ライフサイエンスコーパス: tyrosine

1 rting from the amino acids phenylalanine and tyrosine.

2 racted that the most influential analyte was tyrosine.

3 tation, considering the oxidizable nature of tyrosine.

4 ons of NAP stimulated the phosphorylation of tyrosine-1229 (L1-Y1229) at the ankyrin binding motif of

5 receptor tyrosine kinase Pyk2 phosphorylates tyrosine 131 in the E2 transactivation domain.

6 on of PTPN14 reduced CAV1 phosphorylation on tyrosine-14, as well as suppressed CAV1-enhanced cell mi

7 O-(2-(18)F-fluoroethyl)-l-tyrosine ((18)F-FET) (7 studies, 172 lesions) demonstrat

8 PET using O-(2-(18)F-fluoroethyl)-l-tyrosine ((18)F-FET) has been shown to be a useful tool

9 PET using O-(2-(18)F-fluoroethyl)-l-tyrosine ((18)F-FET) is useful to detect residual tumor

10 Mutation of CD226 at tyrosine 319 (Y319) led to increased CD226 surface expre

11 AMPylated by IbpA from Histophilus somni at tyrosine 32 or by VopS from Vibrio parahaemolyticus at t

12 found two residues in the C-terminal domain, tyrosine 351 and glutamate 355, that influence pH gating

13 phorylation of the FAK family member Pyk2 at tyrosine 402 is decreased in NK92 CD56-KO cells, demonst

14 h a signaling pathway involving direct HDAC5 tyrosine 642 phosphorylation by focal adhesion kinase (F

15 nd centered around the universally conserved tyrosine 837 (Saccharomyces cerevisiae numbering), that

16 -S880) is decreased while phosphorylation of tyrosine-876 on GluA2 (GluA2-Y876) is elevated during ch

17 systems containing one pH- and redox-active tyrosine (alpha(3)Y and peptide A), and two proteins tha

18 ic acid, protocatechuic acid, syringic acid, tyrosine and capsaicin used as controls.

19 rom normally cultured cells was 1.1 mmol/mol tyrosine and decreased significantly in the presence of

20 h supporting enzymatic turnover of substrate tyrosine and forming the organometallic intermediate Ome

21 esized from chitin via any chemical process (tyrosine and l-DOPA).

22 protection of the phenolic hydroxyl in beta-tyrosine and N-Boc protection in lysine.

23 ur proteomic studies identified noncatalytic tyrosine and phosphotyrosine sites that can be liganded

24 ld with three added proline residues between tyrosine and the oxidant.

25 dation evoked by DPTA, suggesting that these tyrosines are targets for NO-dependent downregulation.

26 ity, flexibility and solvent exposure of the tyrosines are the key characteristics of hormonogenic si

27 the hydroxylation acceptor proline precludes tyrosine autophosphorylation and folding of DYRK1, resul

28 and CAR specific and required immunoreceptor tyrosine-based activation motif signaling.

29 e key kinases phosphorylating immunoreceptor tyrosine-based activation motifs (ITAM) in both these re

30 These studies indicate that tyrosine can undergo stable, covalent linkages in fibril

31 entral carbon catabolism flux redirection to tyrosine catabolism.

32 owth and metabolic genes enriched in cognate tyrosine codons.

33 pecific and crucial role for the active site tyrosine, conserved in all CcOs, is suggested.

34 H(2)O(2) at 3 and 24 h of incubation; and a tyrosine-containing entity.

35 In our experiment, tyrosine-containing peptides were selected as surrogate

36 r for site-specific incorporation of 3-nitro-tyrosine could not outcompete near-cognate suppression i

37 Altogether, our study highlights the tyrosine degradation pathway as a regulator of longevity

38 emonstrate that the levels of enzymes in the tyrosine degradation pathway increase with age in wild-t

39 al-specific downregulation of enzymes in the tyrosine degradation pathway significantly extends Droso

40 ased lifespan, and upregulates the levels of tyrosine-derived neuromediators.

41 We present results for capped tyrosine dipeptide, two maquette systems containing one

42 nine requirements (in the presence of excess tyrosine) during early and late gestation using direct a

43 nable the coupling reaction but hormonogenic tyrosines have not been clearly identified, and the lack

44 as approximately 20% and 38% of oxytocin and tyrosine hydroxylase (TH) cells, respectively, were resp

45 ulated phosphoprotein of 32 kDa (DARPP32) or tyrosine hydroxylase (TH) in tissue sections of adult mo

46 with immunofluorescence experiments against tyrosine hydroxylase (TH) or dopamine transporter (DAT).

47 -mediated loss of SDHC in cells that express tyrosine hydroxylase (TH), a compartment where PPGL is k

48 to stimulate VTA glutamate neurons in which tyrosine hydroxylase (TH), and thus DA biosynthesis, was

49 ely labeled with an antiserum raised against tyrosine hydroxylase (TH), the rate-limiting enzyme in c

50 Intriguingly, fibers expressing tyrosine hydroxylase (TH), the rate-limiting enzyme of d

51 pression of the dopamine-synthesizing enzyme tyrosine hydroxylase (TH).

52 minergic neurons marked by the expression of tyrosine hydroxylase (TH).

53 ], dopamine function [striatal expression of tyrosine hydroxylase (Th)], glucocorticoid receptor (GR)

54 Expression of tyrosine hydroxylase 2 in the brain was elevated in cdnf

55 ine cell number and volume and expression of tyrosine hydroxylase and dopamine transporter.

56 ed significant increases in the diameters of tyrosine hydroxylase immunoreactive soma in cave Astyana

57 nt reduction of DANs (~35%) in the SNpc, the tyrosine hydroxylase protein level in the striatum (~60%

58 rain and show that Syt2a is colocalized with tyrosine hydroxylase, a biosynthetic enzyme in the dopam

59 genetics we show the involvement of striatal tyrosine hydroxylase-expressing interneurons in mediatin

60 istance dependence for the CPET oxidation of tyrosine in a model system.

61 ed for the biosynthesis of phenylalanine and tyrosine in bacteria, archaea, plants, and fungi.

62 smic tyrosine residues called immunoreceptor tyrosine inhibitory motifs.

63 tiple sites, yet phosphorylation at specific tyrosines is variable and only a subset of receptors sha

64 nine is an indispensable amino acid and, via tyrosine, is the precursor for the neurotransmitters dop

65 a good source of tryptophan, phenylalanine + tyrosine, isoleucine, histidine, but limiting for lysine

66 ation of the cytoplasmic immunoglobulin tail tyrosine (ITT) motif in transmembrane IgE (mIgE) impairs

67 Using Bruton's tyrosine kinase (BTK) as a clinically relevant model sys

68 Therapeutic targeting of Bruton tyrosine kinase (BTK) has dramatically improved survival

69 Bruton's tyrosine kinase (BTK) is a non-receptor tyrosine kinase

70 Bruton's tyrosine kinase (BTK) is targeted in the treatment of B-

71 clude genes that modulate NFKB, BCL2, Bruton tyrosine kinase (BTK), and apoptosis.

72 receptor pathway, and specifically of Bruton tyrosine kinase (BTK), is a leading therapeutic strategy

73 binders, affects the degradation of Bruton's Tyrosine Kinase (BTK), we serendipitously discover that

74 had a significantly higher level of receptor tyrosine kinase (c-Kit) mRNA.

75 ins associated with insulin, erb-b2 receptor tyrosine kinase (Erbb), and Toll-like receptor signaling

76 way, including LCK proto-oncogene SRC family tyrosine kinase (LCK), LYN proto-oncogene SRC family tyr

77 kinase (LCK), LYN proto-oncogene SRC family tyrosine kinase (LYN), zeta chain of T-cell receptor-ass

78 wth factor (HGF)/MET proto-oncogene receptor tyrosine kinase (MET) and Wnt/beta-catenin signaling pat

79 Pathogenic muscle-specific tyrosine kinase (MuSK)-specific IgG4 autoantibodies in a

80 hat is known about the neurotrophic receptor tyrosine kinase (NTRK) genes in cancer was revealed thro

81 Are the receptor tyrosine kinase (RTK) and JAK-STAT-driven proliferation

82 ulators and mutations that activate receptor tyrosine kinase (RTK) signaling frequently occur in blad

83 delivery of SRC proto-oncogene, nonreceptor tyrosine kinase (SRC) to the plasma membrane and promote

84 ROS generation and spleen tyrosine kinase (Syk) activation induced by heme were cr

85 ed the implication of FcgammaRIIa and spleen tyrosine kinase (Syk) in DC activation and showed that t

86 A depletion of Mincle and its adaptor spleen tyrosine kinase (Syk), and Syk pharmacological inhibitio

87 ole of a nonreceptor tyrosine kinase, spleen tyrosine kinase (SYK), in mediating osteomyelitis.

88 endotoxin (ETX) or sFlt-1 (soluble fms-like tyrosine kinase 1), and in a postnatal model due to prol

89 ngiogenic biomarker(7), the soluble fms-like tyrosine kinase 1:placental growth factor (sFLT1:PlGF) r

90 Tyrosine kinase 2 (TYK2) is a member of the JAK kinase f

91 that MEOX1 knockdown decreased expression of tyrosine kinase 2 (TYK2), signal transducer and activato

92 sence of stem cell factor (SCF) and FMS-like tyrosine kinase 3 ligand (FLT3L) give rise to numerous c

93 gene, Ser/Thr kinase (Pim1); and Fms-related tyrosine kinase 4 (Flt4).

94 Eph family receptor tyrosine kinase A2 (EphA2) is a cellular receptor for KS

95 oidin domain receptor 1 (DDR1) is a receptor tyrosine kinase activated by collagens that can regulate

96 We show that tyrosine kinase activation is not the only rate-limiting

97 ned to intracellular membranes upon receptor tyrosine kinase activation.

98 ions illuminate a new connection between the tyrosine kinase activity of EGFR and innate immune funct

99 linked to insulin resistance through reduced tyrosine kinase activity of the insulin receptor; howeve

100 study found that inhibitors of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK) blocked

101 cell receptor signaling pathway, like Bruton tyrosine kinase and phosphatidylinositol 3 kinase.

102 resulting complex activates the RET receptor tyrosine kinase and subsequent downstream signals.

103 Further, we identify the ABL2 tyrosine kinase as an upstream regulator of HSF1 protein

104 r, ALKBH5 affects mRNA stability of receptor tyrosine kinase AXL in an m(6)A-dependent way.

105 pregulates the protein level of the receptor tyrosine kinase AXL to induce oncogenic signaling in ova

106 lecule-in mregDCs is induced by the receptor tyrosine kinase AXL, while upregulation of interleukin (

107 ely charged phospho-tyrosine on the receptor tyrosine kinase EphB2.

108 protein-protein interactions, with receptor tyrosine kinase ErbB2, and fundamental and clinical data

109 ng driver mutations in the gene encoding the tyrosine kinase FLT3 occur in both leukemias and are par

110 ctor receptor-beta (PDGFRbeta) is a receptor tyrosine kinase found in cells of mesenchymal origin suc

111 ant synaptic substrates, among which are the tyrosine kinase Fyn and glutamate receptors.

112 locus in the proximity of the gene encoding tyrosine kinase FYN as the most affected region in neuro

113 age display screen against EphA2, a receptor tyrosine kinase highly expressed in a number of solid tu

114 n the catalytic domain of the ERBB2 receptor tyrosine kinase in a patient with schwannomatosis-associ

115 sitizes primary ALL cells to chemotherapy or tyrosine kinase inhibition in vitro and in vivo.

116 The development of the tyrosine kinase inhibitor (TKI) imatinib allows patients

117 risk of molecular recurrence after stopping tyrosine kinase inhibitor (TKI) treatment substantially

118 vivo deletion of alpha6 in combination with tyrosine kinase inhibitor (TKI) treatment was more effec

119 identified that exhibited potent activity in tyrosine kinase inhibitor (TKI)-sensitive and TKI-resist

120 y and safety of ripretinib, a switch-control tyrosine kinase inhibitor active against a broad spectru

121 ng both BCRs and TLR-MyD88 by using Bruton's tyrosine kinase inhibitor and histone deacetylase inhibi

122 o a subset of EGFR-mutant NSCLC to attenuate tyrosine kinase inhibitor delivery to the tumors by limi

123 ta are available, second-line therapy with a tyrosine kinase inhibitor may be recommended for appropr

124 exed and carboplatin chemotherapy to an oral tyrosine kinase inhibitor may improve outcomes.

125 hat differ in their mechanism of action (the tyrosine kinase inhibitor pazopanib in MKN45 gastric car

126 g FLT3 inhibitors, such as the multitargeted tyrosine kinase inhibitor sorafenib, improves outcome af

127 ell lymphoma following prior failed Bruton's tyrosine kinase inhibitor therapy, with an overall respo

128 Ibrutinib is a Bruton tyrosine kinase inhibitor with remarkable efficacy again

129 eks of acalabrutinib, a more specific Bruton tyrosine kinase inhibitor, demonstrating that AF is an o

130 Importantly, we showed that tyrosine kinase inhibitor-resistant tumors, with EGFRT79

131 PFS than those without these mutations after tyrosine kinase inhibitors (2.1 vs 3.7 months, p < 0.001

132 at COVID-19 diagnosis, most commonly Bruton tyrosine kinase inhibitors (BTKi's; n = 68/90 [76%]).

133 Although new generations of EGFR-tyrosine kinase inhibitors (EGFR-TKI) have been develope

134 astatic melanoma using immune checkpoint and tyrosine kinase inhibitors (TKI), the majority of stage

135 ey obstacle to the clinical efficacy of EGFR tyrosine kinase inhibitors (TKI).

136 t with the highly effective CML therapeutics tyrosine kinase inhibitors (TKIs) and interferon-alpha (

137 The development of resistance to EGFR Tyrosine kinase inhibitors (TKIs) in NSCLC with activati

138 Preclinical data suggest that EGFR tyrosine kinase inhibitors (TKIs) plus MET TKIs are a po

139 tcome of most patients with CML treated with tyrosine kinase inhibitors (TKIs), a greater number of c

140 r endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors (TKIs).

141 velop drug resistance when treated with EGFR tyrosine kinase inhibitors (TKIs).

142 eral epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors have been developed and appro

143 le in vitro data of treatment with different tyrosine kinase inhibitors of BT-20 triple-negative brea

144 ications to atezolizumab and/or bevacizumab, tyrosine kinase inhibitors sorafenib or lenvatinib may b

145 The long-term effectiveness of tyrosine kinase inhibitors such as the EGFR inhibitor (E

146 We identified several tyrosine kinase inhibitors that inhibit CAR T-cell cytot

147 The activity of MET tyrosine kinase inhibitors varies by MET alteration cate

148 We further show that the activity of the tyrosine kinase ITK acts as a signaling catalyst that ac

149 fused Gene (TFG) fused to the 3' end of RET tyrosine kinase leading to a TFG-RET fusion which transf

150 aplastic lymphoma kinase (Alk) is a receptor tyrosine kinase of the insulin receptor super-family tha

151 target of rapamycin, DNA repair and receptor tyrosine kinase pathways.

152 control of the endothelial-specific receptor tyrosine kinase promoter Tie2.

153 s study, we demonstrate that the nonreceptor tyrosine kinase Pyk2 phosphorylates tyrosine 131 in the

154 hippocampal neurons using a photoactivatable tyrosine kinase receptor (optoFGFR1).

155 Neurotrophic tyrosine kinase receptor 3 (TrkC) is expressed in podocy

156 In the cerebral cortex, the tyrosine kinase receptor ErbB4 is critical for the wirin

157 ion causes an impaired maturation of several tyrosine kinase receptors (RTKs), consistent with a part

158 its effects on neurons by signalling through tyrosine kinase receptors.

159 Using the tyrosine kinase Src as a model, we demonstrate efficient

160 Here, we demonstrate that the tyrosine kinase Src is activated under DNA damage stress

161 omal recruitment of hepatocyte growth factor tyrosine kinase substrate (HRS), which was necessary for

162 ontains the binding motif for endogenous Src tyrosine kinase that constitutively inhibits I(Kv1.5) Di

163 The expression of Fyn, a tyrosine kinase that phosphorylates hnRNPA2, reduces neu

164 on's tyrosine kinase (BTK) is a non-receptor tyrosine kinase that signals downstream of Fc receptors

165 binds to and activates the transmembrane RET tyrosine kinase to signal through intracellular Akt/Erk

166 er, these results identify ALK as a receptor tyrosine kinase transactivated by D2R that promotes its

167 Endothelial (angiopoietin-1, angiopoietin-2, tyrosine kinase with immunoglobulin-like loop epidermal

168 adapter protein Nck (noncatalytic region of tyrosine kinase) to the CD3e subunit of the TCR.

169 Inhibition of Erk1/2, tyrosine kinase, and/or GSK-3beta was implied to be invo

170 effect was reproduced in mice lacking Bruton tyrosine kinase, but not in mice treated with 4 weeks of

171 ion of a differentiation regulatory receptor tyrosine kinase, downregulates the telomerase RNA compon

172 Reducing levels or function of the tyrosine kinase, ephrin type-A receptor 4 (EphA4), has b

173 d discovered a central role of a nonreceptor tyrosine kinase, spleen tyrosine kinase (SYK), in mediat

174 by activating mutations in the KIT receptor tyrosine kinase, such as the exon 11 KIT V559Delta mutat

175 endothelial growth factor, soluble fms-like tyrosine kinase, von Willebrand factor, E-selectin, inte

176 y hypertension and elevated soluble Fms-Like Tyrosine Kinase-1 (sFlt-1).

177 dothelial (angiopoetin-1/2, soluble fms-like tyrosine kinase-1, soluble vascular cell adhesion molecu

178 we demonstrate a design of a sensor for EGFR tyrosine kinase-an important target in cancer research.

179 geting the tumor-associated antigen receptor tyrosine kinase-like orphan receptor 1 (ROR1) infiltrate

180 cleotide exchange factors (GEFs) or receptor tyrosine kinase-mediated and GEF-dependent RAS activatio

181 he ectopic expression of NPM-ALK, a chimeric tyrosine kinase.

182 -cell acute lymphocytic leukaemia in the pre-tyrosine-kinase inhibitor era.

183 calabrutinib is a selective, covalent Bruton tyrosine-kinase inhibitor with activity in chronic lymph

184 treated with regimens that do not contain a tyrosine-kinase inhibitor, despite the use of high-risk

185 Acalabrutinib is a selective, potent Bruton tyrosine-kinase inhibitor.

186 of (68)Ga-NeoBOMB1 in patients with advanced tyrosine-kinase inhibitors-treated GIST using PET/CT.

187 lass fusions can be targeted successfully by tyrosine-kinase inhibitors.

188 naling with the genetic loss of the receptor tyrosine-kinase-driven terminal signaling patterning in

189 Receptor tyrosine kinases (RTKs) are often overexpressed or mutat

190 Receptor tyrosine kinases (RTKs) are single-pass membrane protein

191 Receptor tyrosine kinases (RTKs) play crucial roles in human heal

192 Receptor tyrosine kinases (RTKs), including the FGF receptor, are

193 Stimulation of plasma membrane receptor tyrosine kinases (RTKs), such as the epidermal growth fa

194 are also reports of ligand bias for receptor tyrosine kinases (RTKs).

195 the activation of Src family of cytoplasmic tyrosine kinases (SFKs) and two SFK substrates-CUB-domai

196 K7 is regulated by HER2, and by the receptor tyrosine kinases activated in response to HER2 inhibitio

197 B (PTP1B)-an important regulator of receptor tyrosine kinases and a therapeutic target for the treatm

198 ER3 signaling via the activation of multiple tyrosine kinases and transcriptional upregulation.

199 e through engagement of alternative receptor tyrosine kinases either through upregulation of FGF3 or

200 resistance, activation of multiple receptor tyrosine kinases is a known critical factor that contrib

201 Janus kinases (JAKs) are non-receptor tyrosine kinases that are essential components of the JA

202 of G protein-coupled receptors and receptor tyrosine kinases through direct interactions with small

203 They negatively regulate signaling from tyrosine kinases to the Ras-MAPK pathway.

204 therapeutic target proteins, including MAO, tyrosine kinases, BACE1, steroid receptors, mGlu5 recept

205 n about how EGFR, or possibly other receptor tyrosine kinases, becomes activated.

206 -malate) targeting against multiple receptor tyrosine kinases, exerts potent antiangiogenesis.

207 iates signaling induced by multiple receptor tyrosine kinases, including signaling by the epidermal g

208 nteractions between VDAC1 and other receptor tyrosine kinases, indicating a novel role for this famil

209 gnaling is proximally mediated by Src family tyrosine kinases, the most abundant being Lyn.

210 anine and human gliomas such as the receptor tyrosine kinases, TP53 and cell-cycle pathways, and IDH1

211 Since GPCRs can transactivate receptor tyrosine kinases, we also examined if D2R stimulation ac

212 routy 1 (SPRY1) is an antagonist of receptor tyrosine kinases.

213 the immunosuppressive TAM family of receptor tyrosine kinases.

214 hey were employed for the determination of l-tyrosine (l-Tyr) in human plasma from tyrosinemia-diagno

215 oyable alternative to detect ROR1+ (receptor tyrosine-like orphan receptor one) cancer cells from the

216 , and facilitates the phosphorylation on two tyrosines located within the interdomain cleft of Galpha

217 The non-protein amino acid meta-Tyrosine (m-Tyr) is produced in cells under conditions o

218 analogue of MACE2 containing 2,6-dimethyl-l-tyrosine (MACE4) showed the best potency and in vivo ant

219 quently used adjuvant, with microcrystalline tyrosine (MCT), monophosphoryl lipid A (MPLA) and calciu

220 Microbiome-associated histidine and tyrosine metabolites were increased in both sexes, while

221 bles regulation of biocatalytic activity for tyrosine nucleophilic attack on phosphorus.

222 Phosphorylation of the inhibitory tyrosine of SFKs was almost completely abolished in DKO

223 nteraction with a negatively charged phospho-tyrosine on the receptor tyrosine kinase EphB2.

224 on 325 nm / emission 410 nm) as indicator of tyrosine oxidation and carbonyl content significantly in

225 The rate constants for tyrosine oxidation decreased by 125-fold with three adde

226 The observed shallow distance dependence for tyrosine oxidation is proposed to originate in part from

227 We identified all of the hormonogenic tyrosine pairs in the structure, and verified them using

228 T-cell protein tyrosine phosphatase (TC-PTP), encoded by Ptpn2, has bee

229 Protein-tyrosine phosphatase 1B (PTP1B) is the canonical enzyme

230 Inflammation activates the protein-tyrosine phosphatase 1B (PTP1B), and this could suppress

231 sruptive optical approach to control protein tyrosine phosphatase 1B (PTP1B)-an important regulator o

232 hibitor of the oncogenic phosphatase protein tyrosine phosphatase 4A3 binds to at least one site on h

233 Receptor-type protein tyrosine phosphatase alpha (RPTPalpha) is an important p

234 e interactions between its N-SH2 and protein-tyrosine phosphatase domains are weakened such that SHP2

235 The hematopoietic-specific protein tyrosine phosphatase nonreceptor type 22 (PTPN22) is enc

236 The novel protein tyrosine phosphatase PTPN14 was identified by mass spect

237 1 deficiency led to reduced levels of active tyrosine phosphatase SHP1, which plays a B cell-intrinsi

238 The protein tyrosine phosphatase SHP2 binds to phosphorylated signal

239 The tyrosine phosphatase SHP2 controls the activity of pivot

240 were available, an inhibitor of the protein tyrosine phosphatase SHP2, a critical mediator of RAS si

241 The protein tyrosine phosphatase SHP2, encoded by PTPN11, is ubiquit

242 Protein tyrosine phosphatase sigma (PTPsigma, PTPRS), a receptor

243 ind to the host cellular nonreceptor protein tyrosine phosphatase type 14 (PTPN14) and direct it for

244 s, we demonstrate a role of receptor protein tyrosine phosphatase zeta (RPTPzeta) in PNN structure.

245 ing that this pseudophosphatase functions in tyrosine phosphorylation by competing with active phosph

246 It blocked STAT1 tyrosine phosphorylation induced either by type I IFN or

247 r time frame and that the MCP-1-induced Pyk2 tyrosine phosphorylation is controlled by the Src family

248 face receptors containing ITAM, ITIM or ITSM tyrosine phosphorylation motifs to the promiscuous cell-

249 resistance and decreased insulin-stimulated tyrosine phosphorylation of insulin receptor beta (IRbet

250 a subset of BCR signaling events, including tyrosine phosphorylation of the kinase SYK, the calcium

251 ition occurs isothermally and is governed by tyrosine phosphorylation on LAT.

252 tes of posttranslational modification (e.g., tyrosine phosphorylation), and participate in nonlinear

253 troTyr post-translational modification, like tyrosine phosphorylation, can impact calmodulin sensitiv

254 tion of p53 transcriptional activity through tyrosine phosphorylation.

255 such as IL-17A and IL-6, and increased STAT3 tyrosine phosphorylation.

256 ubunits are post-translationally modified by tyrosine phosphorylation.

257 validation assays, we show that PD-1 targets tyrosine phosphosites that mediate proximal T cell recep

258 Proton-coupled electron transfer (PCET) from tyrosine produces a neutral tyrosyl radical (Y(*)) that

259 y that mutation in dual serine/threonine and tyrosine protein kinase (dstyk) lead to CS-like vertebra

260 we describe the profiling of a non-receptor tyrosine-protein kinase (TYK2) inhibitor which shows a f

261 cell-cell contacts through the receptor-type tyrosine-protein phosphatases kappa led to acquisition o

262 Tyrosine proximity within TG is thought to enable the co

263 an aryl sulfonyl fluoride electrophile at a tyrosine residue (Tyr-82) inhibits guanine exchange fact

264 Importantly, a tyrosine residue (Y203) is essential for ligand recognit

265 Collectively, these results suggest that the tyrosine residue at position 16 is necessary to constrai

266 we report that phosphorylation of a specific tyrosine residue in STING by the epidermal growth factor

267 ting this point, we observed that one of the tyrosine residues (Y954) located in the C-terminal lobe

268 n the discovery of CD31's 2 intracytoplasmic tyrosine residues called immunoreceptor tyrosine inhibit

269 n phosphorylation of the Igf1R on activating tyrosine residues in podocytes.

270 he direct intracellular dephosphorylation of tyrosine residues on the receptor target.

271 This reaction on tyrosine residues required both the TGF-beta1-dependent

272 sion of this chemistry for the activation of tyrosine residues that project into solution from the N

273 GluN2A harbors tyrosine residues that, when phosphorylated by Src famil

274 y interactions with conserved asparagine and tyrosine residues within the binding pocket.

275 ons of proteins, particularly bromination of tyrosine residues, in peroxidasin-expressing PFHR9 cells

276 es, and acyl adducts with lysine and several tyrosine residues.

277 Here we have established a dimeric tyrosine-rich glycopeptide system for probing the corres

278 e, glycine, proline (PRO), tryptophan (TRP), tyrosine, serine and GABA were quantified by gas-chromat

279 utations in genes in cell cycle and receptor tyrosine signaling pathways.

280 y principles to identify a large fraction of tyrosine sites (~30%) on proteins (~44%) that can be lig

281 ating nucleophilic substitution reactions on tyrosine sites of proteins.

282 Genistein (4',5,7-trihydroxyisoflavone), a tyrosine-specific-protein kinase inhibitor, has been sho

283 man telomerase assays determined a conserved tyrosine steric gate regulates ribonucleotide insertion

284 zyme that shows improved activation for some tyrosine substrates.

285 21 amino acid CIF peptide ligands, which are tyrosine sulfated by the tyrosylprotein sulfotransferase

286 In contrast, tyrosine sulfated versions displayed equivalent neutrali

287 t post-translational modifications including tyrosine sulfation and proline hydroxylation within, and

288 e to Ru(bpy)(3)(3+) and proton transfer from tyrosine to a hydrogen phosphate dianion.

289 the key enzyme ensuring the conversion of l-tyrosine to dopaquinone, thereby initiating melanin synt

290 e change of binding site polarity and that a tyrosine to phenylalanine substitution at a binding site

291 olving intramolecular electron transfer from tyrosine to Ru(bpy)(3)(3+) and proton transfer from tyro

292 Depletion of tyrosine tRNA(GUA) or its translationally regulated targ

293 Tyrosine-tRNA(GUA) depletion impaired translation of gro

294 and Ag nanoparticles were synthesized using tyrosine, tryptophan, isonicotinylhydrazide, epigallocat

295 irects the site of O-arylation at a proximal tyrosine (Tyr) residue.

296 The first amino acid-Fmoc-O-TIPS-beta-tyrosine-was prepared in 78% yield (two steps in one pot

297 nvironment influences the PCET properties of tyrosine, we have studied the radical formation behavior

298 goproline peptides linking Ru(bpy)(3)(2+) to tyrosine were shown to exhibit a substantially shallower

299 We previously reported that tyrosine (Y) 138 of HPV-31 E2 is phosphorylated by the f

300 DYRK1A [dual specificity tyrosine-(Y)-phosphorylation-regulated kinase 1 A] is a