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1 hibited Akt kinase activation in response to pervanadate.
2 nd in vivo after stimulation of T cells with pervanadate.
3 rons with the tyrosine phosphatase inhibitor pervanadate.
4 ment with the tyrosine phosphatase inhibitor pervanadate.
5 fect of exogenous PTPase was also blocked by pervanadate.
6 dues are required for current suppression by pervanadate.
7 ment with the tyrosine phosphatase inhibitor pervanadate.
8 er treatment of cells with the PTP inhibitor pervanadate.
9 rane-permeant tyrosine phosphatase inhibitor pervanadate.
10 s Ran-keratin binding after cell exposure to pervanadate.
11 n was sensitive to the general PTP inhibitor pervanadate.
12 vity of PTP-MEG2 and was rapidly reversed by pervanadate.
13 neurofascin isolated from cells treated with pervanadate.
14 ns Zn(2+) and 1,2-naphthoquinone, as well as pervanadate.
15 easing protein tyrosine phosphorylation with pervanadate.
16 tuberin phosphorylation when stimulated with pervanadate.
17 ted with the tyrosine phosphatase inhibitor, pervanadate.
18                                              Pervanadate (200 micromol/L) also induced marked NF-kapp
19 Y(529)FSrc-expressing MEFs were treated with pervanadate (a global phosphatase inhibitor), pTyr(576)/
20                                              Pervanadate, a general tyrosine phosphatase inhibitor, r
21 ulation of 3T3-L1 adipocytes with insulin or pervanadate, a portion of the cytosolic PIKfyve was recr
22 osphorylation of Tiam1 in cells treated with pervanadate, a potent inhibitor of tyrosine phosphatases
23                                    Recently, pervanadate, a protein-tyrosine phosphatase inhibitor, w
24 ansition was examined by treating cells with pervanadate, a reagent that prevents the GE-band 3 compl
25                         Exposure of cells to pervanadate, a stress-inducing agent, stimulated its tyr
26                                              Pervanadate, a tyrosine phosphatase inhibitor, induced r
27 a degree approximately equivalent to that of pervanadate, a well known PTPase inhibitor.
28 h human CEACAM1-L and stimulated with sodium pervanadate, actin was found to co-localize with CEACAM1
29 oth insulin and the insulin-mimetic compound pervanadate activate L6 cell glucose incorporation in do
30 tion, and the tyrosine phosphatase inhibitor pervanadate activate the transcription factor NF-kappaB,
31                                              Pervanadate activates the signaling pathways directly an
32                                    Moreover, pervanadate activation of ErbB-4 cleavage, but not that
33 osphorylation in cells by the application of pervanadate, an extremely potent phosphotyrosine phospha
34 treating gACE- or sACE-expressing cells with pervanadate, an inhibitor of protein Tyr phosphatases.
35 ation of KIR was detected in the presence of pervanadate, an inhibitor of protein tyrosine phosphatas
36                                              Pervanadate, an inhibitor of protein-tyrosine phosphatas
37                                   Hence, the pervanadate and 12-O-tetradecanoylphorbol-13-acetate-ind
38 rrent modulation, we examined the effects of pervanadate and insulin on wild-type and mutant Kv1.3 ch
39                      Treatment of cells with pervanadate and knocking down PTP-1B restores insulin an
40           Inhibition of PTP-1B activity with pervanadate and metformin or knocking down PTP-1B reesta
41 s and occurs in response to stimulation with pervanadate and oxidative stress.
42 ate that the tyrosine phosphatase inhibitors pervanadate and zinc potently inhibited budding of nasce
43 n the presence of the phosphatase inhibitor, pervanadate, and recruits SHP-1 and SHP-2.
44 buted to NF-kappaB activation in response to pervanadate appeared to involve its catalytic p110 subun
45    We now demonstrate that phorbol ester and pervanadate are effective stimuli for HER4 JM-a processi
46                                        Using pervanadate as a means to phosphorylate the BTLA cytopla
47 BTLA function and caution against the use of pervanadate as means to initiate signal transduction cas
48 n tyrosine phosphatase inhibitors Na3VO4 and pervanadate blocked the striking induction of IL-4Ralpha
49 rotein-tyrosine phosphatase (PTP) inhibitor, pervanadate, blocks Cat.G-induced FAK tyrosine dephospho
50                              Upon removal of pervanadate, both tyrosine phosphorylation and MAP kinas
51 nduced by the tyrosine phosphatase inhibitor pervanadate but not by phorbol esters, whereas the other
52 imeric receptor upon treating the cells with pervanadate, but it was unable to recruit ITIM-binding n
53  inhibitors of tyrosine phosphatases such as pervanadate, calpeptin appeared to inhibit a subset of p
54 as a protein tyrosine phosphatase inhibitor, pervanadate, caused depression.
55             Therefore, cell-free exposure to pervanadate causes cysteine to cysteic acid oxidation of
56 ssociate with keratins 8 or 18 (K8/K18) in a pervanadate-dependent manner.
57     The enhancement of cleavage secretion by pervanadate did not require the presence of the cytoplas
58 d by 12-O-tetradecanoylphorbol-13-acetate or pervanadate (each of which is blocked by metalloprotease
59                                       Sodium pervanadate elicited tyrosine phosphorylation of native
60                                     However, pervanadate in the absence of collagen was able to induc
61 wing stimulation with either anti-IgG Abs or pervanadate in the murine B cell lymphoma A20 IIA1.6 and
62 ) are detected after treatment of cells with pervanadate; in yeast, overexpression of a phosphatidyli
63 er, treatment of MO7e cells with H(2)O(2) or pervanadate increased the tyrosine kinase activity of c-
64 tion of untransformed cells with H(2)O(2) or pervanadate increased tyrosine phosphorylation of each o
65 fied in response to v-Src co-transfection or pervanadate incubation.
66 e capacity to flux Ca2+ after treatment with pervanadate, indicating that tyrosine dephosphorylation
67                                              Pervanadate induced the tyrosine phosphorylation of gamm
68 to TCR/CD3 ligation, treatment of cells with pervanadate induced tyrosine phosphorylation of either P
69 uced degranulation while having no effect on pervanadate-induced degranulation.
70 GF) or lysophosphatidic acid receptors or by pervanadate-induced inhibition of tyrosine phosphatases
71      This was evident from the inhibition of pervanadate-induced NF-kappaB activation and reporter ge
72                                          The pervanadate-induced proteolysis occurs in NIH 3T3 cells
73                                          The pervanadate-induced suppression of current and much of t
74 ent of WT tissue with carnosol inhibited the pervanadate-inducible expression of tyrosine-phosphoryla
75              Zn(2+), 1,2-naphthoquinone, and pervanadate inhibited dephosphorylation of the reporter
76       We investigated the mechanism by which pervanadate inhibits the degradation of IkappaBalpha.
77 ccur upon exposure to H2O2 or vanadate or if pervanadate is excluded during cell solubilization.
78                             This response to pervanadate is not dependent on protein kinase C activat
79                                        Last, pervanadate is shown to stimulate the proteolytic cell s
80 tes a similar cleavage of ErbB-4 but, unlike pervanadate, is not sensitive to pyrrolidine dithiocarbo
81 ctor alpha (TNF-alpha) or the strong oxidant pervanadate leads to loss of cell-surface EMCN and incre
82 y inactive form of SHP2 or pretreatment with pervanadate markedly increased EGF-stimulated Gab1 tyros
83                                     CD40- or pervanadate-mediated I kappa B tyrosine phosphorylation
84                                          The pervanadate-mediated Ran cysteine --> cysteic acid oxida
85     Src kinase inhibitors markedly decreased pervanadate-mediated tyrosine phosphorylation of PTEN.
86                     Amphiregulin cleavage by pervanadate occurred in the absence of a cytoplasmic dom
87 ists on phosphorylation of beta-catenin, and pervanadate, on that of p120-catenin.
88 ing the effects of a powerful PTP inhibitor, pervanadate, on the activation of the mitogen-activated
89  cells expressing active Src or treated with pervanadate or a G protein-coupled receptor ligand (CXCL
90                 Our results demonstrate that pervanadate or H/R treatment leads to tyrosine phosphory
91 rylation and NF kappa B activation following pervanadate or H/R treatment.
92   As shown previously, treatment with either pervanadate or insulin suppresses Kv1.3 current in these
93                   PTPase inhibitors, such as pervanadate or phenylarsine oxide, inhibited hot spot di
94                                              Pervanadate or platelet-derived growth factor induced lo
95 iam1 co-localized with IRSp53 in response to pervanadate or platelet-derived growth factor.
96  attenuated RGS16 phosphorylation induced by pervanadate or receptor stimulation.
97 lycerate mutase, direct inhibition of GEs by pervanadate, or oxidation, which are the major side effe
98 ration of the tyrosine phosphatase inhibitor pervanadate, produced a sizable increase in presynaptic
99                                 In contrast, pervanadate (PV) activates NF-kappaB and induces tyrosin
100                        Hydrogen peroxide and pervanadate (PV) treatment stimulates eNOS tyrosine phos
101                                              Pervanadate (PV), a tyrosine phosphatase inhibitor, indu
102 hat are briefly exposed to the PTP inhibitor pervanadate (PV), resulting in tyrosine phosphorylation
103  absence of tyrosine phosphatase inhibitors (pervanadate [PV], phenylarsine oxide [PAO]) and a serine
104 by the phosphotyrosine phosphatase inhibitor pervanadate (PVN).
105 sible CHC phosphorylation in the presence of pervanadate reduced both constitutive and ligand-induced
106                             Furthermore, the pervanadate-regulated sheddase activity is sensitive to
107 WT intestine with the phosphatase inhibitor, pervanadate, removed E-cadherin and beta-catenin from th
108            The protein phosphatase inhibitor pervanadate reproduces the alterations in subcellular di
109                 Treatment of HeLa cells with pervanadate resulted in a marked inhibition of PTP activ
110  endogenous focal adhesion kinase induced by pervanadate resulted in a similar reduction of localizat
111  phosphatase inhibitors such as vanadate and pervanadate resulted in the tyrosine phosphorylation of
112                    Stimulation of cells with pervanadate resulted in tyrosine phosphorylation of PZR
113 enylalanine-induced polarization, 0.5 microM pervanadate returned cell polarization to nearly normal
114                                              Pervanadate reversed the gamma-T3-induced down-regulatio
115 ells with the tyrosine phosphatase inhibitor pervanadate significantly enhanced IFN-gamma-inducible J
116 l substrates were identified in lysates from pervanadate-stimulated Jurkat cells using PTPN22-D195A/C
117 , or -19, is critical for phorbol ester- and pervanadate-stimulated release of TNFalpha in mouse embr
118 on B cell antigen receptor (BCR) ligation or pervanadate stimulation and associates with phospholipas
119                             Following either pervanadate stimulation or TCR engagement, both Siglecs
120 9A, -C, and -G2 are phosphorylated following pervanadate stimulation, whereas Ly-49D is not; 2) mAb-i
121 d with similar kinetics following TCR/CD3 or pervanadate stimulation.
122  after inhibition of tyrosine phosphatase by pervanadate suggested that KIR2DL1-H36A is selectively p
123 ut only following treatment with vanadate or pervanadate, suggesting that endogenous phosphorylation
124 ncreased in breast cancer cells treated with pervanadate, suggesting that PTEN contains sites for tyr
125                        It is noteworthy that pervanadate suppressed the ability of PMF to inhibit the
126                               We report that pervanadate suppresses oxygen-dependent changes in glyco
127  concentrations of the phosphatase inhibitor pervanadate, this caused the CR4-uPAR oscillations to be
128                                     However, pervanadate-treated cells also revealed a slower migrati
129 ently phosphorylated in v-Src-transfected or pervanadate-treated cells at two tyrosines conserved in
130  enhancement of cleavage secretion of ACE in pervanadate-treated cells was specifically blocked by an
131 lower migrating species of IkappaBalpha from pervanadate-treated cells was tyrosine-phosphorylated as
132  Munc18c phosphorylation levels increased in pervanadate-treated cells, suggesting that phosphorylati
133 everal tyrosine-phosphorylated proteins from pervanadate-treated cells.
134  with a marked reduction in pyrin binding in pervanadate-treated cells.
135  inactive mutant form of SHP-1 as well as in pervanadate-treated cells.
136 t 130-kDa tyrosine-phosphorylated protein in pervanadate-treated HeLa cell lysates which was preferen
137 ern of tyrosine phosphorylation was found in pervanadate-treated Jurkat T cells stably expressing CTL
138 ere found in soluble fractions prepared from pervanadate-treated Jurkat T-cells.
139   When CEACAM1-L was immunoprecipitated from pervanadate-treated MC38/CEACAM1-L cells and the associa
140 alyses using detergent lysates prepared from pervanadate-treated MIN6 beta cells revealed that the ty
141 recognized tyrosine phosphorylated pp36 from pervanadate-treated rat thymocytes.
142 one S-transferase (GST) fusion proteins with pervanadate-treated S2 cell lysates.
143                        When overexpressed in pervanadate-treated U937 cells, FDF03 was tyrosine-phosp
144                                              Pervanadate treatment causes a time- and concentration-d
145  alpha-Syn is phosphorylated within 2 min of pervanadate treatment in alpha-Syn-transfected cells.
146 at of the wild-type protein, indicating that pervanadate treatment induces an alternate mechanism of
147 s phosphorylated at tyrosine residue(s) upon pervanadate treatment of cells and then recruits the pro
148 oop and carboxy-terminal tyrosines following pervanadate treatment of cells expressing c-MET.
149                                              Pervanadate treatment of N2a neuroblastoma cells resulte
150 hat immunoprecipitation of Ly-49D, following pervanadate treatment or specific Ab cross-linking, copr
151                Immunochemical analyses after pervanadate treatment showed that each of the mutant mol
152                                 Furthermore, pervanadate treatment validated the phosphorylation even
153  FcRH3 was tyrosine phosphorylated following pervanadate treatment, and its coligation with the BCR i
154  Use of [(32)P]orthophosphate incorporation, pervanadate treatment, and phosphotyrosine-specific anti
155 ion sites of c-Cbl in T cells in response to pervanadate treatment, as well as in response to TcR/CD3
156 idation, which are the major side effects of pervanadate treatment.
157  beta-cells following glucose stimulation or pervanadate treatment.
158 edox activation of NFkappaB following H/R or pervanadate treatment.
159 ion following hypoxia/reoxygenation (H/R) or pervanadate treatment.
160 2B4 became tyrosine phosphorylated following pervanadate-treatment of transfected cells and recruited
161                                              Pervanadate triggers Ran-K8/K18 binding and a gel-migrat
162 AChR phosphorylation, stimulated by agrin or pervanadate, was inhibited by blocking Src-class kinases
163 ns and observed that lower concentrations of pervanadate were needed to cause an increase in phospho-
164                        Consistent with this, pervanadate, which increases cellular tyrosine phosphory
165    However, when maximally phosphorylated by pervanadate, Y391 and, to a lesser extent, Y421 were suf
166 eatment of the cells with the PTP inhibitors pervanadate, Zn(2+), and 1,2-naphthoquinone (76%, 69%, a
167 eincubation of the cells with the inhibitors pervanadate, Zn(2+), and 1,2-naphthoquinone (91%, 88%, a

 
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