ライフサイエンスコーパス: pervanadate

1 nd in vivo after stimulation of T cells with pervanadate.

2 rons with the tyrosine phosphatase inhibitor pervanadate.

3 ment with the tyrosine phosphatase inhibitor pervanadate.

4 fect of exogenous PTPase was also blocked by pervanadate.

5 dues are required for current suppression by pervanadate.

6 ment with the tyrosine phosphatase inhibitor pervanadate.

7 er treatment of cells with the PTP inhibitor pervanadate.

8 rane-permeant tyrosine phosphatase inhibitor pervanadate.

9 s Ran-keratin binding after cell exposure to pervanadate.

10 n was sensitive to the general PTP inhibitor pervanadate.

11 vity of PTP-MEG2 and was rapidly reversed by pervanadate.

12 ns Zn(2+) and 1,2-naphthoquinone, as well as pervanadate.

13 neurofascin isolated from cells treated with pervanadate.

14 easing protein tyrosine phosphorylation with pervanadate.

15 tuberin phosphorylation when stimulated with pervanadate.

16 ted with the tyrosine phosphatase inhibitor, pervanadate.

17 hibited Akt kinase activation in response to 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 y inactive form of SHP2 or pretreatment with pervanadate markedly increased EGF-stimulated Gab1 tyros

82 CD40- or pervanadate-mediated I kappa B tyrosine phosphorylation

83 The pervanadate-mediated Ran cysteine --> cysteic acid oxida

84 Src kinase inhibitors markedly decreased pervanadate-mediated tyrosine phosphorylation of PTEN.

85 Amphiregulin cleavage by pervanadate occurred in the absence of a cytoplasmic dom

86 ists on phosphorylation of beta-catenin, and pervanadate, on that of p120-catenin.

87 ing the effects of a powerful PTP inhibitor, pervanadate, on the activation of the mitogen-activated

88 cells expressing active Src or treated with pervanadate or a G protein-coupled receptor ligand (CXCL

89 Our results demonstrate that pervanadate or H/R treatment leads to tyrosine phosphory

90 rylation and NF kappa B activation following pervanadate or H/R treatment.

91 As shown previously, treatment with either pervanadate or insulin suppresses Kv1.3 current in these

92 PTPase inhibitors, such as pervanadate or phenylarsine oxide, inhibited hot spot di

93 Pervanadate or platelet-derived growth factor induced lo

94 iam1 co-localized with IRSp53 in response to pervanadate or platelet-derived growth factor.

95 attenuated RGS16 phosphorylation induced by pervanadate or receptor stimulation.

96 lycerate mutase, direct inhibition of GEs by pervanadate, or oxidation, which are the major side effe

97 ration of the tyrosine phosphatase inhibitor pervanadate, produced a sizable increase in presynaptic

98 In contrast, pervanadate (PV) activates NF-kappaB and induces tyrosin

99 Hydrogen peroxide and pervanadate (PV) treatment stimulates eNOS tyrosine phos

100 Pervanadate (PV), a tyrosine phosphatase inhibitor, indu

101 hat are briefly exposed to the PTP inhibitor pervanadate (PV), resulting in tyrosine phosphorylation

102 absence of tyrosine phosphatase inhibitors (pervanadate [PV], phenylarsine oxide [PAO]) and a serine

103 by the phosphotyrosine phosphatase inhibitor pervanadate (PVN).

104 sible CHC phosphorylation in the presence of pervanadate reduced both constitutive and ligand-induced

105 Furthermore, the pervanadate-regulated sheddase activity is sensitive to

106 WT intestine with the phosphatase inhibitor, pervanadate, removed E-cadherin and beta-catenin from th

107 The protein phosphatase inhibitor pervanadate reproduces the alterations in subcellular di

108 Treatment of HeLa cells with pervanadate resulted in a marked inhibition of PTP activ

109 endogenous focal adhesion kinase induced by pervanadate resulted in a similar reduction of localizat

110 phosphatase inhibitors such as vanadate and pervanadate resulted in the tyrosine phosphorylation of

111 Stimulation of cells with pervanadate resulted in tyrosine phosphorylation of PZR

112 enylalanine-induced polarization, 0.5 microM pervanadate returned cell polarization to nearly normal

113 Pervanadate reversed the gamma-T3-induced down-regulatio

114 ells with the tyrosine phosphatase inhibitor pervanadate significantly enhanced IFN-gamma-inducible J

115 l substrates were identified in lysates from pervanadate-stimulated Jurkat cells using PTPN22-D195A/C

116 , or -19, is critical for phorbol ester- and pervanadate-stimulated release of TNFalpha in mouse embr

117 on B cell antigen receptor (BCR) ligation or pervanadate stimulation and associates with phospholipas

118 Following either pervanadate stimulation or TCR engagement, both Siglecs

119 9A, -C, and -G2 are phosphorylated following pervanadate stimulation, whereas Ly-49D is not; 2) mAb-i

120 d with similar kinetics following TCR/CD3 or pervanadate stimulation.

121 after inhibition of tyrosine phosphatase by pervanadate suggested that KIR2DL1-H36A is selectively p

122 ut only following treatment with vanadate or pervanadate, suggesting that endogenous phosphorylation

123 ncreased in breast cancer cells treated with pervanadate, suggesting that PTEN contains sites for tyr

124 It is noteworthy that pervanadate suppressed the ability of PMF to inhibit the

125 We report that pervanadate suppresses oxygen-dependent changes in glyco

126 concentrations of the phosphatase inhibitor pervanadate, this caused the CR4-uPAR oscillations to be

127 However, pervanadate-treated cells also revealed a slower migrati

128 ently phosphorylated in v-Src-transfected or pervanadate-treated cells at two tyrosines conserved in

129 enhancement of cleavage secretion of ACE in pervanadate-treated cells was specifically blocked by an

130 lower migrating species of IkappaBalpha from pervanadate-treated cells was tyrosine-phosphorylated as

131 Munc18c phosphorylation levels increased in pervanadate-treated cells, suggesting that phosphorylati

132 everal tyrosine-phosphorylated proteins from pervanadate-treated cells.

133 with a marked reduction in pyrin binding in pervanadate-treated cells.

134 inactive mutant form of SHP-1 as well as in pervanadate-treated cells.

135 t 130-kDa tyrosine-phosphorylated protein in pervanadate-treated HeLa cell lysates which was preferen

136 ern of tyrosine phosphorylation was found in pervanadate-treated Jurkat T cells stably expressing CTL

137 ere found in soluble fractions prepared from pervanadate-treated Jurkat T-cells.

138 When CEACAM1-L was immunoprecipitated from pervanadate-treated MC38/CEACAM1-L cells and the associa

139 alyses using detergent lysates prepared from pervanadate-treated MIN6 beta cells revealed that the ty

140 recognized tyrosine phosphorylated pp36 from pervanadate-treated rat thymocytes.

141 one S-transferase (GST) fusion proteins with pervanadate-treated S2 cell lysates.

142 When overexpressed in pervanadate-treated U937 cells, FDF03 was tyrosine-phosp

143 Pervanadate treatment causes a time- and concentration-d

144 alpha-Syn is phosphorylated within 2 min of pervanadate treatment in alpha-Syn-transfected cells.

145 at of the wild-type protein, indicating that pervanadate treatment induces an alternate mechanism of

146 s phosphorylated at tyrosine residue(s) upon pervanadate treatment of cells and then recruits the pro

147 oop and carboxy-terminal tyrosines following pervanadate treatment of cells expressing c-MET.

148 Pervanadate treatment of N2a neuroblastoma cells resulte

149 hat immunoprecipitation of Ly-49D, following pervanadate treatment or specific Ab cross-linking, copr

150 Immunochemical analyses after pervanadate treatment showed that each of the mutant mol

151 Furthermore, pervanadate treatment validated the phosphorylation even

152 FcRH3 was tyrosine phosphorylated following pervanadate treatment, and its coligation with the BCR i

153 Use of [(32)P]orthophosphate incorporation, pervanadate treatment, and phosphotyrosine-specific anti

154 ion sites of c-Cbl in T cells in response to pervanadate treatment, as well as in response to TcR/CD3

155 idation, which are the major side effects of pervanadate treatment.

156 edox activation of NFkappaB following H/R or pervanadate treatment.

157 ion following hypoxia/reoxygenation (H/R) or pervanadate treatment.

158 2B4 became tyrosine phosphorylated following pervanadate-treatment of transfected cells and recruited

159 Pervanadate triggers Ran-K8/K18 binding and a gel-migrat

160 AChR phosphorylation, stimulated by agrin or pervanadate, was inhibited by blocking Src-class kinases

161 ns and observed that lower concentrations of pervanadate were needed to cause an increase in phospho-

162 Consistent with this, pervanadate, which increases cellular tyrosine phosphory

163 However, when maximally phosphorylated by pervanadate, Y391 and, to a lesser extent, Y421 were suf

164 eatment of the cells with the PTP inhibitors pervanadate, Zn(2+), and 1,2-naphthoquinone (76%, 69%, a

165 eincubation of the cells with the inhibitors pervanadate, Zn(2+), and 1,2-naphthoquinone (91%, 88%, a