ライフサイエンスコーパス: tyrosine

1 at serves as a factory for the production of tyrosine.

2 The role of tyrosine-1 (Tyr1) remains incompletely understood, as, f

3 ion with a dominant negative CAV1 mutated at tyrosine 14 reduced the interaction.

4 on of AMP activated protein kinase (Ampk) at tyrosine 172 and of unc-51 like autophagy activating kin

5 Tyrosine 18 is both a disease- and nondisease-state modi

6 brain tumor studies using (18)F-fluoro-ethyl-tyrosine ((18)F-FET) (n = 31) and (68)Ga-DOTANOC (n = 7)

7 id transport using O-(2-(18)F-fluoroethyl)-l-tyrosine ((18)F-FET) and proton MR spectroscopy (MRS) im

8 ents using dynamic O-(2-(18)F-fluoroethyl)-l-tyrosine ((18)F-FET) PET.

9 which undergoes conformational changes upon tyrosine-221 phosphorylation by EGFR.

10 ctase and SbCCR1, residues threonine-154 and tyrosine-310 were pinpointed as being involved in bindin

11 Phosphorylation of PTK6 tyrosine 342 (PY342) promotes activation, while phosphor

12 Its binding to mRNA is regulated by tyrosine 396 phosphorylation, and this particular modifi

13 romotes activation, while phosphorylation of tyrosine 447 (PY447) regulates auto-inhibition.

14 These observations demonstrate that tyrosine 470 and 88 are critical for allosteric modulato

15 phosphorylation of cytochrome c by replacing tyrosine 48 with p-carboxy-methyl-l-phenylalanine (pCMF)

16 tochrome c phosphorylation-in particular, at tyrosine 48-is a key modulator of mitochondrial signalin

17 he most commonly mutated amino acid residue, tyrosine 537, in the estrogen-responsive MCF7 breast can

18 of human Hsp90alpha at the highly conserved tyrosine 627 has previously been reported to reduce clie

19 Site-directed mutagenesis indicates that tyrosine 645 in this loop has an important role in the s

20 We discovered tyrosine 78 of Atoh1 is phosphorylated by a Jak2-mediate

21 Phosphorylation of tyrosine 78 stabilizes Atoh1, increases Atoh1's transcri

22 at is controlled by a key residue in DENND3, tyrosine 940.

23 e preseasonal short-course booster AIT using tyrosine-absorbed grass pollen allergoids containing the

24 ure was monitored via the anodic reaction of tyrosine and tryptophan residues.

25 d the shikimate-derived aromatic amino acids tyrosine and tryptophan.

26 Wistar rats were treated with alpha-methyl-L-tyrosine and tyrosol.

27 d from the decarboxylation of the amino acid tyrosine, and is therefore present at important concentr

28 leucine, methionine, lysine, phenylalanine, tyrosine, and tryptophan.

29 To determine how many and which tyrosines are required to enable EGF receptor-mediated s

30 matory bleeding through (hem) immunoreceptor tyrosine-based activation motif-dependent mechanisms irr

31 er identified the membrane-proximal internal tyrosine-based sorting motif YXXL as a determinant that

32 Substitution of glutamic acid for tyrosine between the Syk SH2 domains (Syk-Y130E) led to

33 sidues, and successive substitution of these tyrosines breaks the interaction between ShcD and Grb2,

34 ese were identified as L-phenylalanine and L-tyrosine but it may be that metabolically-related compou

35 The identity of the tubulin tyrosine carboxypeptidase (TCP) responsible for detyrosi

36 residues and the bound l-phenylalanine and l-tyrosine, conferring the deamination reaction through ei

37 used by a variety of peptides, in particular tyrosine-containing peptides.

38 Betalains are tyrosine-derived red-violet and yellow plant pigments kn

39 I intermediate to the reactive deprotonated tyrosine, forming Tyr(*).

40 ode the enzymes dopa decarboxylase (Ddc) and tyrosine hydroxylase (ple).

41 pha), specific to pain-sensing C-fibers, and tyrosine hydroxylase (Th), specific to low-threshold mec

42 he diagnosis of PD and demonstrated >300,000 tyrosine hydroxylase (TH)-positive grafted cells per sid

43 s, including reductions in the expression of tyrosine hydroxylase and catechol-O-methyltransferase (C

44 f D2S but not D2L prevents the inhibition of tyrosine hydroxylase phosphorylation and, thereby, of do

45 m neurons expressing Per2 and Per3 and their tyrosine hydroxylase phosphorylation is regulated in a c

46 tered mRNA expression of dopamine receptors, tyrosine hydroxylase, and dopamine transporter genes in

47 nt did not alter Fos-immunoreactivity within tyrosine hydroxylase-immunolabeled neurons of VTA, but d

48 Dopamine- and tyrosine hydroxylase-immunopositive cells (TH cells) mod

49 sphorylation of the autophosphorylation site tyrosine in the SRC family kinase (SFK) FYN as well as T

50 ies of EGF receptors that contained only one tyrosine in their C-terminal tail.

51 ropriate level of protein phosphorylation on tyrosine is essential for cells to react to extracellula

52 ely correlated with susceptibility to Bruton tyrosine kinase (BTK) and SYK inhibitors in MCL.

53 Ibrutinib, a Bruton tyrosine kinase (BTK) inhibitor approved for the treatme

54 Ibrutinib, a Bruton's tyrosine kinase (BTK) inhibitor, targets BCR signaling a

55 Bruton tyrosine kinase (BTK) is a key enzyme in B-cell developm

56 Recent data suggest that Bruton's tyrosine kinase (BTK) is an emerging therapeutic target

57 Ibrutinib, an oral inhibitor of Bruton's tyrosine kinase (BTK), at a once-daily dose of 420 mg ac

58 significance of KIT proto-oncogene receptor tyrosine kinase (KIT) and platelet-derived growth factor

59 aplastic lymphoma kinase (Alk) and leucocyte tyrosine kinase (Ltk) were identified as "orphan" recept

60 the macrophage efferocytosis receptor c-Mer tyrosine kinase (MerTK) reduces efferocytosis and promot

61 y mediating degradation of Torso, a receptor tyrosine kinase (RTK) and major determinant of somatic c

62 The receptor tyrosine kinase (RTK) AXL has been intrinsically linked

63 We report several receptor tyrosine kinase (RTK) ligands increase RhoA-guanosine tr

64 road implications for understanding receptor tyrosine kinase (RTK) signaling specificity.

65 Inhibitors that target the receptor tyrosine kinase (RTK)/Ras/mitogen-activated protein kina

66 Spleen tyrosine kinase (Syk) is an intracellular nonreceptor ty

67 Here we show that spleen tyrosine kinase (SYK) is upregulated during brown adipoc

68 osinylation and specifically recruits spleen tyrosine kinase (Syk), initiating cellular activation.

69 igen receptor (BCR)-proximal effector spleen tyrosine kinase (SYK), which we identified as an HSP90 c

70 ins that interact with neurotrophic receptor tyrosine kinase 1, a receptor also known as TrkA that up

71 In a mouse model of basal ErbB2 receptor tyrosine kinase 2 (ErbB2)-positive breast cancer (ErbB2(

72 xis, connecting genetic aberrations in FLT3, tyrosine kinase 2 (TYK2), platelet-derived growth factor

73 Context ERBB2 (erb-b2 receptor tyrosine kinase 2 or HER2) is currently the only biomark

74 Inhibition of proline-rich tyrosine kinase 2 restores insulin-induced and shear str

75 Erb-B2 receptor tyrosine kinase 4 (ErbB4) is a kinase that can signal vi

76 or release, as well as Lyn kinase and spleen tyrosine kinase activation and signaling through mechani

77 Src tyrosine kinase activity and tyrosine phosphorylation of

78 Cediranib (AZD2171) is a potent inhibitor of tyrosine kinase activity associated with vascular endoth

79 Genetic or pharmacologic inhibition of EGFR tyrosine kinase activity or downstream MEK activity atte

80 Furthermore, this study reveals key tyrosine kinase and DNA methylation pathways in liposarc

81 un N-terminal kinase (JNK), the Axl receptor tyrosine kinase and extracellular signal-regulated kinas

82 otein that is required for activation of SRC tyrosine kinase and simultaneously coordinates the atten

83 ve ligand-induced dimerization of a receptor tyrosine kinase at the cell surface and directly measure

84 Importantly, we discover that receptor tyrosine kinase AXL is a transcriptional target of BCL6

85 oncogene activates the cellular nonreceptor tyrosine kinase c-Src and recruits the Hippo pathway eff

86 ctive oxygen species, thus preventing spleen tyrosine kinase dephosphorylation and perpetuating MC si

87 type of FLT3 mutation: point mutation in the tyrosine kinase domain (TKD) or internal tandem duplicat

88 at WHSC1L1 mono-methylates lysine 721 in the tyrosine kinase domain of EGFR, and that this methylatio

89 ceptor while retaining the transmembrane and tyrosine kinase domains.

90 nectin type III (FN3) domain of the receptor tyrosine kinase EphB2.

91 The receptor tyrosine kinase ephrin type-A receptor 2 (EphA2) was ide

92 gesterone receptors, along with the receptor tyrosine kinase ERB2 (HER2), that define most mammary ca

93 Spleen tyrosine kinase expression was found in human and murine

94 one of the most recently identified receptor tyrosine kinase families.

95 The receptor tyrosine kinase family consisting of Tyro3, Axl, and Mer

96 Tie1 and Tie2, members of the tyrosine kinase family with immunoglobulin and EGF homol

97 ene (MAN2A1) and the last 6 exons in the FER tyrosine kinase gene (FER), called MAN2A1-FER.

98 ers tumor cells more susceptible to receptor tyrosine kinase inhibition in a preclinical glioblastoma

99 ents at diagnosis and following conventional tyrosine kinase inhibitor (TKI) treatment.

100 Combined treatment with an EGFR tyrosine kinase inhibitor and Akt inhibitor causes apopt

101 al metastases who had never received an EGFR tyrosine kinase inhibitor and patients with leptomeninge

102 of EGFR, HER2, and HER3 signalling with the tyrosine kinase inhibitor AZD8931 will control growth of

103 The epidermal growth factor receptor tyrosine kinase inhibitor erlotinib in combination with

104 The tyrosine kinase inhibitor erlotinib poorly penetrates th

105 and safety with that of the reversible EGFR tyrosine kinase inhibitor gefitinib in the first-line tr

106 er substantiated by the rescue effect of the tyrosine kinase inhibitor genistein, and the more specif

107 limumab in combination, and nivolumab plus a tyrosine kinase inhibitor in metastatic renal cell carci

108 Vandetanib is a novel tyrosine kinase inhibitor of VEGFR2, RET, and EGFR, all

109 S metastases who had either never received a tyrosine kinase inhibitor or who had been pretreated wit

110 had progressed after treatment with an EGFR tyrosine kinase inhibitor received AZD3759 at 50 mg, 100

111 The diversity and unpredictability of EGFR tyrosine kinase inhibitor resistance mechanisms presents

112 tually all patients succumb to acquired EGFR tyrosine kinase inhibitor resistance that occurs via div

113 r developing new treatments to overcome EGFR tyrosine kinase inhibitor resistance.

114 odel of mBC resistance to the antiangiogenic tyrosine kinase inhibitor sunitinib.

115 ls at CML diagnosis on molecular response to tyrosine kinase inhibitor therapy in early chronic-phase

116 first-line epidermal growth factor receptor tyrosine kinase inhibitor therapy, and T790M mutation, o

117 nergistic growth inhibition in multiple EGFR tyrosine kinase inhibitor-resistant non-small-cell lung

118 despite treatment with ibrutinib, a Bruton's tyrosine kinase inhibitor.

119 activity of oral BGJ398, a selective FGFR1-3 tyrosine kinase inhibitor.

120 inhibitor or who had been pretreated with a tyrosine kinase inhibitor.

121 astases who had been pretreated with an EGFR tyrosine kinase inhibitor.

122 The BCR-ABL specific tyrosine kinase inhibitors (TKI) changed the outcome of

123 Mutant-selective EGFR tyrosine kinase inhibitors (TKI), such as osimertinib, a

124 tumor cells sensitive to treatment with EGFR tyrosine kinase inhibitors (TKI).

125 and epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) are treatment options

126 Tyrosine kinase inhibitors (TKIs) are used in the clinic

127 Tyrosine kinase inhibitors (TKIs) of the EGF receptor (E

128 c myeloid leukemia (CP-CML) are treated with tyrosine kinase inhibitors (TKIs).

129 hocytic leukemia/lymphoma 2 (BCL2), and many tyrosine kinase inhibitors (TKIs).

130 on of skin toxicity in patients treated with tyrosine kinase inhibitors at levels not detectable via

131 Trials comparing the addition of tyrosine kinase inhibitors to conventional therapy are r

132 Bruton tyrosine kinase inhibitors were active in progressive CL

133 l glioma mouse model, we assessed a panel of tyrosine kinase inhibitors with different selectivity pr

134 Epidermal growth factor receptor tyrosine kinase inhibitors, including gefitinib, erlotin

135 ion of novel targets for two clinically used tyrosine kinase inhibitors, nilotinib and osimertinib.

136 ure, with the emergence of clinically useful tyrosine kinase inhibitors.

137 utic considerations, including new and novel tyrosine kinase inhibitors.

138 Bruton tyrosine kinase is a clinically validated target in mant

139 The Tec tyrosine kinase is expressed in many cell types, includi

140 cription 5 (STAT5s) are crucial effectors of tyrosine kinase oncogenes in myeloid leukemias.

141 We show that the tyrosine kinase PTK6 (BRK) is a PTEN substrate.

142 l of CD1c(+) DC activation via regulation of tyrosine kinase receptor AXL, an important inhibitory DC

143 The tyrosine kinase receptor EGFR is expressed in Schwann ce

144 nteracts with the calcium pump PMCA2 and the tyrosine kinase receptor ErbB2/HER2 in normal mammary ep

145 ants of Neuregulin 1 (NRG1) and its neuronal tyrosine kinase receptor ErbB4 are associated with risk

146 growth factor receptor alpha (PDGFRalpha), a tyrosine kinase receptor, is up-regulated in hepatic ste

147 y of growth factors that are ligands for the tyrosine kinase receptor, Tie2.

148 ion prevalence in the ephrin (EPH) family of tyrosine kinase receptors was 10-fold higher in primary

149 The ErbB/HER family comprises four distinct tyrosine kinase receptors, EGFR/ErbB1/HER1, ErbB2/HER2,

150 Stabilization was independent of tyrosine kinase signaling and the actin cytoskeleton, su

151 The Abl tyrosine kinase signaling network controls cell migratio

152 ses CBL and CBL-B are negative regulators of tyrosine kinase signaling with established roles in the

153 ssible role for regulation of RNA binding by tyrosine kinase signaling.

154 ne, while hepatocyte growth factor-regulated tyrosine kinase substrate as the top negative correlated

155 lation of hepatocyte growth factor-regulated tyrosine kinase substrate, were further confirmed in liv

156 lived positive signals driven by the protein tyrosine kinase Syk; slow, long-lived negative signals d

157 t-derived growth factor receptor, a receptor tyrosine kinase) and H-Ras generates strong, synergistic

158 via the SFK (Src family kinase)-Syk (spleen tyrosine kinase)-PLCgamma2 (phospholipase Cgamma2) pathw

159 athophysiological roles for the MET receptor tyrosine kinase, a multifunctional receptor that mediate

160 The tyrosine kinase, c-Src, participates in mu opioid recept

161 In the mammalian brain the ubiquitous tyrosine kinase, C-Src, undergoes splicing to insert sho

162 The two isoforms of the Bcr-Abl tyrosine kinase, p210 and p190, are associated with diff

163 on in a manner that is dependent on Bruton's tyrosine kinase, p38 MAPK, and TANK-binding kinase 1 (TB

164 monstrated by the individual use of Bruton's tyrosine kinase, p38 MAPK, and TBK1 inhibitors.

165 eviously that Janus kinase 3, a non-receptor tyrosine kinase, plays a crucial role in AJ formation th

166 mutations that activate receptor-associated tyrosine kinase, vascular endothelial growth factor, and

167 kinase (Syk) is an intracellular nonreceptor tyrosine kinase, which has been implicated as central im

168 main (ICD) in addition to classical receptor tyrosine kinase-activated signaling cascades.

169 ld-type RAS amplification increases receptor tyrosine kinase-dependent activation of RAS more potentl

170 ies reveal an adaptive feedback mechanism in tyrosine kinase-driven cancers associated with reactivat

171 y specifically destroying the Torso Receptor Tyrosine Kinase.

172 lpha1) and signals through activation of RET tyrosine kinase.

173 ating alterations in members of the receptor tyrosine kinase/Ras/Raf pathway including EGFR and KRAS

174 rm of MerTK (myeloid-epithelial-reproductive tyrosine kinase; ie, soluble MER), a critical biomarker

175 ansplantation vs long-term administration of tyrosine-kinase inhibitors) as well as on MRD testing.

176 discovery that work in concert with protein tyrosine kinases (PTK) in controlling cellular homeostas

177 Receptor tyrosine kinases (RTK) are major regulators of key biolo

178 ns leading to oncogenic variants of receptor tyrosine kinases (RTKs) are frequent events during tumor

179 of small organic molecules against receptor tyrosine kinases (RTKs) has been shown to be a valuable

180 one of the most commonly amplified receptor tyrosine kinases (RTKs) in glioblastoma (GBM).

181 e (Ltk) were identified as "orphan" receptor tyrosine kinases (RTKs) with oncogenic potential.

182 tors comprise the largest family of receptor tyrosine kinases (RTKs), with fourteen receptors divided

183 ANCE STATEMENT The Src family of nonreceptor tyrosine kinases acts in signaling pathways that regulat

184 Mutant receptor tyrosine kinases are mislocalized in the endoplasmic ret

185 One of these receptor tyrosine kinases could be MET, the receptor for hepatocy

186 bulin and EGF homology domains, are receptor tyrosine kinases found primarily in endothelial cells wi

187 The key role of tyrosine kinases in this process is further substantiate

188 mitant targeting of EGFR and the nonreceptor tyrosine kinases PYK2/FAK synergistically inhibits the p

189 f cell-surface receptors and Abl nonreceptor tyrosine kinases that participate in actin cytoskeleton

190 any G protein-coupled receptors and receptor tyrosine kinases, activate phospholipase C (PLC) isozyme

191 gulator of not only GPCRs, but also receptor tyrosine kinases, including the highly cancer relevant i

192 otein phosphatase 2A (PP2A), YAP, Src family tyrosine kinases, Shc, phosphatidylinositol 3-kinase (PI

193 to the well-studied ErbB family of receptor tyrosine kinases.

194 sion wavelength (em: 302-313 nm) peak of the tyrosine-like component occurred in the reserved sanitar

195 These tyrosine-like components were gradually evacuated in the

196 anges of the fluorescence indexes related to tyrosine-like substances were well correlated with the c

197 activity to be used for the treatment of the tyrosine metabolism-related diseases.

198 riphenylene) by hydroquinone (H2Q), N-acetyl-tyrosine (N-Ac-Tyr) or guanosine-5'-monophosphate (GMP)

199 Installation of the radical trap 3-amino tyrosine (NH2Y) by amber codon suppression at positions

200 ve reaction monitoring were used to quantify tyrosine nitration of in vivo samples and when hemopexin

201 ptide (CGRP), substance P (SP), neuropeptide tyrosine (NPY), and the nitric oxide synthesizing enzyme

202 ed extracellular phosphorylation of a single tyrosine (p*Y504) in a highly conserved region of the fi

203 te antigen-related (Lar), a receptor protein tyrosine phosphatase (RPTP) and the only known Drosophil

204 essive activity of striatal-enriched protein tyrosine phosphatase (STEP) in the brain has been detect

205 Here, we have identified T cell protein tyrosine phosphatase (TC-PTP), also known as PTPN2, as a

206 The T-cell protein tyrosine phosphatase (TCPTP) pathway consists of signali

207 EC and its phosphatases, EC-specific protein tyrosine phosphatase (VE-PTP) and Src homology phosphata

208 ding claudin-5, vascular endothelial-protein tyrosine phosphatase (VE-PTP), and von Willebrand factor

209 m of Src homology region 2 domain-containing tyrosine phosphatase 1 (SHP-1) along with the T. cruzi T

210 ransport into hepatocytes to inhibit protein-tyrosine phosphatase 1B (PTP1B) activity, which acts to

211 ermeability via vascular endothelial-protein tyrosine phosphatase inhibition limits mycobacterial gro

212 The protein tyrosine phosphatase nonreceptor type 12 (PTPN12) is a m

213 a tumor suppressor function for the protein tyrosine phosphatase PTP1B in myeloid lineage cells, wit

214 The plasma membrane-associated tyrosine phosphatase PTPRO is frequently transcriptional

215 als by signaling through presynaptic protein tyrosine phosphatase receptor delta.

216 nventional T cell proliferation in vitro via tyrosine phosphatase SHP-1-dependent uncoupling of IL-2R

217 ctly regulated the catalytic activity of the tyrosine phosphatase SHP-1.

218 in prior panel testing: a pathogenic protein tyrosine phosphatase, non-receptor type 11 (PTPN11) vari

219 wo catalytically inactive mutants of protein-tyrosine phosphatase-like myo-inositol phosphatases (PTP

220 n ubiquitously expressed cytoplasmic protein tyrosine phosphatase.

221 Protein tyrosine phosphatases (PTP) are exciting and novel targe

222 ribute to proper signal transduction.Protein-tyrosine phosphatases (PTPs) are thought to be major tar

223 involves reversible inactivation of protein tyrosine phosphatases (PTPs) through the oxidation and r

224 er (PRLs), the most oncogenic of all protein-tyrosine phosphatases (PTPs), play a critical role in me

225 Classical protein-tyrosine phosphatases can exhibit substrate specificity

226 Protein tyrosine phosphatases have received little attention in

227 itory receptor with the potential to mediate tyrosine phosphatases SHP-1/-2 dependent signaling.

228 the Src homology 2 domain-containing protein-tyrosine phosphatases Shp1 and Shp2, knockout and transg

229 ity of the receptor and non-receptor protein-tyrosine phosphatases that down-regulate Met phosphoryla

230 Bis-o-nitrobenzyl protection of tyrosine phosphate enabled its incorporation into DHFR a

231 Accordingly, SOS1, ARHGEF1, and DOCK2 are tyrosine phosphorylated upon chemokine signaling with ti

232 e phosphatase fold that unexpectedly targets tyrosine-phosphorylated peptides.

233 Cool-associated tyrosine-phosphorylated protein 1 (Cat-1) is a signaling

234 authors demonstrate iSNAP, a tool to detect tyrosine phosphorylation and activate desired protein en

235 130Cas targeting to FAs is essential for its tyrosine phosphorylation and downstream signaling.

236 ximal IGF-1R signaling events, including IRS tyrosine phosphorylation and recruitment of PI3K, are no

237 ects of SH2 domain overexpression on protein tyrosine phosphorylation by quantitative Western and far

238 hat IRF4 is activated through c-Src-mediated tyrosine phosphorylation in virus-transformed cells.

239 Tyrosine phosphorylation is a vital mechanism that contr

240 Reversible tyrosine phosphorylation is a widespread post-translatio

241 Blocking the tyrosine phosphorylation of C-Raf with Src family inhibi

242 endothelial function, mediated by increased tyrosine phosphorylation of eNOS and excess Nox2-derived

243 Over-expression of VHR decreased tyrosine phosphorylation of FAK and decreasing VHR promo

244 diated activation of TrkB- and TrkB-mediated tyrosine phosphorylation of NMDA receptors.

245 nd time-dependent manner that coincides with tyrosine phosphorylation of STAT5.

246 d barrier function and excessive Src-related tyrosine phosphorylation of the adherens junction protei

247 Src tyrosine kinase activity and tyrosine phosphorylation of VE-cadherin were increased i

248 Src activity and tyrosine phosphorylation of VE-cadherin were increased i

249 of keratin primary amino acid sequences, and tyrosine phosphorylation predictions, extracted from pub

250 Second, we found conservation of tyrosine phosphorylation within the RNP1 and RNP2 consen

251 significant, dose-dependent increase in EGFR tyrosine phosphorylation, particularly of sites correspo

252 cts in HEK 293T cells and observed increased tyrosine phosphorylation, suggesting increased ABL1 kina

253 and SYK-dependent counterregulation of MyD88 tyrosine phosphorylation, we have demonstrated that the

254 2) phosphatase, which in turn regulates ShcD tyrosine phosphorylation.

255 f CLEC-2 signaling, i.e. the CLEC-2 receptor tyrosine phosphorylation.

256 ugh endocytosis and degradation triggered by tyrosine phosphorylation.

257 ation of FAK and decreasing VHR promoted FAK tyrosine phosphorylation.

258 nsertion in DSTYK (dual serine-threonine and tyrosine protein kinase) in all four affected family mem

259 We show that Abelson tyrosine-protein kinase 2 (Abl2) has a key role in regul

260 Initial sorting is based on tyrosine-protein kinase Kit (c-Kit) expression that enri

261 In both contests, we employed the tyrosine-protein kinase Yes as an example target protein

262 the side chain structures of phosphorylated tyrosine (pY) are partitioned into two conserved conform

263 (involved in cell cycle control) and NTRK3 (tyrosine receptor kinase that undergoes rearrangement in

264 irected mutagenesis of RCAR1 showed that its tyrosine residue is critical for AHG1 interaction and re

265 We show that EgtB contains a conserved tyrosine residue that reacts via proton-coupled electron

266 mo phosphorylation on a conserved C-terminal tyrosine residue.

267 involving this carboxylate and the following tyrosine residue.

268 regulated by the phosphorylation of a single tyrosine residue.

269 nal covalent oxidative modifications on four tyrosine residues and one tryptophan residue of hemopexi

270 orylate extracellular serine, threonine, and tyrosine residues of numerous proteins have been identif

271 I1 compared to wild-type FLI1 and depends on tyrosine residues that are necessary for phase transitio

272 nt mutagenesis of the PTB domain and the CH1 tyrosine residues, and successive substitution of these

273 mon pathway to sulfate CCR5 on extracellular tyrosine residues, facilitating CCR5 recognition by the

274 in, where Jak3 directly phosphorylated three tyrosine residues, viz.

275 ia an NPP7-specific aromatic box composed of tyrosine residues.

276 Importantly, three of the four modified tyrosines, some of which have more than one modification

277 are enzymes that catalyze post-translational tyrosine sulfation of proteins.

278 llen-expressed P. rhoeas threonine-aspartate-tyrosine (TDY) MAPK, PrMPK9-1 Rather few data relating t

279 A tyrosine that hydrogen bonds to propionate 2 in a positi

280 wo principal components (PC1-tryptophan, PC2-tyrosine) that captured significant variance in the fluo

281 ndent 4-HPAA synthase that directly converts tyrosine to 4-HPAA.

282 ylation and deamination enzymatic steps from tyrosine to the key intermediate 4-hydroxyphenylacetalde

283 h to quantify the contribution of individual tyrosines to cation binding using the HP1 chromodomain a

284 asmic tail region of M2, and in particular a tyrosine-to-alanine mutation at residue 76 (Y76A), were

285 from the reaction between peroxynitrite and tyrosine (Try).

286 the formation of 3-Nitrotyrosine (3-NT) from Tyrosine (Tyr) by adding a nitro group (-NO2) with nitra

287 oxidative decarboxylation of the C-terminal tyrosine (Tyr-30) on the mycofactocin precursor peptide

288 glucagon-like peptide 1 (GLP-1), and peptide tyrosine tyrosine (PYY)] were measured, and ad libitum e

289 yrate, 3-hydroxybutyrate/3-aminoisobutyrate, tyrosine, valine and 3-hydroxyisovalerate exhibited the

290 arginine, leucine/isoleucine, phenylalanine, tyrosine, valine and proline significantly associated wi

291 luorescent non-canonical amino acid coumarin-tyrosine was genetically encoded at Y671, a residue prox

292 period and lower activity were measured when tyrosine was located in the middle of the peptide chain.

293 e since exposition of hydrophobic amino acid tyrosine was modified.

294 Key ingredients (tryptophan and tyrosine) were shown not to affect their total concentra

295 by phosphorylation of a threonine (T) and a tyrosine (Y) in its activation loop.

296 phosphorylation event involving a conserved tyrosine (Y) in the bovine papillomavirus 1 (BPV-1) E2 p

297 We demonstrate that two tyrosines (Y24 and Y48) bind to a Kme3-histone tail pept

298 e, we show by site-directed mutagenesis that tyrosine (Y382-384) within the P2X7R C-terminus is diffe

299 II isoforms and by a conserved non-catalytic tyrosine, Y640 in topo IIalpha and Y656 in topo IIbeta.

300 Redox-active tyrosines (Ys) play essential roles in enzymes involved