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1                                              Tyr pocket mutations selectively impair PLK1 binding to
2                                              Tyr(126) of Zap70 directly bound to PKCtheta, and the in
3                                              Tyr-172, Tyr-654, Tyr-855, and Tyr-1510 were phosphoryla
4 sidues in the Nef dimer interface (Leu(112), Tyr(115), and Phe(121)) and demonstrated attenuated homo
5                  During catalysis, Arg(169), Tyr(185), and Tyr(187) are responsible for neutralizing
6                                     Tyr-172, Tyr-654, Tyr-855, and Tyr-1510 were phosphorylated on IQ
7 incorporation of 3,5-dichlorotyrosine (Cl(2)-Tyr) and 3,5-difluorotyrosine (F(2)-Tyr) to replace Tyr2
8 e (Cl(2)-Tyr) and 3,5-difluorotyrosine (F(2)-Tyr) to replace Tyr272 in the GAO(V) previously optimize
9 the specific SHCA tyrosine residues Tyr-239, Tyr-240, and Tyr-313.
10   We noted that phosphorylation of Tyr(297), Tyr(246), and Tyr(336) of Shb is required for EphB2-ephr
11 aromatic triad of three amino acids, Phe(36)-Tyr(51)-Phe(64), is a unique SUMO signature that is abse
12 simulations suggested that an Asp-156-Arg-39-Tyr-202 triad creates a hydrogen-bonded network to facil
13                           Mutation of NPF6.4 Tyr-370 to His (Y370H) resulted in saturable high-affini
14 four active-site residues, Phe-316, His-583, Tyr-766, and His-767.
15 .phenylazophenol complex identified Phe(59), Tyr(101), and Lys(134) as contacting the 4-hydroxyphenyl
16     Absence of IGF-1R or mutation of Tyr-60, Tyr-133, or Tyr-250 in PCNA abrogated its ubiquitination
17 ed residues - Gln(232/585)-Asp(262)/Asn(623)-Tyr(322/666) (the constriction triads).
18                            Tyr-172, Tyr-654, Tyr-855, and Tyr-1510 were phosphorylated on IQGAP1 when
19 ts three conserved aromatic residues Trp-71, Tyr-87, and Phe-89 at the center of this pocket.
20 xtended to include a fourth Trp (W369) and a Tyr (Y319) residue at the protein surface that imparts a
21 bation of the edge-to-face conformation by a Tyr to Phe substitution significantly decreased stabilit
22 finic C27 followed by HAT to the C26* from a Tyr.
23                        Here, we identified a Tyr-16-Phe (Y16F) change in the NS4A transmembrane domai
24                       Recent studies using a Tyr-CreER driven mouse model have drawn contradictory co
25  hydroquinone (H2Q), N-acetyl-tyrosine (N-Ac-Tyr) or guanosine-5'-monophosphate (GMP) was investigate
26                 Here, we identify amino acid Tyr (Y) 155 of the RLC as a novel regulatory site that s
27 pon heptamerization, packing of trans-acting Tyr(290) against cis-acting Arg(349) compels Arg(349) to
28           The first contained a redox-active Tyr in beta subunits (F41Y), a substitution present in H
29                                  An adaptive Tyr-to-Cys substitution at amino acid 42 was discovered
30 7)Lu-DOTA-PP-F11 ((177)Lu-DOTA-(dGlu)(6)-Ala-Tyr-Gly-Trp-Met-Asp-Phe-NH(2)), and whether the use of p
31 )Lu-DOTA-PP-F11N ((177)Lu-DOTA-(dGlu)(6)-Ala-Tyr-Gly-Trp-Nle-Asp-Phe-NH(2)) performs better than refe
32 nigastrin analog (177)Lu-DOTA-(d-Glu)(6)-Ala-Tyr-Gly-Trp-Nle-Asp-PheNH(2) ((177)Lu-PP-F11N) is a suit
33 ran/gelatin hydrolysate films containing Ala-Tyr peptide were developed and characterised for their p
34 ely (177)Lu-DOTA-MG11 ((177)Lu-DOTA-dGlu-Ala-Tyr-Gly-Trp-Met-Asp-Phe-NH(2)) and (177)Lu-DOTA-PP-F11 (
35                      Methods: DOTA-D-Glu-Ala-Tyr-Gly-Trp-(N-Me)Nle-Asp-1-Nal-NH(2) (DOTA-MGS5) radiol
36            The model dipeptide Fmoc-Tyr(All)-Tyr(All) was used to explore different reaction conditio
37 etathesis (RCM) involving tyrosine(O-allyl) (Tyr(All)), but desallyl products limited the yields of t
38 rating that kinase activity and Tyr-1022 and Tyr-1162 of ERBB4, as well as the intact phosphotyrosine
39 ABL1 or the homologous residues Tyr(116) and Tyr(161) in ABL2 induces only minor structural perturbat
40 2A overexpression, we show that Tyr-1292 and Tyr-1387 but not Tyr-1325 are responsible for the effect
41 vealed that two pol eta residues, Phe-18 and Tyr-92, behave as steric gates to influence sugar select
42    During catalysis, Arg(169), Tyr(185), and Tyr(187) are responsible for neutralizing the negative c
43   The solvent accessibilities of Tyr-213 and Tyr-216 suggested that these tyrosines move to new parti
44 ses ADAMTS2 and ADAMTS14 between Asp-218 and Tyr-219, 50 amino acids downstream of the BMP1 cleavage
45 ly conserved tyrosine residues, Tyr-2387 and Tyr-2391, in the Poltheta active site.
46 SHCA tyrosine residues Tyr-239, Tyr-240, and Tyr-313.
47 ion-hole histidine residues with Tyr-246 and Tyr-344.
48 t phosphorylation of Tyr(297), Tyr(246), and Tyr(336) of Shb is required for EphB2-ephrinB1 boundary
49 hobic interactions with Trp-37, Phe-260, and Tyr-443.
50 ilic residues of tetraspanin 33, Trp-283 and Tyr-282, were required for its interaction with PLEKHA7.
51  and the interdomain B residues Tyr(315) and Tyr(319) were indirectly required for binding to PKCthet
52                                  Phe-316 and Tyr-766 variants retained catalytic activity, albeit wit
53 oforms bearing monosaccharides at Tyr(4) and Tyr(4') shows that the glycopeptides with either alpha-
54 at while the active site residues Asp-40 and Tyr-16 maintain their electric field contributions at al
55                                  Phe(59) and Tyr(101) substitutions with His and Phe, respectively, r
56 f two UNG2 phosphorylation sites (Thr(6) and Tyr(8)) located within its PCNA-interacting motif (PIP-b
57 es lining the SBS-A1 site, two (Gln(700) and Tyr(717)) promoted alternan elongation.
58 and focal adhesion kinase (FAK) Ser(722) and Tyr(576).
59  a beta(3)-homo amino acid in position 8 and Tyr(11) substitutions.
60               Tyr-172, Tyr-654, Tyr-855, and Tyr-1510 were phosphorylated on IQGAP1 when phosphotyros
61  simultaneous phosphorylation of Tyr(89) and Tyr(134) in ABL1 or the homologous residues Tyr(116) and
62 it by demonstrating that kinase activity and Tyr-1022 and Tyr-1162 of ERBB4, as well as the intact ph
63  from the D-ring hydroxyl of 17-HOPC-CoA and Tyr-344 as the general acid that protonates the propiony
64    FPheK reacted with adjacent Lys, Cys, and Tyr residues in thioredoxin in high yields.
65 n of three dipeptides, Tyr-Gly, Phe-Gly, and Tyr-Ala, from raw water demonstrates a useful applicatio
66  oxidation at certain sites of Met, His, and Tyr, conversion of histidine to aspartate and hydroxyasp
67 nd hydroxo(Cu) ligands, while the Cu(II) and Tyr(*) are ferromagnetically coupled due their delocaliz
68 volved with specific preferences for Ser and Tyr ligands, respectively, and that the structural contr
69 s involving sidechains of Gln, Asn, Ser, and Tyr residues, both along and transverse to the fibril gr
70 guously identified the core 1 structures and Tyr-10 attachment sites of the glycopeptides, we did not
71 these phenomena, we compared the Ser/Thr and Tyr phosphoproteomes of murine lung epithelial cells ear
72 ase undergoes autophosphorylation on Thr and Tyr residues and phosphorylates a classical eukaryotic p
73  composed of a dual specificity (Ser/Thr and Tyr) kinase domain tethered to a calmodulin-like domain
74 re DEPC labeling reactivity of Ser, Thr, and Tyr residues in intact proteins with peptide fragments f
75 enhanced reactivity of certain Ser, Thr, and Tyr residues occurs due to higher local concentrations o
76 akly nucleophilic side chains (Ser, Thr, and Tyr) can be modified by DEPC in addition to other residu
77 g the signals of interest from other Trp and Tyr residues.
78 as required for expression of Dct, Tyrp1 and Tyr, genes that are regulated by SOX10 and MITF and for
79 tional contacts involving Glu(4) of XCL1 and Tyr(117) and Arg(273) of XCR1.
80 nds, derived from the hexapeptide acetyl-Arg-Tyr-Arg-Leu-Arg-Tyr-NH(2) (1), reported to be a Y(4)R pa
81 m the hexapeptide acetyl-Arg-Tyr-Arg-Leu-Arg-Tyr-NH(2) (1), reported to be a Y(4)R partial agonist wi
82 of 1 resulted in a tetrapeptide (Arg-Leu-Arg-Tyr-NH(2)), being a Y(4)R partial agonist with unchanged
83 dicted to bind the minimal FLAG peptide (Asp-Tyr-Lys-Asp) were grafted onto a single-chain variable f
84 e demonstrated that phosphorylation of AR at Tyr-267 by Ack1/TNK2 tyrosine kinase results in nuclear
85  of 18 glycoforms bearing monosaccharides at Tyr(4) and Tyr(4') shows that the glycopeptides with eit
86          In contrast, calmodulin nitrated at Tyr-138 produced more nitric oxide and did so more effic
87 itro eNOS assays with calmodulin nitrated at Tyr-99 revealed that this nitration reduces nitric-oxide
88 rated that the absence of phosphorylation at Tyr(399) caused PTPROt to dephosphorylate Src at the act
89                 Recently, phosphorylation at Tyr-67 by the FGF15/19 signaling-activated nonreceptor t
90 6) In contrast, phosphorylation of PTPROt at Tyr(399) enabled PTPROt to recruit Src through Grb2 and
91 that reversible phosphorylation of PTPROt at Tyr(399) is a molecular switch that selects between its
92 umours, ALK directly phosphorylates SMAD4 at Tyr 95.
93 cogene, nonreceptor tyrosine kinase (SRC) at Tyr(198) We demonstrate that PANX1-mediated ATP release
94 involves a hydrogen bond interaction between Tyr-73 of mCD1d and the amide group oxygen of alphaGSAs.
95 e activity possibly by the promotion of BIN2 Tyr(200) autophosphorylation, and subsequently represses
96                           The bioelectrodes (Tyr/ZnO-rGO/ITO) were designed by covalently immobilizin
97 cyclohexanol, 4-methylumbelliferone, and Boc-Tyr-OMe), an amine (propargylamine, diethylamine, morpho
98                    3,5-Di-I-Tyr-Ala and N-Br-Tyr-Ala were detected in treated water but not in the co
99 ues flanking the SP motif, such as the bulky Tyr(1) next to Ser(2), prevent the formation of such con
100 as shown by X-ray crystallography, partly by Tyr-172 inserting into a cavity in the activation domain
101 g form as in the wild-type, i.e., Cu(II)-(Cl-Tyr(*)-Cys) or Cu(II)-(F-Tyr(*)-Cys).
102  analyses revealed that the highly conserved Tyr-86 residue in E. coli TrmD is essential to discrimin
103 ations ablating an evolutionarily conserved, Tyr-lined pocket in human PLK1 PBD trigger cellular anom
104 .e., biogenesis) leading to the key covalent Tyr-His cross-link in CcO.
105   This loop contains a functionally critical Tyr at position 71.
106 -platelet aggregates by cleaving the cryptic Tyr(1605)-Met(1606) bond in the VWF A2 domain.
107 consists of a cysteine-tyrosine radical (Cys-Tyr(*)) as a copper ligand.
108 a-c[d-Cys-Aph(Hor)-d-Aph(Cbm)-Lys-Thr-Cys]-d-Tyr-NH2), an antagonist with selectivity for sstr subtyp
109 tion and quantification of three dipeptides, Tyr-Gly, Phe-Gly, and Tyr-Ala, from raw water demonstrat
110 ctivity for the proximal Tyr in Asp-directed Tyr modification.
111   While the distance between the H(+) donor (Tyr) and acceptor (O(Cu)) results in a barrier to PT, th
112 on studies after injection with (177)Lu-DOTA-Tyr(3)-octreotate or (177)Lu-DOTA-JR11.
113  with surfactant to release the encapsulated Tyr.
114 ains five putative canonical surface-exposed Tyr-based endocytic motifs.
115 e, i.e., Cu(II)-(Cl-Tyr(*)-Cys) or Cu(II)-(F-Tyr(*)-Cys).
116 e assessed whether ZINC40099027 promotes FAK-Tyr-397 phosphorylation and wound healing in Caco-2 mono
117 8F variant (i) fails to accumulate the first Tyr* and (ii) makes an altered major product, identifyin
118                     The model dipeptide Fmoc-Tyr(All)-Tyr(All) was used to explore different reaction
119  interfacial self-assembly of peptides (Fmoc-Tyr(H(2) PO(3) )-OH) with magnetic nanoparticles (MNPs)
120 ects were blunted by substitution of Phe for Tyr-67 in FXR.
121        Our results reveal critical roles for Tyr(1) in differentiating the phosphorylation states of
122  the reactive deprotonated tyrosine, forming Tyr(*).
123                                     The free Tyr could then initiate the transformation of tyrosine t
124 cle, we detect 3-NT and discriminate it from Tyr with Differential Pulse Voltammetry (DPV) as it is a
125                                Thus, PT from Tyr precedes O-O elongation and is rate-limiting, consis
126 M proteins via the recognition of functional Tyr motifs also operates in plants.
127 y, respectively, in place of the gatekeeping Tyr found in mSCD1.
128                    Optimal conditions to get Tyr-Tyr covalent binding between invertase and the suppo
129 een the carbonyl groups from the Thr-Val-Gly-Tyr-Gly signature filter sequence and the permeant ions
130                                     However, Tyr and Trp are not functionally interchangeable, and th
131 veal that proofreading activity to hydrolyze Tyr-tRNA(Phe) is increased during oxidative stress, whil
132 hy was performed with (125)I-JR11 and (125)I-Tyr(3)-octreotide in cancers from prostate, breast, colo
133                                     3,5-Di-I-Tyr-Ala and N-Br-Tyr-Ala were detected in treated water
134 osphorylation of the PI 3-kinase-interacting Tyr-751 residue of PDGFRbeta, thus activating Akt.
135 tegies should be applicable to RCM involving Tyr(All) and similar residues in peptide and peptidomime
136 libration slope = 4%, n = 3), and accurate l-Tyr quantification in plasma samples with low relative e
137 mycin A, cyclo (l-Pro-l-Val), cyclo (l-Pro-l-Tyr), bikaverin, kojic acid and 3-nitropropionic acid we
138         High analytical performance toward l-Tyr (linear range of 0.5-100 muM, LOD = 0.1 muM), intere
139 loyed for the determination of l-tyrosine (l-Tyr) in human plasma from tyrosinemia-diagnosed patients
140 n of the hexapeptide VEALYL (Val-Glu-Ala-Leu-Tyr-Leu), the B-chain residue 12-17 segment of insulin t
141 with the standard PRRT agent, (177)Lu-LuDOTA-Tyr(3)-octreotate ((177)Lu-LuTATE).
142  effectively form covalent adducts with Lys, Tyr, and His residues, given that these agents were cell
143  warheads to form covalent adducts with Lys, Tyr, and His residues.
144 ctive gamma-turn conformation of the Bip-Lys-Tyr tripeptide in Urocontrin ([Bip(4)]URP), which modula
145  a minimalistic self-assembling peptide, Lys-Tyr-Tyr (KYY) with strong propensity to form supramolecu
146                                            m-Tyr resistant mutants were isolated and found to have al
147  under conditions of oxidative stress, and m-Tyr has been shown to be toxic to a broad range of biolo
148 l protection against hazardous cytoplasmic m-Tyr accumulation.
149  checkpoint by the PheRS, this toxicity of m-Tyr may result from interfering with amino acid metaboli
150              To determine the mechanism of m-Tyr toxicity, we utilitized a strain of E. coli that exp
151 sult in less uptake or increased efflux of m-Tyr.
152 erentially expressed after the addition of m-Tyr.
153 -dense protein aggregates, indicating that m-Tyr destabilized a large fraction of the proteome.
154 tein stress response, and cells exposed to m-Tyr contained large, electron-dense protein aggregates,
155   The global responses of E. coli cells to m-Tyr were assessed by RNA-seq, and >500 genes were differ
156 ase (PheRS) is required for resistantce to m-Tyr.
157  The non-protein amino acid meta-Tyrosine (m-Tyr) is produced in cells under conditions of oxidative
158          These findings indicate that when m-Tyr has passed the QC checkpoint by the PheRS, this toxi
159            However, the mechanism by which m-Tyr damages cells is unclear.
160 first-time-in-humans trial of (64)Cu-MeCOSar-Tyr(3)-octreotate ((64)Cu-SARTATE) to assess its safety
161        We specifically detected SRC-mediated Tyr(198) phosphorylation at the plasma membrane and obse
162                                     Mutating Tyr-430 in the alpha5 M4 domain changed alpha5-selectivi
163 this residue, but instead labeled the nearby Tyr(62) within this same binding pocket.
164 , we show that Tyr-1292 and Tyr-1387 but not Tyr-1325 are responsible for the effect of leptin.
165 , carrying the core 1 Galbeta3GalNAcalpha1-O-Tyr-10 structure, to (1) identify by HCD LC-MS/MS the de
166               The solvent accessibilities of Tyr-213 and Tyr-216 suggested that these tyrosines move
167 t step results in sequential accumulation of Tyr radicals, which are suppressed without detriment to
168 tion of PheRS editing caused accumulation of Tyr-tRNAPhe (5%), but not deacylated tRNAPhe during amin
169 both analytes, confirming the aggregation of Tyr-Au NPs induced by spermine and spermidine, which res
170 stic surface plasmon resonance (SPR) band of Tyr-Au NPs was red-shifted to 596 and 616nm and the emis
171 t DM1 linked to the C-terminal side chain of Tyr(3)-octreotate.
172 successfully applied to the determination of Tyr in dairy products and fermented drinks with good rec
173 ne, which results to restore fluorescence of Tyr on the surfaces of Au NPs.
174         Asp-82 also enhanced the function of Tyr as a redox-active amino acid in the rHbS betaF41Y/K8
175                       Subsequent mutation of Tyr(117) and Arg(273) led to diminished binding and acti
176             Absence of IGF-1R or mutation of Tyr-60, Tyr-133, or Tyr-250 in PCNA abrogated its ubiqui
177                       The phosphorylation of Tyr(1) further prohibited Ssu72 binding to pSer(2) and t
178             We noted that phosphorylation of Tyr(297), Tyr(246), and Tyr(336) of Shb is required for
179 Pyk2 (particularly by the phosphorylation of Tyr(402)) in primary human peripheral blood monocytes.
180 evealed that simultaneous phosphorylation of Tyr(89) and Tyr(134) in ABL1 or the homologous residues
181 ly, our data suggest that phosphorylation of Tyr-1510 of IQGAP1 alters cell function.
182 er than the corresponding phosphorylation of Tyr-223 by MKK4 with or without arrestin-3.
183 YK for rapid LYN-mediated phosphorylation of Tyr-352 and then Tyr-348 of the SH2-kinase linker, which
184 und that leptin increases phosphorylation of Tyr-418 in Src, an indicator of kinase activation.
185 5A variants revealed that phosphorylation of Tyr-93 located within domain 1 of NS5A, but not of any o
186 ide chain is packed by the aromatic rings of Tyr(312) and Trp(273), as well as the hydrocarbon side c
187                              Substitution of Tyr for Ala and Gly in ADS1.2 and ADS1.4, respectively,
188 his communication reports the elegant use of Tyr-loaded liposomes (TLL) toward in situ sensitization
189 icles via the recognition of motifs based on Tyr or di-Leu in their cytoplasmic tails.
190     IQGAP1 was phosphorylated exclusively on Tyr-1510 under conditions with enhanced MET or c-Src sig
191 ere on Ser or Thr residues, but none were on Tyr.
192 of IGF-1R or mutation of Tyr-60, Tyr-133, or Tyr-250 in PCNA abrogated its ubiquitination.
193 Pro hydroxylation, Hyp glycosylation, and/or Tyr sulfation.
194 conformational change does not affect Phe or Tyr activation or the aminoacylation activity of PheRS.
195 bone amidate and an oxygenic residue (Ser or Tyr) ligate to two of the cluster's Fe centers.
196 ose typically conserved among GA 3-oxidases, Tyr(93), Met(106), and Thr(202), respectively, conferred
197 onjugated zinc oxide-reduced graphene oxide (Tyr/ZnO-rGO) nanocomposite system as a biosensing test-b
198 ant was further modified by replacing the P1 Tyr residue with para-substituted Phe derivatives, gener
199  unaffected by mutating phosphorylated p190A-Tyr(308), but disrupted by a S296A mutation, targeting t
200                                Using a PANX1 Tyr(198)-specific antibody, SFK inhibitors, SRC knockdow
201 volves constitutive phosphorylation of PANX1 Tyr(198) by SRC.
202 fted to 596 and 616nm and the emission peak (Tyr) at 410nm was gradually increased with increasing co
203 olecules and the amino acid side chains Phe, Tyr, and Trp.
204 His583 to Ala, Asp, Asn, Glu, Gln, Lys, Phe, Tyr, and Trp showed that although both the Cu(Z) and Cu(
205 with enhanced specificity for phosphorylated Tyr(992) (pTyr(992)) of EGFR.
206  These findings indicate that phosphorylated Tyr-93 in NS5A plays an important role during viral repl
207 ating protein p85alpha in a phosphorylation (Tyr(397))-dependent manner, preventing Rab5-GTP loading,
208 ty of amino acids were composed of Val, Pro, Tyr, Met, Leu, Trp, Phe, Lys and Glu.
209 re achieved in the O-arylation at a proximal Tyr residue in a number of cases, including a peptide-sm
210  that gave high selectivity for the proximal Tyr in Asp-directed Tyr modification.
211 FAK phosphorylation, without activating Pyk2-Tyr-402 or Src-Tyr-419.
212 BL1 complex also suppressed downstream RAD51 Tyr-315 phosphorylation.
213 osphorylatable IQGAP1 construct by replacing Tyr-1510 with alanine.
214  residue Tyr(527) and its activating residue Tyr(416) Whereas wild-type and PTPROt knockout mice exhi
215 phA1 phosphorylate the Cx32CT domain residue Tyr(243) Unlike for Cx43, the tyrosine phosphorylation o
216 phorylate Src both at its inhibitory residue Tyr(527) and its activating residue Tyr(416) Whereas wil
217 fluoride electrophile at a tyrosine residue (Tyr-82) inhibits guanine exchange factor Rgl2-mediated n
218                       The catalytic residue, Tyr(250) , is under the hydrogen bond network to facilit
219  to PKCtheta, and the interdomain B residues Tyr(315) and Tyr(319) were indirectly required for bindi
220  Tyr(134) in ABL1 or the homologous residues Tyr(116) and Tyr(161) in ABL2 induces only minor structu
221 e catalytic interface unveiled that residues Tyr(195) (-3 subsite) and Trp(234) (-5 subsite) from dis
222 ation of the specific SHCA tyrosine residues Tyr-239, Tyr-240, and Tyr-313.
223  the two highly conserved tyrosine residues, Tyr-2387 and Tyr-2391, in the Poltheta active site.
224 almodulin sensitivity for calcium and reveal Tyr site-specific gain or loss of functions for calmodul
225  central to the RPN2-RPN13 interaction, RPN2 Tyr-950, is phosphorylated in Jurkat cells.
226 asome is enhanced by phosphorylation of RPN2 Tyr-950, have important implications for efforts to deve
227  causing CYP2B6 downregulation, and selected Tyr and Cys residues for mutation based on predicted sol
228 previously identified a series of sialylated Tyr-10 O-glycosylated Abeta peptides, 15-20 residues lon
229                              Both the single Tyr-41 and Asp-82 constructs lowered the oxygen affinity
230 ng the binding of Grb2 and Shc to the single-Tyr EGF receptors.
231 f the signaling capabilities of these single-Tyr EGF receptors indicated that they can activate a ran
232 o dephosphorylate Src at the inhibitory site Tyr(527), thus stimulating Src activity.
233  a putative C-terminal phosphorylation site, Tyr(399), in endogenous PTPROt was replaced with phenyla
234                                Specifically, Tyr-encapsulated and detection antibody-functionalized l
235 o observed for a eukaryotic dual-specificity Tyr phosphorylation-regulated kinase class.
236 ility, in part by dephosphorylating Spetin1 (Tyr(246)), a poorly described component of the cytoskele
237 tion, without activating Pyk2-Tyr-402 or Src-Tyr-419.
238                                 Substituting Tyr-213 within this hinge with smaller uncharged amino a
239                                     Sulfated Tyr in such compounds was stable in neutral buffer.
240 ro-apoptotic Ser(727) p-STAT1 and suppressed Tyr(705)-p-STAT3 for up to 72 h in the rat cochlea.
241  in the cochlea, which leads to pro-survival Tyr(705)-p-STAT3 activation.
242 igh concentrations of betalains, synthesizes Tyr via plastidic arogenate dehydrogenases (TyrAa /ADH)
243      We show that the loss of the C-terminal Tyr-Ala-Met-Leu motif is responsible for P0 mislocalizat
244 f arteries from hypertensive humans and that Tyr(198) phosphorylation is detectable in these samples,
245                                We found that Tyr 96, Glu 201, Arg 204, and Trp 234 in the presumptive
246 rated these findings, and we also found that Tyr-251 is critical for LAIR-1's inhibitory function.
247 hysical results presented here indicate that Tyr-15 plays a key role in the dimerization of the globi
248            Our results further indicate that Tyr-397 is the dominant site of c-Abl phosphorylation bo
249 -CoA desaturase (mSCD1) it was proposed that Tyr-104, a surface residue located at the distal end of
250 mmunoprecipitation experiments revealed that Tyr-251 in LAIR-1 binds CSK.
251 g mutant GluN2A overexpression, we show that Tyr-1292 and Tyr-1387 but not Tyr-1325 are responsible f
252  dimer are under tension and suggesting that Tyr-15 plays a role in both this tension and the globin
253 rmal vascular hemodynamics and suggests that Tyr(198)-phosphorylated PANX1 is involved in hypertensiv
254 e GABA-mediated activation and suggests that Tyr(87) prevents inhibitory effects of GABA.
255                                          The Tyr-Au NPs were successfully used as a dual probe for co
256                                          The Tyr-to-Phe substitution in Y(898)KAI reduced BRI1 intern
257 ecific edge-to-face conformation between the Tyr(51)-Phe(64) pair of interacting aromatics is vital t
258  that Y155 is phosphorylated in vitro by the Tyr kinase domain of epidermal growth factor (EGF) recep
259  step of the iconic PCET process used by the Tyr(z)-His190 redox relay in photosystem II to oxidize w
260 e mitotic defects caused by mutations in the Tyr pocket, further evidencing its essential function, a
261 positively charged amino acids result in the Tyr-84 swing, amino acids that are negatively charged in
262 ime proposed to be a key intermediate in the Tyr-His cofactor biogenesis.
263 ule inhibitor, Polotyrin, which occupies the Tyr pocket.
264 alling a canonical Met ligand in lieu of the Tyr found at the heme of MauG associated with electron t
265 al studies revealed that perturbation of the Tyr(51)-Phe(64) conformation disrupts several long-range
266 s, coupled to a 10- angstrom movement of the Tyr-loop.
267                  The response studies of the Tyr/ZnO-rGO/ITO bioelectrode revealed ultrafast (0.34 +/
268 ic role as genomic insulators, shielding the Tyr locus from the expression patterns of adjacent genes
269 esulting structure, which we have termed the Tyr-lock peptide family, is stabilized by a tyrosine res
270            Modeling studies suggest that the Tyr 85 adduct stabilizes the Keap1-Cul3 complex, thereby
271                            We found that the Tyr-950 phosphorylation enhances binding to RPN13.
272 and donate back a hydrogen bond upshifts the Tyr(*) potential into a range where it can effectively o
273 del wherein substrate discrimination via the Tyr pocket in the human PLK1 PBD regulates mitotic chrom
274 way for electrons to reduce the heme via the Tyr-41 side chain.
275    Of note, one of these by-products was the Tyr-based "cofactor" trihydroxyphenylalanine quinone (TP
276 mediated phosphorylation of Tyr-352 and then Tyr-348 of the SH2-kinase linker, which facilitates acti
277 tein kinase substrate in vitro This dual Thr-Tyr kinase activity is also observed for a eukaryotic du
278  evaluated by the ability to predict Ser/Thr/Tyr phosphorylation sites in the disordered proteome.
279        The most frequent mutation was His to Tyr at amino acid 44; additional escape mutants had a Hi
280 ydrogen-bonded via another water molecule to Tyr-131.
281 lamino)-5-oxopentanoic acid), conjugated to (Tyr(3))-octreotate, called (64)Cu-CuSarTATE, was demonst
282 sts of a mononuclear iron coordinated by two Tyr side-chain phenolates and one carboxylate from Glu.
283 elop an amperometric biosensor for tyramine (Tyr) measurement in food and beverages.
284 ngest on chromosome 7 containing tyrosinase (Tyr).
285 , which is embedded in the mouse tyrosinase (Tyr) gene, to evaluate whether targeted gene conversion
286                  Using the mouse tyrosinase (Tyr) locus as an experimental model, a gene whose mutati
287 osensor architecture is based on tyrosinase (Tyr(ase)) immobilization on glassy carbon electrode modi
288                             With tyrosinase (Tyr) and TiO(2) as representative enzyme and electrode,
289 ntioselectively converting L- or D-tyrosine (Tyr) into dityrosine (diTyr).
290  site of O-arylation at a proximal tyrosine (Tyr) residue.
291 7 of fumitremorgin B, posited that tyrosine (Tyr or Y) 224 serves as HAT intermediary to separate the
292 enylalanylglycine (Phe-Gly), tyrosylalanine (Tyr-Ala), and tyrosylglycine (Tyr-Gly), under chloramina
293 yrosylalanine (Tyr-Ala), and tyrosylglycine (Tyr-Gly), under chloramination in the presence of Br(-)
294 34-encoded antibodies with unmutated Ala-Val-Tyr and Asn-His-Ser motifs, which recognize both erythro
295 odel, we propose a catalytic mechanism where Tyr-294 acts as the general base abstracting a proton fr
296 olution, the Y15A and Y15G variants in which Tyr-15 is replaced with Ala or Gly, respectively, are mo
297 ations common to both viral genotypes, while Tyr phosphorylations showed little overlap.
298 air of oxyanion-hole histidine residues with Tyr-246 and Tyr-344.
299 ecular switch and works synergistically with Tyr-73 to control NKT cell activity.
300 e that recognizes the proline-rich Pro-Pro-x-Tyr (PPxY) motif contained in specific target proteins.

 
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