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1 varphi is a hydrophobic amino acid and pY is phosphotyrosine).
2 cific for phosphoserine, phosphothreonine or phosphotyrosine.
3 to bind phosphorylated substrates including phosphotyrosine.
4 ractions beyond the classical recognition of phosphotyrosine.
5 signaling interactions beyond recognition of phosphotyrosine.
6 s analyzed using specific antibodies against phosphotyrosine.
7 und peptides containing phosphothreonine and phosphotyrosine.
8 a BV-tag-labeled monoclonal antibody against phosphotyrosine.
9 tual amino acid sequence and position of the phosphotyrosines.
10 "knocked-in" EpoR mutant lacking cytoplasmic phosphotyrosines.
11 ated with the unusual SH2 recognition of two phosphotyrosines.
12 hifts in the spectroscopic identification of phosphotyrosines.
14 osphotyrosine 1003 or indirectly via Grb2 to phosphotyrosine 1356 in the multisubstrate binding domai
17 mortem samples, there was an accumulation of phosphotyrosine 39 alpha-synuclein in brain tissues and
20 ne 416 (stimulatory site) and down-regulated phosphotyrosine 527 (inhibitory site) in retinal cells,
21 Transgenic osteoclasts showed a lower c-Src phosphotyrosine 527 level, greater c-Src kinase activity
27 re, we investigated the possibility that the phosphotyrosine adaptor protein ShcA regulates nephrin t
28 bstitute tyrosine 104 with chemically stable phosphotyrosine analogue (p-Carboxymethyl-L-phenylalanin
29 alidation of the predicted sites using a pan-phosphotyrosine and a site-specific antibody, which we g
30 an increase in PI3K enzyme activity in anti-phosphotyrosine and anti-IGF-1R immunoprecipitates of RO
32 to the synapse, suppressing accumulation of phosphotyrosine and myosin without affecting F-actin.
34 that cis-interactions between the C-terminal phosphotyrosines and SH2 domain within the protein tyros
35 iched in TCR, protein kinase C-theta, ZAP70, phosphotyrosine, and HS1), forming what we term a podo-s
36 blots were performed for MKP-1, phospho-JNK, phosphotyrosine, and protein kinase Cdelta (PKCdelta).
37 binding partner, suggesting that Nck couples phosphotyrosine- and phosphoinositide-dependent signals.
38 gets and represents a key connection linking phosphotyrosine- and phosphoserine/threonine-mediated on
41 ith EGFR antibody followed by detection with phosphotyrosine antibody revealed that erlotinib effecti
42 is of mouse oocytes and zygotes with an anti-phosphotyrosine antibody revealed that fertilization sti
45 suggest a model in which dynamic changes in phosphotyrosine-based signaling confer plasticity to the
49 , we define a novel mechanism where the CCM2 phosphotyrosine binding (PTB) domain binds the ubiquitin
50 ion of KRIT1 and CCM2 and find that the CCM2 phosphotyrosine binding (PTB) domain displays a preferen
51 cellular experiments now show that the Mint1 phosphotyrosine binding (PTB) domain that binds to APP i
53 rtually every human Src homology 2 (SH2) and phosphotyrosine binding (PTB) domain, as well as microar
55 protein containing pleckstrin homology (PH), phosphotyrosine binding (PTB), and leucine zipper motifs
59 otein containing pleckstrin homology domain, phosphotyrosine binding domain and leucine zipper motif)
60 uncation mutant consisting of the N-terminal phosphotyrosine binding domain blocks PP1-Axin interacti
61 erface with MDM2, only one region within the phosphotyrosine binding domain of NUMB (amino acids 113-
63 eta phosphorylation site also located in the phosphotyrosine binding domain, threonine 206, had no ph
64 g of proteins that contain Src homology 2 or phosphotyrosine binding domains and whether mechanisms i
65 e to investigate the effect of disruption of phosphotyrosine binding of the N-terminal SH2 domain of
66 eport the discovery of malonate bound in the phosphotyrosine binding pocket of the apo-Grb7-SH2 struc
67 analogues were designed on the basis of the phosphotyrosine binding pocket of the Src SH2 domain and
69 to design inhibitors blocking its SH2 domain phosphotyrosine binding site that is responsible for bot
70 s between the two SH2 domains distant to the phosphotyrosine binding sites, Syk dissociates from the
72 59249, p.Arg125Trp) in the N-terminal TBC1D1 phosphotyrosine-binding (PTB) domain has shown a replica
73 sent the detailed structural analysis of Shc phosphotyrosine-binding (PTB) domain in complex with the
74 step in this process involves interaction of phosphotyrosine-binding (PTB) domain in the N-terminal h
75 rystal structure at 1.37-A resolution of the phosphotyrosine-binding (PTB) domain of ARH in complex w
76 These characteristics are conserved in the phosphotyrosine-binding (PTB) domain of beta-amyloid pre
78 mprises a pleckstrin-homology (PH) domain, a phosphotyrosine-binding (PTB) domain, and C-terminal sit
79 ontaining a pleckstrin-homology (PH) domain, phosphotyrosine-binding (PTB) domain, and leucine zipper
80 ontaining a pleckstrin homology (PH) domain, phosphotyrosine-binding (PTB) domain, and leucine zipper
86 ay of interactions that likely includes both phosphotyrosine-binding and SH3-domain-containing protei
87 Tyr(313)-phosphorylated hinge region and its phosphotyrosine-binding C2 domain that controls PKCdelta
88 variants that differ in the length of their phosphotyrosine-binding domain (PTB) and proline-rich re
89 tor-like protein that contains an N-terminal phosphotyrosine-binding domain and a C-terminal Src homo
90 if is predicted to bind directly to the Numb phosphotyrosine-binding domain and is critical for Numb
91 cterize such interaction networks within the phosphotyrosine-binding domain of insulin receptor subst
94 n containing a pleckstrin-homology domain, a phosphotyrosine-binding domain, and a leucine zipper mot
95 ant, inactive IRS-1 protein (deletion of the phosphotyrosine-binding domain, PTB) and does not requir
100 Unlike the monomeric nature of the SH2 and phosphotyrosine-binding domains, the architecture of the
105 hat, in the nematode Caenorhabditis elegans, phosphotyrosine-binding pseudo-phosphatases are key regu
106 mology 2 (SH2) and kinase domains and to the phosphotyrosine-binding site of the SH2 domain, respecti
107 KCtheta and specifically required a putative phosphotyrosine-binding site within its N-terminal C2 do
108 Through 7 phosphoinositide 3-kinase (PI3K) phosphotyrosine-binding sites, ErbB3 is able to recruit
109 ture/function approach, we now show that the phosphotyrosine-binding, but not the Src homology 2, dom
110 ich involves a transesterification to form a phosphotyrosine bond within the RepD active site, is clo
114 y 2 (SH2) domain-containing proteins and the phosphotyrosine-containing counterparts play significant
116 cking methods to identify phosphoserine- and phosphotyrosine-containing peptides as possible substrat
117 ng the nSH2-helical domain contact caused by phosphotyrosine-containing peptides binding to the enzym
118 hat the Vav2 SH2 domain binds selectively to phosphotyrosine-containing peptides corresponding to cor
119 ime-resolved luminescence of Tb(3+)-chelated phosphotyrosine-containing peptides, which facilitated e
121 inase inhibitor, K-252a, and purification of phosphotyrosine-containing proteins allowed for definiti
122 ings demonstrate that FAK depletion switches phosphotyrosine-containing proteins from focal adhesions
123 se families, stimulate the ubiquitination of phosphotyrosine-containing proteins, including receptor
125 rexpression in HEK293 cells increases global phosphotyrosine content, promotes anchorage-independent
126 ession levels, probe signal is linked to the phosphotyrosine-correlated activation state of the ERBB2
127 ing and dissociation of effectors containing phosphotyrosine-dependent binding modules such as Src ho
128 , it binds SHP-1 and SHP-2 phosphatases in a phosphotyrosine-dependent manner, facilitating their rec
129 cal importance, how vascular cells integrate phosphotyrosine-dependent signaling to elicit cytoskelet
131 structure and dynamics of complexes of three phosphotyrosine-derived peptides with the Src SH2 domain
132 rowth factor, there are only two established phosphotyrosine-docking sites (Tyr-490 and Tyr-785 on Tr
133 or tyrosine kinases generally act by forming phosphotyrosine-docking sites on their own endodomains t
135 we combine this approach with immunoaffinity phosphotyrosine enrichment, enabling the identification
137 e ShK-170 (ShK-L5), containing an N-terminal phosphotyrosine extension of the Stichodactyla helianthu
138 l-cysteine-l-phenylalanine, or l-cysteine-l-phosphotyrosine formed on crystallographically textured
139 osine (160-fold), sulfotyrosine (3600-fold), phosphotyrosine (>8000-fold), and phosphoserine (>8000-f
141 ures is comparable to the specificity of the phosphotyrosine immonium ion for phosphotyrosine peptide
142 s, the characteristic 16O1- and 18O1-labeled phosphotyrosine immonium ions at m/z 216.043 and 218.047
144 vity in cell extracts using traditional anti-phosphotyrosine immunodetection and chemifluorescence.
145 Proteome analysis was based on 2D-DIGE, phosphotyrosine immunoprecipitations followed by 1D SDS-
146 ur finding that v-Src increased the level of phosphotyrosine in cellular proteins in RSV-transformed
148 amplified cell lines also contained elevated phosphotyrosine in EGFR, Her2, and Erbb3, but the elevat
151 sequences of approximately 100 aa that bind phosphotyrosines in signaling proteins and thereby media
152 tion of PLC-gamma1 by Itk requires a direct, phosphotyrosine-independent interaction between the Src
153 ec kinases and provides evidence of a novel, phosphotyrosine-independent regulatory role for the ubiq
155 depends on a tyrosine in DCL1 (Y442) but is phosphotyrosine-independent, a highly unusual feature fo
157 O6 is present on peripheral adaptor protein, phosphotyrosine interacting with PH domain and leucine z
160 ternative methods for membrane anchoring and phosphotyrosine interaction in cytoplasmic kinases, and
161 concomitant decline of Ca(2+) dampens the C2-phosphotyrosine interaction so that PLCgamma2 activation
162 94Asn]) in the gene for the Adaptor Protein, Phosphotyrosine Interaction, PH domain, and leucine zipp
163 1 and APPL2 proteins (APPL (adaptor protein, phosphotyrosine interaction, pleckstrin homology (PH) do
164 e affinities and specificities of SH2 domain-phosphotyrosine interactions have been well characterize
167 yrosine relaxase enzymes can accommodate two phosphotyrosine intermediates within their divalent meta
168 egion 2600-2605 and incorporated unprotected phosphotyrosine into IkappaB-alpha using a modified gene
169 bosomes capable of incorporating unprotected phosphotyrosine into proteins from a phosphotyrosyl-tRNA
170 show that the elevated EGFR, Her2, and Erbb3 phosphotyrosine is dependent on FGFR2, revealing EGFR fa
171 aling leads to aberrant expression of RON, a phosphotyrosine kinase receptor, and that signaling by R
172 resulting in the activation of the specific phosphotyrosine kinases SRC, LYN, and SYK and the concom
174 B cell activation was indicated by high phosphotyrosine levels in caps and patches, expression o
175 otion is reinforced by their decreased total phosphotyrosine levels, mirroring a postactivated stage,
176 rise to both increased growth and decreased phosphotyrosine levels; cellular PTP activity can theref
178 required for the precise positioning of the phosphotyrosine linkage for nucleophilic attack by the 3
182 itors (TKIs), which has uncovered widespread phosphotyrosine-mediated regulation of drug transporters
183 provide insight into Eya's participation in phosphotyrosine-mediated signaling networks by demonstra
184 ssibility of integrating the newly developed phosphotyrosine mimetic moiety into inhibitors designed
186 The interaction is independent of both a phosphotyrosine motif and a proline-rich sequence, the c
187 ich bears a dimeric fold that recognizes the phosphotyrosine motifs of E-cadherin, cortactin, DOK1, a
188 ntains a sterile-alpha motif (SAM) domain, 3 phosphotyrosine motifs, a proline-rich region, and a Src
192 rc homology (SH) 2 domain binds two specific phosphotyrosines on cortactin, a known Abl/Arg substrate
198 order to visualize synaptic accumulation of phosphotyrosine, paxillin, F-actin, and the major motor
203 method, targeted ECD allows analysis of both phosphotyrosine peptides and lower abundance phosphopept
204 e identification of 3168 unique nonredundant phosphotyrosine peptides in two LC-MS/MS runs from 8 mg
205 spectrometric data set of affinity-purified phosphotyrosine peptides obtained from normal and cancer
206 city of the phosphotyrosine immonium ion for phosphotyrosine peptides, allowing the efficient data co
207 Proteomic analysis revealed several novel phosphotyrosine peptides, including Harvey rat sarcoma o
208 the opposite direction to that of canonical phosphotyrosine peptides, which may contribute to their
210 activity and suggested the involvement of a phosphotyrosine phosphatase 1b (PTP1b) in this process.
211 VEGFR2 by calpain via its substrate protein phosphotyrosine phosphatase 1B (PTP1B), and the relevanc
212 on of suppressor of cytokine signaling-3 and phosphotyrosine phosphatase 1B, two negative regulators
215 g in hematopoietic cells is regulated by the phosphotyrosine phosphatase SHP-1, which is not implied
216 cal probes for second-site screening against phosphotyrosine phosphatases (PTPs) using NMR-based tech
217 phosphotyrosine signaling-tyrosine kinases, phosphotyrosine phosphatases, and Src Homology 2 (SH2) d
218 ing mechanism was ROS-mediated inhibition of phosphotyrosine phosphatases, which antagonize receptor
221 signaling pathways in HNSCC, we compared the phosphotyrosine profiles of a panel of HNSCC cell lines
222 highlights the application and potential of phosphotyrosine profiling for identifying clinically rel
223 ted under these conditions with quantitative phosphotyrosine profiling identified 193 differentially
225 ome similarity to that of low-molecular-mass phosphotyrosine protein phosphatase, although Ssu72 has
231 t nature of hydrogen bonding interactions in phosphotyrosine (pTyr) and sulfotyrosine (sTyr) residues
232 these effects, we analyzed the stability of phosphotyrosine (pTyr) sites in ovarian and colon tumors
233 e kinases, 38 tyrosine phosphatases, and 123 phosphotyrosine (pTyr)-binding SH2 proteins, all higher
237 specificity is highly biased toward a single phosphotyrosine (pY) motif among many potential pYXNX Gr
238 to discover a BCR-ABL fusion in H929 cells: phosphotyrosine (pY) peptide IP, p85 regulatory subunit
239 th similar affinities to known Stat3-binding phosphotyrosine (pY) peptide motifs, including those of
240 veal hypothesized novel EPOR/JAK2 targets, a phosphotyrosine (PY) phosphoproteomics approach was appl
243 H2 ligand, a constrained mimic, in which the phosphotyrosine (pY) residue is preorganized in the boun
244 e binding of Src-homology 2 (SH2) domains to phosphotyrosine (pY) sites is critical for the autoinhib
245 for specific and absolute quantification of phosphotyrosine (pY) under the assistance of a protein t
246 reventing dephosphorylation of substrate Lck phosphotyrosine (pY)-505 versus preventing dephosphoryla
247 VHZ efficiently catalyzes the hydrolysis of phosphotyrosine (pY)-containing peptides but exhibits no
250 RTK(571-999) in incubations with recombinant phosphotyrosine-recognition sequences expressed as GST-f
251 hrough binding of the Nck1 SH2 domain to the phosphotyrosine residue at position 602 (Y602) of the Ep
252 consisting of an N-capped d-tetrapeptide, a phosphotyrosine residue, and a diester or a diamide grou
253 inds of D-tetrapeptide containing one or two phosphotyrosine residues and with the N-terminal capped
255 SH2 domain of STAT6 to block recruitment to phosphotyrosine residues on IL-4 or IL-13 receptors and
256 interaction between the STATc SH2 domain and phosphotyrosine residues on Pyk2 that are generated by a
258 dephosphorylation on the critical 1007-1008 phosphotyrosine residues, implying JAK2 inhibition and t
259 of neighboring negatively charged N-terminal phosphotyrosine residues, promoting swelling of caveolae
261 necessary for the formation of invadopodia, phosphotyrosine-rich structures which degrade the extrac
262 ns from 8 mg of HeLa peptides, each with 80% phosphotyrosine selectivity, at a peptide FDR of 0.2%.
264 , weakening of the inhibitory intramolecular phosphotyrosine-SH2 interaction, and amplification of a
265 ivision, NMY-2 is required for SRC-dependent phosphotyrosine signaling and acts in parallel with WNT-
266 in the modulation of point contact dynamics, phosphotyrosine signaling at filopodial tips, and lamell
268 e performed a quantitative comparison of the phosphotyrosine signaling network and resulting phenotyp
269 etic nephropathy, has been shown to activate phosphotyrosine signaling pathways in human podocytes.
272 Yet the three-part toolkit that regulates phosphotyrosine signaling-tyrosine kinases, phosphotyros
274 ll receptor signal transduction by enhancing phosphotyrosine signals and intracellular calcium fluxes
279 SP) and an SH2 domain that binds to multiple phosphotyrosine sites in the adhesion protein nephrin, l
281 e purified phosphorylated protein bound to a phosphotyrosine specific antibody and permitted NF-kappa
282 mong the first to recognize the potential of phosphotyrosine-specific antibodies, Parsons and colleag
283 , substrates, and pathways through which the phosphotyrosine-specific ubiquitin ligases regulate dive
284 escence colocalization of Muc1/TLR5 and Muc1/phosphotyrosine staining patterns in mouse airway epithe
285 principally recognizes the phosphate of its phosphotyrosine substrate and further stabilizes the tyr
287 A peptide bound in the active site mimics a phosphotyrosine substrate, affords insight into substrat
288 ability, ShK-192, contains a nonhydrolyzable phosphotyrosine surrogate, a methionine isostere, and a
289 Src family kinases, decreased the amount of phosphotyrosine syntrophin and decreased the level of ac
291 N-Fmoc and O-Et protected phosphoserine and phosphotyrosine to prepare molecularly imprinted monolit
293 rts have established that GIV is involved in phosphotyrosine (Tyr(P))-based signaling in response to
294 differing only in their N-terminal residue, phosphotyrosine vs lysine, coassemble as stacks of antip
295 n the human genome that show specificity for phosphotyrosine, we identified six PTPs by quantitative
297 yl amino propionic acid (pCAP), an analog of phosphotyrosine, which can be incorporated into peptides
298 coumaryl amino propionic acid, an analog of phosphotyrosine, which can be incorporated into peptides
299 rosine phosphatase that targets two critical phosphotyrosines within GIV and antagonizes phospho-GIV-
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