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1 varphi is a hydrophobic amino acid and pY is phosphotyrosine).
2 f that forms a direct salt bridge with bound phosphotyrosine.
3 cific for phosphoserine, phosphothreonine or phosphotyrosine.
4 mutant Y138F displayed reduced FGFR3-induced phosphotyrosine.
5  to bind phosphorylated substrates including phosphotyrosine.
6 ractions beyond the classical recognition of phosphotyrosine.
7 signaling interactions beyond recognition of phosphotyrosine.
8 s analyzed using specific antibodies against phosphotyrosine.
9 und peptides containing phosphothreonine and phosphotyrosine.
10 hifts in the spectroscopic identification of phosphotyrosines.
11 tual amino acid sequence and position of the phosphotyrosines.
12 "knocked-in" EpoR mutant lacking cytoplasmic phosphotyrosines.
13 ated with the unusual SH2 recognition of two phosphotyrosines.
14  a potential GADD34 phosphatase, recognizing phosphotyrosine 262.
15                Although Stat5 binds to EPO-R phosphotyrosine 343, the initial Stat5-deficient mice di
16 mortem samples, there was an accumulation of phosphotyrosine 39 alpha-synuclein in brain tissues and
17            This study further indicates that phosphotyrosine 39 alpha-synuclein is a potential diseas
18 tivation led to an age-dependent increase in phosphotyrosine 39 alpha-synuclein.
19 ne 416 (stimulatory site) and down-regulated phosphotyrosine 527 (inhibitory site) in retinal cells,
20  Transgenic osteoclasts showed a lower c-Src phosphotyrosine 527 level, greater c-Src kinase activity
21 shing indicated that SOCS6 binds directly to phosphotyrosines 591 and 919 of Flt3.
22 lpha1-antitrypsin deficiency, and editing of phosphotyrosine 701 in STAT1, the activity switch of the
23                        Localization requires phosphotyrosine, Abl and Src family tyrosine kinases, an
24                                     However, phosphotyrosine accounts for less than 1% of all phospho
25              Crystallography of the cores of phosphotyrosine-activated dimers of STAT1 (132-713) and
26 re, we investigated the possibility that the phosphotyrosine adaptor protein ShcA regulates nephrin t
27 bstitute tyrosine 104 with chemically stable phosphotyrosine analogue (p-Carboxymethyl-L-phenylalanin
28 alidation of the predicted sites using a pan-phosphotyrosine and a site-specific antibody, which we g
29  an increase in PI3K enzyme activity in anti-phosphotyrosine and anti-IGF-1R immunoprecipitates of RO
30 ntrols both steady-state and poststimulation phosphotyrosine and calcium levels.
31 ed diversity in SH2 domain interactions with phosphotyrosine and classify the C-terminal SH2 domain o
32  to the synapse, suppressing accumulation of phosphotyrosine and myosin without affecting F-actin.
33 ing complexes using a bilayered mechanism of phosphotyrosine and proline-rich anchoring motifs.
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 binding partner, suggesting that Nck couples phosphotyrosine- and phosphoinositide-dependent signals.
37 gets and represents a key connection linking phosphotyrosine- and phosphoserine/threonine-mediated on
38                                         Anti-phosphotyrosine antibodies were used to purify tyrosine
39                                              Phosphotyrosine antibody immunoprecipitation and mass sp
40          There were small increases in total phosphotyrosine at the anergic synapse along with signif
41                                              Phosphotyrosine-based peptidomimetic inhibitors, which m
42  suggest a model in which dynamic changes in phosphotyrosine-based signaling confer plasticity to the
43                                      Because phosphotyrosine-based signaling in hematopoietic cells i
44                                              Phosphotyrosine-based signaling plays a vital role in ce
45                                    Nck links phosphotyrosine-based signaling to Arp2/3-dependent acti
46 rosine binding (PTB) domain, namely atypical phosphotyrosine binding (aPTB) domain.
47 , we define a novel mechanism where the CCM2 phosphotyrosine binding (PTB) domain binds the ubiquitin
48 ion of KRIT1 and CCM2 and find that the CCM2 phosphotyrosine binding (PTB) domain displays a preferen
49 cellular experiments now show that the Mint1 phosphotyrosine binding (PTB) domain that binds to APP i
50 rtually every human Src homology 2 (SH2) and phosphotyrosine binding (PTB) domain, as well as microar
51 ough experimentation, we discovered a unique phosphotyrosine binding (PTB) domain, namely atypical ph
52 s of a Pleckstrin Homology (PH) domain and a Phosphotyrosine Binding (PTB) domain.
53 These proteins associate with TBC1D1 via its phosphotyrosine binding (PTB) domains and their interact
54 protein containing pleckstrin homology (PH), phosphotyrosine binding (PTB), and leucine zipper motifs
55 tions with PKC-theta occurred independent of phosphotyrosine binding and Fyn.
56          The cell fate determinant Numb is a phosphotyrosine binding domain (PTB)-containing endocyti
57 ses mapped the ERalpha binding domain to the phosphotyrosine binding domain 2 (PTB2).
58 otein containing pleckstrin homology domain, phosphotyrosine binding domain and leucine zipper motif)
59 uncation mutant consisting of the N-terminal phosphotyrosine binding domain blocks PP1-Axin interacti
60 erface with MDM2, only one region within the phosphotyrosine binding domain of NUMB (amino acids 113-
61 AB-6.2 bound to and colocalized with the PDZ/phosphotyrosine binding domain protein LIN-10.
62 eta phosphorylation site also located in the phosphotyrosine binding domain, threonine 206, had no ph
63 g of proteins that contain Src homology 2 or phosphotyrosine binding domains and whether mechanisms i
64 e to investigate the effect of disruption of phosphotyrosine binding of the N-terminal SH2 domain of
65 eport the discovery of malonate bound in the phosphotyrosine binding pocket of the apo-Grb7-SH2 struc
66                                          The phosphotyrosine binding region, but not the PDZ-binding
67 to design inhibitors blocking its SH2 domain phosphotyrosine binding site that is responsible for bot
68                       Hakai acts through its phosphotyrosine-binding (HYB) domain, which bears a dime
69 e assessed in Src homology 2 domain (SH2) or phosphotyrosine-binding (PTB) domain deletion mutants by
70 59249, p.Arg125Trp) in the N-terminal TBC1D1 phosphotyrosine-binding (PTB) domain has shown a replica
71 sent the detailed structural analysis of Shc phosphotyrosine-binding (PTB) domain in complex with the
72 step in this process involves interaction of phosphotyrosine-binding (PTB) domain in the N-terminal h
73 rystal structure at 1.37-A resolution of the phosphotyrosine-binding (PTB) domain of ARH in complex w
74   These characteristics are conserved in the phosphotyrosine-binding (PTB) domain of beta-amyloid pre
75                        Here we show that the phosphotyrosine-binding (PTB) domain protein Ced-6, a we
76 mprises a pleckstrin-homology (PH) domain, a phosphotyrosine-binding (PTB) domain, and C-terminal sit
77 ontaining a pleckstrin homology (PH) domain, phosphotyrosine-binding (PTB) domain, and leucine zipper
78 ontaining a pleckstrin-homology (PH) domain, phosphotyrosine-binding (PTB) domain, and leucine zipper
79                            Dab2, through its phosphotyrosine-binding (PTB) domain, inhibits platelet
80 e intrinsic EGFR kinase, as well as the ShcD phosphotyrosine-binding (PTB) domain.
81 ophic factor receptors predominantly via its phosphotyrosine-binding (PTB) domain.
82 proteins containing Src homology 2 (SH2) and phosphotyrosine-binding (PTB) domains, which recognize p
83 ing modules such as Src homology 2 (SH2) and phosphotyrosine-binding (PTB) domains.
84 orylated and bind proteins containing SH2 or phosphotyrosine-binding (PTB) domains.
85 ay of interactions that likely includes both phosphotyrosine-binding and SH3-domain-containing protei
86 Tyr(313)-phosphorylated hinge region and its phosphotyrosine-binding C2 domain that controls PKCdelta
87 Src SH2 domain strictly depends on an intact phosphotyrosine-binding competent SH2 domain and on tyro
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                               Similarly, the phosphotyrosine-binding domain of IRS-1 mediates a direc
92        This interaction occurred between the phosphotyrosine-binding domain of SH2D5 and an NxxF moti
93 n containing a pleckstrin-homology domain, a phosphotyrosine-binding domain, and a leucine zipper mot
94 omain linked to a PH domain and a C-terminal phosphotyrosine-binding domain.
95 ein receptor family members by recognizing a phosphotyrosine-binding domain.
96             However, CFTR does not possess a phosphotyrosine-binding domain.
97  proteins containing a Src homology 2 and/or phosphotyrosine-binding domain.
98   Unlike the monomeric nature of the SH2 and phosphotyrosine-binding domains, the architecture of the
99 pter protein that possesses an SH2 and a PTB phosphotyrosine-binding motif.
100 e SH2 domain surface, far from the classical phosphotyrosine-binding pocket.
101 cture of the HYB domain is essential for the phosphotyrosine-binding property of Hakai.
102 hat, in the nematode Caenorhabditis elegans, phosphotyrosine-binding pseudo-phosphatases are key regu
103 mology 2 (SH2) and kinase domains and to the phosphotyrosine-binding site of the SH2 domain, respecti
104 KCtheta and specifically required a putative phosphotyrosine-binding site within its N-terminal C2 do
105   Through 7 phosphoinositide 3-kinase (PI3K) phosphotyrosine-binding sites, ErbB3 is able to recruit
106 ture/function approach, we now show that the phosphotyrosine-binding, but not the Src homology 2, dom
107 ich involves a transesterification to form a phosphotyrosine bond within the RepD active site, is clo
108 1-associated DNA breaks via hydrolysis of 3'-phosphotyrosine bonds.
109                               We report that phosphotyrosine-cholesterol conjugates effectively and s
110  competent position at rates that mirror the phosphotyrosine cleavage kinetics.
111 y 2 (SH2) domain-containing proteins and the phosphotyrosine-containing counterparts play significant
112 hose of the Src homology 2 (SH2) domain with phosphotyrosine-containing peptide motifs (pTyr), are ub
113 cking methods to identify phosphoserine- and phosphotyrosine-containing peptides as possible substrat
114 ng the nSH2-helical domain contact caused by phosphotyrosine-containing peptides binding to the enzym
115 hat the Vav2 SH2 domain binds selectively to phosphotyrosine-containing peptides corresponding to cor
116 ime-resolved luminescence of Tb(3+)-chelated phosphotyrosine-containing peptides, which facilitated e
117 tic ER microsomes identified 49 high scoring phosphotyrosine-containing peptides.
118 ings demonstrate that FAK depletion switches phosphotyrosine-containing proteins from focal adhesions
119 se families, stimulate the ubiquitination of phosphotyrosine-containing proteins, including receptor
120                                   The SLP-76 phosphotyrosine-containing sequence, pY(173)IDR, does no
121 osine-binding (PTB) domains, which recognize phosphotyrosine-containing short linear motifs (SLiMs).
122 rexpression in HEK293 cells increases global phosphotyrosine content, promotes anchorage-independent
123 ession levels, probe signal is linked to the phosphotyrosine-correlated activation state of the ERBB2
124 ing and dissociation of effectors containing phosphotyrosine-dependent binding modules such as Src ho
125 , it binds SHP-1 and SHP-2 phosphatases in a phosphotyrosine-dependent manner, facilitating their rec
126 cal importance, how vascular cells integrate phosphotyrosine-dependent signaling to elicit cytoskelet
127 ss of 170amu to Tyr411 to yield the o-cresyl phosphotyrosine derivative.
128 structure and dynamics of complexes of three phosphotyrosine-derived peptides with the Src SH2 domain
129 ochemical analyses reveal that Apn2 resolves phosphotyrosine-DNA conjugates, terminal 2',3'-cyclic ph
130 rowth factor, there are only two established phosphotyrosine-docking sites (Tyr-490 and Tyr-785 on Tr
131 or tyrosine kinases generally act by forming phosphotyrosine-docking sites on their own endodomains t
132  (linker for activation of T cells)-Grb2-SOS phosphotyrosine-driven phase transition at the membrane.
133                                              Phosphotyrosine enrichment used immunoprecipitation and
134 we combine this approach with immunoaffinity phosphotyrosine enrichment, enabling the identification
135                 This regulation depends upon phosphotyrosine-EphrinB2 signalling repressing c-jun N-t
136 e ShK-170 (ShK-L5), containing an N-terminal phosphotyrosine extension of the Stichodactyla helianthu
137 tamic acid (E) mutant Y138E, which can mimic phosphotyrosine, failed to induce transient DNA replicat
138 tamic acid (E) mutant Y131E, which may mimic phosphotyrosine, failed to stimulate transient DNA repli
139  l-cysteine-l-phenylalanine, or l-cysteine-l-phosphotyrosine formed on crystallographically textured
140 osine (160-fold), sulfotyrosine (3600-fold), phosphotyrosine (>8000-fold), and phosphoserine (>8000-f
141                                              Phosphotyrosine hydrolysis by protein tyrosine phosphata
142           We employed proteomic screening by phosphotyrosine immunoaffinity purification and tandem m
143      Proteome analysis was based on 2D-DIGE, phosphotyrosine immunoprecipitations followed by 1D SDS-
144 ur finding that v-Src increased the level of phosphotyrosine in cellular proteins in RSV-transformed
145 on in IFNLR1 mimics the mode of binding of a phosphotyrosine in classical SH2 domains.
146 ephosphorylation cascade directed in part at phosphotyrosine in myosin.
147  Src homology 2 domain binds directly to two phosphotyrosines in HS1.
148  sequences of approximately 100 aa that bind phosphotyrosines in signaling proteins and thereby media
149 tion of PLC-gamma1 by Itk requires a direct, phosphotyrosine-independent interaction between the Src
150       Second, we identified a non-canonical, phosphotyrosine-independent STAT3 activation motif withi
151                   Hence, this interaction is phosphotyrosine-independent, and GRB10 SH2 can bind the
152 O6 is present on peripheral adaptor protein, phosphotyrosine interacting with PH domain and leucine z
153 and Tyr-1162 of ERBB4, as well as the intact phosphotyrosine-interacting SH2 domain of VAV3, are nece
154 each in calponin homology 1 (CH1) domain and phosphotyrosine interaction domain (PID) of Shc.
155                                              Phosphotyrosine Interaction Domain containing 1 (PID1; N
156 concomitant decline of Ca(2+) dampens the C2-phosphotyrosine interaction so that PLCgamma2 activation
157 94Asn]) in the gene for the Adaptor Protein, Phosphotyrosine Interaction, PH domain, and leucine zipp
158 1 and APPL2 proteins (APPL (adaptor protein, phosphotyrosine interaction, pleckstrin homology (PH) do
159 e affinities and specificities of SH2 domain-phosphotyrosine interactions have been well characterize
160 ins and thus can serve as competitors of SH2-phosphotyrosine interactions.
161 egion 2600-2605 and incorporated unprotected phosphotyrosine into IkappaB-alpha using a modified gene
162 bosomes capable of incorporating unprotected phosphotyrosine into proteins from a phosphotyrosyl-tRNA
163                Unexpectedly, coordination of phosphotyrosine is achieved by a modified binding pocket
164  resulting in the activation of the specific phosphotyrosine kinases SRC, LYN, and SYK and the concom
165 methyl-d-aspartic acid receptor subunit NR2B phosphotyrosine labeling.
166      B cell activation was indicated by high phosphotyrosine levels in caps and patches, expression o
167 bonate proportionally dictates total protein phosphotyrosine levels obtained after stimulation with e
168 otion is reinforced by their decreased total phosphotyrosine levels, mirroring a postactivated stage,
169 ommunication through the control of cellular phosphotyrosine levels.
170  rise to both increased growth and decreased phosphotyrosine levels; cellular PTP activity can theref
171 ng into a SH2-like domain in the presence of phosphotyrosine ligands.
172  required for the precise positioning of the phosphotyrosine linkage for nucleophilic attack by the 3
173 valently bound to its substrate 5'-end via a phosphotyrosine linkage.
174                        Here, we reconstitute phosphotyrosine-mediated assembly of extended linker for
175 itors (TKIs), which has uncovered widespread phosphotyrosine-mediated regulation of drug transporters
176  provide insight into Eya's participation in phosphotyrosine-mediated signaling networks by demonstra
177                  These results indicate that phosphotyrosine-mediated signaling through Shb is essent
178 a highly potent and selective monoacid-based phosphotyrosine mimetic for mPTPB inhibition.
179 ssibility of integrating the newly developed phosphotyrosine mimetic moiety into inhibitors designed
180            Here we have incorporated a novel phosphotyrosine mimetic, which is an unusual amino acid
181                               SOCS2 binds to phosphotyrosine-modified epitopes as degrons for ubiquit
182     The interaction is independent of both a phosphotyrosine motif and a proline-rich sequence, the c
183 onserved architecture that recognizes linear phosphotyrosine motifs and is present in a wide range of
184 on DNA damage, the cytoskeleton, SH2-binding phosphotyrosine motifs and motif mimicry by pathogenic b
185 ich bears a dimeric fold that recognizes the phosphotyrosine motifs of E-cadherin, cortactin, DOK1, a
186 ntains a sterile-alpha motif (SAM) domain, 3 phosphotyrosine motifs, a proline-rich region, and a Src
187                   The competitiveness of two phosphotyrosines, namely pY542 and pY580, for cis-intera
188 s in a Ca(2+)-regulated manner to a distinct phosphotyrosine of SLP65.
189 he interaction of the Grb2 SH2 domain with a phosphotyrosine on LAT.
190 rc homology (SH) 2 domain binds two specific phosphotyrosines on cortactin, a known Abl/Arg substrate
191 5 regulatory subunit of PI3K, which binds to phosphotyrosines on EpoR.
192 pHis or 3-pHis; they do not cross-react with phosphotyrosine or the other pHis isomer.
193  with peroxidase-like activity to facilitate phosphotyrosine (p-Tyr) oxidation.
194                                          The phosphotyrosines (p-Tyr) then recruit a subset of approx
195 vation of Ras and ERK but not for other FGFR phosphotyrosine pathways.
196  order to visualize synaptic accumulation of phosphotyrosine, paxillin, F-actin, and the major motor
197                                The series of phosphotyrosine peptide derivatives comprises the natura
198            We evaluated active kinases using phosphotyrosine peptide enrichment and quantitative mass
199                                              Phosphotyrosine peptide enrichment and quantitative mass
200 n and displaces fluorescein-labeled GpYLPQTV phosphotyrosine peptide from binding to STAT3.
201 method, targeted ECD allows analysis of both phosphotyrosine peptides and lower abundance phosphopept
202 e identification of 3168 unique nonredundant phosphotyrosine peptides in two LC-MS/MS runs from 8 mg
203  spectrometric data set of affinity-purified phosphotyrosine peptides obtained from normal and cancer
204    Proteomic analysis revealed several novel phosphotyrosine peptides, including Harvey rat sarcoma o
205  the opposite direction to that of canonical phosphotyrosine peptides, which may contribute to their
206  activity and suggested the involvement of a phosphotyrosine phosphatase 1b (PTP1b) in this process.
207  VEGFR2 by calpain via its substrate protein phosphotyrosine phosphatase 1B (PTP1B), and the relevanc
208 on of suppressor of cytokine signaling-3 and phosphotyrosine phosphatase 1B, two negative regulators
209 3-kinase (PI3K) or SRC homology 2-containing phosphotyrosine phosphatase 2 (SHP2).
210  Tyr-1510 were phosphorylated on IQGAP1 when phosphotyrosine phosphatase activity was inhibited in ce
211 ich is stimulated by Ephrin A1 (EfnA1) or by phosphotyrosine phosphatase inhibition.
212 g in hematopoietic cells is regulated by the phosphotyrosine phosphatase SHP-1, which is not implied
213  phosphotyrosine signaling-tyrosine kinases, phosphotyrosine phosphatases, and Src Homology 2 (SH2) d
214 ing mechanism was ROS-mediated inhibition of phosphotyrosine phosphatases, which antagonize receptor
215 alyzed phosphorylation is counterbalanced by phosphotyrosine phosphatases.
216                            LAR-type receptor phosphotyrosine-phosphatases (LAR-RPTPs) are presynaptic
217  Polyomaviruses have shown the importance of phosphotyrosine, PI3K, and p53 in transformation.
218 signaling pathways in HNSCC, we compared the phosphotyrosine profiles of a panel of HNSCC cell lines
219  highlights the application and potential of phosphotyrosine profiling for identifying clinically rel
220 ted under these conditions with quantitative phosphotyrosine profiling identified 193 differentially
221                 We integrated a quantitative phosphotyrosine profiling method with 'spike-in' stable
222 ome similarity to that of low-molecular-mass phosphotyrosine protein phosphatase, although Ssu72 has
223 hanced binding to the critical actin-binding phosphotyrosine protein, cortactin.
224 pressed within cells and can covalently trap phosphotyrosine proteins on exposure to light.
225 ylated peptides, corresponding to 844 unique phosphotyrosine proteins.
226                              Analysis of the phosphotyrosine proteome in paclitaxel-resistant tumor c
227                                      Using a phosphotyrosine proteomics approach, we screened the HNS
228 t nature of hydrogen bonding interactions in phosphotyrosine (pTyr) and sulfotyrosine (sTyr) residues
229  these effects, we analyzed the stability of phosphotyrosine (pTyr) sites in ovarian and colon tumors
230 he amino-terminal C2 domain of PKCtheta as a phosphotyrosine (pTyr)-binding domain.
231                                              Phosphotyrosine (pTyr)-dependent signaling is critical f
232 ng interactions involving the SH2 domain and phosphotyrosine(pTyr)-based inhibitors.
233                        SH2 domains recognize phosphotyrosine (pY) in the context of particular sequen
234 specificity is highly biased toward a single phosphotyrosine (pY) motif among many potential pYXNX Gr
235 g sequence-specific antibodies (Abs) against phosphotyrosine (pY) motifs embedded in folded polypepti
236  to discover a BCR-ABL fusion in H929 cells: phosphotyrosine (pY) peptide IP, p85 regulatory subunit
237 th similar affinities to known Stat3-binding phosphotyrosine (pY) peptide motifs, including those of
238 veal hypothesized novel EPOR/JAK2 targets, a phosphotyrosine (PY) phosphoproteomics approach was appl
239          Succinate- and cyclopropane-derived phosphotyrosine (pY) replacements were incorporated into
240  inhibition increased the exchange rate of a phosphotyrosine (pY) reporter (dSH2) at IACs.
241 H2 ligand, a constrained mimic, in which the phosphotyrosine (pY) residue is preorganized in the boun
242 e binding of Src-homology 2 (SH2) domains to phosphotyrosine (pY) sites is critical for the autoinhib
243  for specific and absolute quantification of phosphotyrosine (pY) under the assistance of a protein t
244 reventing dephosphorylation of substrate Lck phosphotyrosine (pY)-505 versus preventing dephosphoryla
245  VHZ efficiently catalyzes the hydrolysis of phosphotyrosine (pY)-containing peptides but exhibits no
246 otein interaction domain that directs myriad phosphotyrosine (pY)-signaling pathways.
247 ) and carboxyphenylalanine (cF) as mimics of phosphotyrosine (pY).
248 RTK(571-999) in incubations with recombinant phosphotyrosine-recognition sequences expressed as GST-f
249 hrough binding of the Nck1 SH2 domain to the phosphotyrosine residue at position 602 (Y602) of the Ep
250  consisting of an N-capped d-tetrapeptide, a phosphotyrosine residue, and a diester or a diamide grou
251 inds of D-tetrapeptide containing one or two phosphotyrosine residues and with the N-terminal capped
252                                 We find that phosphotyrosine residues on ErbB1 have half-lives of a f
253  SH2 domain of STAT6 to block recruitment to phosphotyrosine residues on IL-4 or IL-13 receptors and
254 interaction between the STATc SH2 domain and phosphotyrosine residues on Pyk2 that are generated by a
255 d a ShcA mutant (R175Q) that no longer binds phosphotyrosine residues via its PTB domain.
256  dephosphorylation on the critical 1007-1008 phosphotyrosine residues, implying JAK2 inhibition and t
257 of neighboring negatively charged N-terminal phosphotyrosine residues, promoting swelling of caveolae
258                 By interacting with specific phosphotyrosine residues, they provide regulatable prote
259  necessary for the formation of invadopodia, phosphotyrosine-rich structures which degrade the extrac
260 ns from 8 mg of HeLa peptides, each with 80% phosphotyrosine selectivity, at a peptide FDR of 0.2%.
261  are transcription factors that dimerize via phosphotyrosine-SH2 domain interactions.
262 estern blot phosphorylated Jak1, Jak3, and a phosphotyrosine signal attributed to the gamma(c)-chain,
263 ivision, NMY-2 is required for SRC-dependent phosphotyrosine signaling and acts in parallel with WNT-
264 in the modulation of point contact dynamics, phosphotyrosine signaling at filopodial tips, and lamell
265 e performed a quantitative comparison of the phosphotyrosine signaling network and resulting phenotyp
266 etic nephropathy, has been shown to activate phosphotyrosine signaling pathways in human podocytes.
267            Multiple angiogenic cues modulate phosphotyrosine signaling to promote vasculogenesis and
268                              Until recently, phosphotyrosine signaling was thought to be restricted t
269    Yet the three-part toolkit that regulates phosphotyrosine signaling-tyrosine kinases, phosphotyros
270 nding the evolutionary origins of SH2 domain-phosphotyrosine signaling.
271 ll receptor signal transduction by enhancing phosphotyrosine signals and intracellular calcium fluxes
272 h lower levels of early signaling events and phosphotyrosine signals at the pSMAC.
273           The family of Nck adaptors couples phosphotyrosine signals with actin dynamics and therefor
274                                Mutation of a phosphotyrosine site of the essential STPK PknB reduces
275         Moreover, hierarchical clustering of phosphotyrosine sites could accurately classify these le
276 SP) and an SH2 domain that binds to multiple phosphotyrosine sites in the adhesion protein nephrin, l
277 studies identified noncatalytic tyrosine and phosphotyrosine sites that can be liganded by SuTEx frag
278 ated basal autophosphorylation at five known phosphotyrosine sites.
279 e purified phosphorylated protein bound to a phosphotyrosine specific antibody and permitted NF-kappa
280 mong the first to recognize the potential of phosphotyrosine-specific antibodies, Parsons and colleag
281 , substrates, and pathways through which the phosphotyrosine-specific ubiquitin ligases regulate dive
282 escence colocalization of Muc1/TLR5 and Muc1/phosphotyrosine staining patterns in mouse airway epithe
283  principally recognizes the phosphate of its phosphotyrosine substrate and further stabilizes the tyr
284 zation of HYB(DeltaC) can be induced using a phosphotyrosine substrate peptide.
285  A peptide bound in the active site mimics a phosphotyrosine substrate, affords insight into substrat
286 ough some crystal contact surfaces involving phosphotyrosines suggested the possibility of tyrosine p
287 ability, ShK-192, contains a nonhydrolyzable phosphotyrosine surrogate, a methionine isostere, and a
288              Here, we present a method named phosphotyrosine Targeting by Recombinant Ab Pair, or pY-
289 lar calcium and accumulated higher levels of phosphotyrosine than control T cells.
290  N-Fmoc and O-Et protected phosphoserine and phosphotyrosine to prepare molecularly imprinted monolit
291              Despite harboring two potential phosphotyrosine (Tyr(P)) recognition domains, SH2D5 bind
292 rts have established that GIV is involved in phosphotyrosine (Tyr(P))-based signaling in response to
293  differing only in their N-terminal residue, phosphotyrosine vs lysine, coassemble as stacks of antip
294 n the human genome that show specificity for phosphotyrosine, we identified six PTPs by quantitative
295 itored by either yeast-growth curves or anti-phosphotyrosine Western blots.
296 yl amino propionic acid (pCAP), an analog of phosphotyrosine, which can be incorporated into peptides
297  coumaryl amino propionic acid, an analog of phosphotyrosine, which can be incorporated into peptides
298 is binding of its tandem SH2 domains to dual phosphotyrosines within FcepsilonRIgamma-ITAMs (immunore
299 rosine phosphatase that targets two critical phosphotyrosines within GIV and antagonizes phospho-GIV-
300 a marked increase in binding affinity of the phosphotyrosine-Y699 with the mutant histidine.

 
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