596 and 616nm and the emis

192 an unanticipated intramolecular collapse of Tyr(93) in kringle-1 onto Trp(547) in the protease domai

193 tudies revealed an aromatic cage composed of Tyr-362, Ser-369, and Trp-385 that accommodate the tri-m

194 Therefore, dephosphorylation of Tyr(P)(346) may be considered an important "checkpoint"

195 ions of TULA-2-mediated dephosphorylation of Tyr(P)(346) may include deactivation of receptor-activat

196 substantial degree, by dephosphorylation of Tyr(P)(346), a regulatory site of Syk, which becomes pho

197 yses, and uncovered coordinated evolution of Tyr and betalain biosynthetic pathways in Caryophyllales

198 ne, which results to restore fluorescence of Tyr on the surfaces of Au NPs.

199 The importance of Tyr(179) in regulating Pi release was supported by site-

200 SLP-76 SAM domain (DeltaSAM) or mutation of Tyr-113, Tyr-128, and Tyr-145 to phenylalanine (3Y3F).

201 mental findings and suggest that mutation of Tyr-23 changes the pore profile at the gate formed by re

202 Absence of IGF-1R or mutation of Tyr-60, Tyr-133, or Tyr-250 in PCNA abrogated its ubiqui

203 Nitration of Tyr often causes loss of protein activity and is linked

204 Oxidation of Tyr-Ala-Ala-Ala-Arg (YAAAR) produces Tyr-O radicals by c

205 ctivity through increased phosphorylation of Tyr-216 in pleural mesothelial cells and GSK-3beta mobil

206 appear to result from optimizing the pKa of Tyr-111, which acts as the catalytic acid during l-alani

207 These results suggest that relaxation of Tyr pathway regulation increased Tyr production and cont

208 To characterize the role of Tyr(215), effects of substitutions of the tyrosine (Y215

209 V1 mutants, containing the whole spectrum of Tyr(511) substitutions, and tested their response to bot

210 Our data show that only substitutions of Tyr(511) to aromatic amino acids were able to mimic, alb

211 etic approaches to investigate the timing of Tyr(162) intercalation for AAG.

212 ylates Beclin1, a core autophagy protein, on Tyr-233 and that this post-translational modification li

213 ng site of hemopexin, and we found that one, Tyr-199, interacts directly with the heme ring D propion

214 of IGF-1R or mutation of Tyr-60, Tyr-133, or Tyr-250 in PCNA abrogated its ubiquitination.

215 , we found that phosphorylation of Thr(6) or Tyr(8) on UNG2 can impede PCNA binding without affecting

216 endogenous readthrough, namely Gln, Lys, or Tyr at UAA or UAG PTCs and Trp, Arg, or Cys at UGA PTCs.

217 unaffected by mutating phosphorylated p190A-Tyr(308), but disrupted by a S296A mutation, targeting t

218 ive reactivity toward Lys and, particularly, Tyr side chains, and can be used to target nonenzymes (e

219 fted to 596 and 616nm and the emission peak (Tyr) at 410nm was gradually increased with increasing co

220 ng e.g. 4.8% Lys, 2.7% Met+Cys, and 7.7% Phe+Tyr.

221 ase in PiPT revealed that Tyr(179) in Pho84 (Tyr(150) in PiPT) is not part of the Pi binding site.

222 Synergy requires receptor phospho-Tyr and two anionic lipids (phosphatidylserine and PIP2)

223 Phosphorylated Tyr-1021 in PDGFRbeta was the primary interaction site f

224 blation also promoted STAT3 phosphorylation (Tyr(705)) to LPS stimulation, but this STAT3 activation

225 lationship between tyrosine phosphorylation (Tyr(P)) and serine phosphorylation (Ser(P)) of IRS-2 aft

226 new site for c-Abl-mediated phosphorylation, Tyr-397.

227 hed that GIV is involved in phosphotyrosine (Tyr(P))-based signaling in response to growth factor sti

228 nt tyrosine in the substrate binding pocket (Tyr(215) in Aerococcus viridans LOX) that is partially r

229 B residues Tyr(440) and Tyr(444) Previously, Tyr(440) was observed to coordinate heme iron in an IsdB

230 tion of Tyr-Ala-Ala-Ala-Arg (YAAAR) produces Tyr-O radicals by combined electron and proton transfer

231 ted in diminished Ser(P)-IRS-2 and prolonged Tyr(P)-IRS-2 as well.

232 odifications of tRNA(UUU)(Lys) and tRNA(QUA)(Tyr) has the opposite effect of decreasing errors.

233 The CTD comprises the repeated Tyr-Ser-Pro-Thr-Ser-Pro-Ser motif with potential epigene

234 Mutating the equivalent residue, Tyr-280/Tyr-261, in Erk1/Erk2 significantly impaired Erk

235 iodination of thyroglobulin (TG) at residues Tyr(5) and Tyr(130), whereas thyroidal T3 production may

236 ally required active site conserved residues Tyr(40), Asp(181), and Arg(100)and a reacting duplex 5'-

237 nterface that is centered on IFNAR1 residues Tyr(240) and Tyr(274) binding the C and N termini of the

238 y a key interface created by IFNAR1 residues Tyr(240) and Tyr(274) interacting with IFN-beta residues

239 ll molecule binding site, including residues Tyr-37(I:07/1.39), Trp-86(II:20/2.60), and Phe-109(III:0

240 porphyrin ring interacts with IsdB residues Tyr(440) and Tyr(444) Previously, Tyr(440) was observed

241 e of VAO reveals that two tyrosine residues, Tyr-108 and Tyr-503, are positioned to facilitate this d

242 tation of two pore-lining tyrosine residues, Tyr-23 and Tyr-149 in sheep AQP0, to the corresponding r

243 Therefore, we hypothesize that the rTRPV1 Tyr(511) residue entraps vanilloids in their binding sit

244 E7, which recognizes the pan-opioid sequence Tyr-Gly-Gly-Phe at the N terminus of most endogenous opi

245 tic mutation of tyrosine residues in Gly/Ser-Tyr-Gly/Ser motifs of the IDR reduced this effect, depen

246 at normally accommodates a conserved Tyr-Ser-Tyr motif from TPX2, blocking the AURKA-TPX2 interaction

247 GF receptor, they bound poorly to the single-Tyr EGF receptors, even those that bound full-length Grb

248 ng the binding of Grb2 and Shc to the single-Tyr EGF receptors.

249 The ability of the single-Tyr receptors to signal correlated with their ability to

250 f the signaling capabilities of these single-Tyr EGF receptors indicated that they can activate a ran

251 There are four phosphorylated sites (Tyr-4, Tyr-19, Tyr-20, and Tyr-205) in ARH1.

252 For one of these sites (Tyr-447) we demonstrated the contribution of MEK/ERK-dep

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

254 Specifically, Tyr(135) and Val(141) on the DEa loop were shown to be c

255 osphorylation event, was necessary for STAT1 Tyr-701 phosphorylation.

256 igh concentrations of betalains, synthesizes Tyr via plastidic arogenate dehydrogenases (TyrAa /ADH)

257 r binding, whereas the AC413/rAmy C-terminal Tyr had little or no influence on binding.

258 oxidative decarboxylation of the C-terminal Tyr of the substrate peptide MftA in a reaction that req

259 We conclude that Tyr-315 is essential for coordinating ssDNA interaction

260 These results indicate that Tyr-108 and Tyr-503 are responsible for the activation o

261 Our results further indicate that Tyr-397 is the dominant site of c-Abl phosphorylation bo

262 rison and biochemical studies indicated that Tyr 97 and His 138 are key residues for catalytic reacti

263 electrophysiological analysis indicates that Tyr-542 interacts with both the pore domain and voltage

264 e model for Pi release in PiPT revealed that Tyr(179) in Pho84 (Tyr(150) in PiPT) is not part of the

265 To conclude, we suggest that Tyr(511)-mediated anchoring of vanilloids in their bindi

266 pase-9 in vitro or in cells, suggesting that Tyr-153 is not phosphorylated by c-Abl.

267 The Tyr-Au NPs were successfully used as a dual probe for co

268 cals involving electron abstraction from the Tyr phenol ring and N-terminal amino group in combinatio

269 , in contrast to AppABLUF, modulation in the Tyr (Y8) pKa has a profound impact on the forward photor

270 positively charged amino acids result in the Tyr-84 swing, amino acids that are negatively charged in

271 s simulations revealed an interaction of the Tyr(11) residue of NT[8-13] with an acidic residue (Glu(

272 Second, we provided the Tyr and 3-NT discrimination with DPV and compared with t

273 ishing a functional Gd(3+) binding site, the Tyr-541 residue participates in fine-tuning Gd(3+)-sensi

274 site-directed mutagenesis, we found that the Tyr-542 residue is critical for establishing a functiona

275 Thr/Tyr kinase (TTK)/monopolar spindle 1 kinase (Mps-1) is a

276 ions of Pho84 in which a residue adjacent to Tyr(179), Asp(178), is protonated revealed a conformatio

277 ase domain and hypothesize that RNA bound to Tyr-315 may be sufficient to competitively inhibit ssDNA

278 of this residue, which is a Tyr in LodA, to Tyr or Ala eliminates the cooperativity and destabilizes

279 BvADHalpha exhibited relaxed sensitivity to Tyr.

280 n-human study of (18)F-fluoroethyl triazole [Tyr(3)] octreotate ((18)F-FET-betaAG-TOCA) in patients w

281 arious planar (including aromatic (Phe, Trp, Tyr, and His)/amide (Asn and Gln)/Guanidine (Arg)) side-

282 lly bound by the peptides: (a) Trp58, Trp59, Tyr 62, Asp96, Arg195, Asp197, Glu233, His299, Asp300 an

283 scence of the tryptophan (Trp) and tyrosine (Tyr) amino acid residues present in the leuprolide nonap

284 ted that iodination of a conserved tyrosine (Tyr(B26)) enhances key properties of a rapid-acting clin

285 erted proton uptake from conserved tyrosine (Tyr-87) and histidine (His-38) residues within the activ

286 and in ESSI MS, of dopamine (DA), tyrosine (Tyr) and N,N-dimethyl-p-phenylenediamine (DMPA), were ev

287 ion of 3-Nitrotyrosine (3-NT) from Tyrosine (Tyr) by adding a nitro group (-NO2) with nitrating agent

288 zed from the aromatic amino acid l-tyrosine (Tyr) and replaced the otherwise ubiquitous phenylalanine

289 decarboxylation of the C-terminal tyrosine (Tyr-30) on the mycofactocin precursor peptide MftA; howe

290 ng specific cleavage C-terminal to tyrosine (Tyr) and tryptophan (Trp) residues provides a potential

291 N terminus, SLP-76 has three key tyrosines (Tyr-113, Tyr-128, and Tyr-145, "3Y") as well as a steril

292 s, tyrosylglycine (Tyr-Gly), tyrosylalanine (Tyr-Ala), and phenylalanylglycine (Phe-Gly), reacted wit

293 rst, three model dipeptides, tyrosylglycine (Tyr-Gly), tyrosylalanine (Tyr-Ala), and phenylalanylglyc

294 de was utilized for the determination of UA, Tyr and AP in human blood serum and urine samples.

295 higher electrocatalytic activity towards UA, Tyr and AP by not only shifting their oxidation potentia

296 actor, oxidized Gd-MoFeP features an unusual Tyr coordination to its P-cluster along with ligation by

297 ed by one-step reduction of Au(3+) ion using Tyr as a reducing and capping agent under microwave irra

298 ivated conformations of the channel, whereas Tyr-545 contributes to the slow kinetics of deactivation

299 with the carboxylate group interacting with Tyr-385 and Ser-530 at the top of the channel.

300 d receptor ligand, analogs H-Tyr-c[D-Lys-Xxx-Tyr-Gly] were synthesized and their biological activity