ライフサイエンスコーパス: phosphatase inhibitor

1 ompletely resistant to this serine-threonine phosphatase inhibitor.

2 ation was blocked by okadaic acid, a Ser/Thr phosphatase inhibitor.

3 slocation, which is partially prevented by a phosphatase inhibitor.

4 ed kinases, 8 phosphatases, and 1 endogenous phosphatase inhibitor.

5 te, with and without levamisole, an alkaline phosphatase inhibitor.

6 was attenuated by a broad spectrum tyrosine phosphatase inhibitor.

7 ity for targeting MYC protein through PHLPP2 phosphatase inhibitors.

8 roteins, and resistance to all known Ser/Thr phosphatase inhibitors.

9 rundown of the channel is prevented by lipid phosphatase inhibitors.

10 orylation of TRPM8 that could be reversed by phosphatase inhibitors.

11 l patch clamp in the presence and absence of phosphatase inhibitors.

12 of PP1 because it was not mimicked by other phosphatase inhibitors.

13 could not be inhibited by general kinase or phosphatase inhibitors.

14 g levels, and was not prevented by kinase or phosphatase inhibitors.

15 hosphatase unaffected by a number of classic phosphatase inhibitors.

16 brane in the presence or absence of tyrosine phosphatase inhibitors.

17 es based on studies using protein kinase and phosphatase inhibitors.

18 nt based on studies using protein kinase and phosphatase inhibitors.

19 activated by ligands, kinase activators, or phosphatase inhibitors.

20 treatment with serine/threonine and tyrosine phosphatase inhibitors.

21 ounds in SSG were effective protein tyrosine phosphatase inhibitors.

22 ion are inhibited by type 1 serine/threonine phosphatase inhibitors.

23 1 binding was also blocked by these tyrosine phosphatase inhibitors.

24 the development of dual-specificity protein phosphatase inhibitors.

25 e receptor was determined in the presence of phosphatase inhibitors.

26 brain followed by incubation with or without phosphatase inhibitors.

27 riments were conducted using JNK and protein phosphatase inhibitors.

28 coronary artery smooth muscle cells, protein phosphatase inhibitor 1 (I-1 target) is highly expressed

29 ls have been identified, the role of protein phosphatase inhibitor 1 (I-1) in the acquisition or main

30 Protein phosphatase inhibitor-1 (I-1) has been proposed as a reg

31 Protein phosphatase inhibitor-1 (I-1) is the classic type-1 phos

32 PKC-alpha directly phosphorylates protein phosphatase inhibitor-1 (I-1), altering the activity of

33 trained by its endogenous inhibitor, protein phosphatase inhibitor-1 (PPI-1).

34 ve at low nM for recombinant SHP-1, tyrosine phosphatase inhibitor-1 (TPI-1) selectively increased SH

35 Protein phosphatase inhibitor-1 is a prototypical mediator of cr

36 ivation of its endogenous regulator, protein phosphatase inhibitor-1.

37 he absence of these serine/threonine protein phosphatase inhibitors, 17beta-estradiol attenuated glut

38 of effective concentrations of these protein phosphatase inhibitors, 17beta-estradiol protection agai

39 overexpression of Glc8, the yeast homolog of phosphatase inhibitor-2 (I-2).

40 identified by yeast two-hybrid using protein phosphatase inhibitor-2 (Inh2) as bait.

41 ted by Glc8, the yeast ortholog of mammalian phosphatase inhibitor-2.

42 itors okadaic acid, microcystin, and protein phosphatase inhibitor-2.

43 el human transmembrane protein KPI-2 (Kinase/Phosphatase/Inhibitor-2) that was identified by yeast tw

44 osure level by 5 mm Ca(NO(3))(2) and protein phosphatase inhibitors (75 nm okadaic acid or 1 mum Na(3

45 mM sodium orthovanadate (a protein tyrosine phosphatase inhibitor) abolished the reduction in Kv1.5

46 Metavanadate, a general protein phosphatase inhibitor, also enhanced SOC activity in ins

47 E(2), cAMP-raising agents, serine/threonine phosphatase inhibitor and activation of protein kinase C

48 s markedly enhanced on treating cells with a phosphatase inhibitor and decreases dramatically on K8 S

49 t in ligand design for vanadium complexes as phosphatase inhibitors and are consistent with other sma

50 tal muscle were treated with pharmacological phosphatase inhibitors and assessed for AS160 Ser(588) a

51 cell proliferation by BRCA1 was prevented by phosphatase inhibitors and by interfering RNA knockdown

52 etic screening, we tested a library of known phosphatase inhibitors and identified several compounds

53 ed the modulation of NHERF-1 dimerization by phosphatase inhibitors and identified the phosphorylatio

54 studies using a panel of protein kinase and phosphatase inhibitors and in-gel kinase assays in these

55 d for high-throughput screening of kinase or phosphatase inhibitors and is a valuable tool for drug d

56 The data suggest that calcineurin phosphatase inhibitors and prednisone can be safely redu

57 Protein phosphatase inhibitors and reduced expression of PP2A-Ca

58 el was experimentally validated by employing phosphatase inhibitors and the p38(MAPK) inhibitor SB203

59 t 1, and protein kinase C-potentiated myosin phosphatase inhibitor) and integrins were reduced in SRF

60 AMP), Bay K 8644 (BayK), Okadaic acid (OA, a phosphatase inhibitor), and phosphatase 2A (PP2A) in non

61 onic rejection, its synergy with calcineurin phosphatase inhibitors, and its inhibitory effects on he

62 cking moiety of rationally designed tyrosine phosphatase inhibitors, and they readily entered live ce

63 Protein phosphatase inhibitors are often considered as tumor pro

64 reveal the potential utility of EYA tyrosine phosphatase inhibitors as therapeutic agents in inhibiti

65 Dual specific phosphatase inhibitors as well as siRNA to DUPD1, comple

66 ophils with okadaic acid, a serine/threonine phosphatase inhibitor, at the concentrations that induce

67 Treatment of T cells with tyrosine phosphatase inhibitors attenuates inactivation by HSV, a

68 d sodium vanadate, a potent protein-tyrosine phosphatase inhibitor, blocked IL-8 production in a dose

69 Finally, phosphatase inhibitors blunted both KV1-C peptide-mediat

70 When prepared in the presence of phosphatase inhibitors, both WT- and SF-MRP1-enriched me

71 The specific phosphotyrosine phosphatase inhibitor, bpV(phen), diminished the stimula

72 tase inhibitor-1 (I-1) is the classic type-1 phosphatase inhibitor, but its presence and role in cAMP

73 to phorbol esters, growth factors or protein phosphatase inhibitors, but has not been observed during

74 hepatoma cell line was inhibited by tyrosine phosphatase inhibitors, but not by the proteasomal inhib

75 +/- 6 %) by prior treatment with the protein phosphatase inhibitor calyculin A (100 nM) and were not

76 The serine/threonine phosphatase inhibitor calyculin A (5 nM) sensitized A7r5

77 ition of PKA reduced KATP current, while the phosphatase inhibitor calyculin A caused a small increas

78 to reach half-maximal force) induced by the phosphatase inhibitor calyculin A in the presence of Ca(

79 onophore ionomycin, and the serine/threonine phosphatase inhibitor calyculin A increased Ser(23) alph

80 lation induced by the cell-permeable protein phosphatase inhibitor calyculin A is rapidly followed by

81 The phosphatase inhibitor calyculin A partially reverses the

82 Interestingly, treating cells with the phosphatase inhibitor calyculin A permitted the accumula

83 and the response to EH is potentiated by the phosphatase inhibitor calyculin A.

84 lanine or restoring phosphorylation with the phosphatase inhibitor calyculin abolished the difference

85 icates that either OCS or treatment with the phosphatase inhibitor calyculin-A (CLA) increase Na(+) t

86 The addition of the serine/threonine phosphatase inhibitors calyculin A and microcystin also

87 Treatment of cells with phosphatase inhibitors calyculin A and okadaic acid enha

88 slow rate of GRK site dephosphorylation, the phosphatase inhibitors calyculin A and okadaic acid fail

89 Use of the phosphatase inhibitors calyculin and okadaic acid indica

90 Importantly, phosphatase inhibitors (calyculin A and okadaic acid) we

91 nase C (PKC) activator (12,13-dibutyrate) or phosphatase inhibitors (calyculin A and okadaic acid), h

92 okadaic acid but not that induced by another phosphatase inhibitor, calyculin A (CA), which is a resu

93 cked by either 2-deoxyglucose or the protein phosphatase inhibitor, calyculin A, and the effects of c

94 The serine/threonine protein phosphatase inhibitor, calyculin A, but not the PP2A-spe

95 A phosphatase inhibitor, calyculin A, does not change this

96 dulin mutants or pretreatment with a protein phosphatase inhibitor, calyculin A.

97 Staurosporine and the phosphatase inhibitor, cantharidin, delay the asymmetric

98 Furthermore, we show that protein tyrosine phosphatase inhibitors cause the selective accumulation

99 Treatment of starved cells with a phosphatase inhibitor caused CDC2 gene overexpression.

100 ls, treatment of transgenic fly tissues with phosphatase inhibitors caused keratin network collapse,

101 nd esophagus cultures, with serine/threonine phosphatase inhibitors causes a dramatic increase in K4-

102 arin and spermine but not by either the acid phosphatase inhibitors citrate and tartrate or the prote

103 Preincubation of ECs with protein tyrosine phosphatase inhibitors completely blocked dbpB activatio

104 d was not blocked by a spectrum of kinase or phosphatase inhibitors, consistent with suppression due

105 Tautomycin (TTM), a potent protein phosphatase inhibitor, consists of a polyketide chain co

106 Human and rabbit CC both express the phosphatase inhibitor CPI-17, the myosin phosphatase reg

107 inhibition of myosin phosphatase, the myosin phosphatase inhibitor CPI17, or direct phosphorylation o

108 ctivation of hClC-2 at pH(o) 7.4, as long as phosphatase inhibitors (cyclosporin A or endothal) were

109 cell death in B104 cells by the calcineurin phosphatase inhibitor, cyclosporin A, abrogated both int

110 The calcineurin phosphatase inhibitor cyclosporine A, which blocks KC te

111 bited by cell treatment with the calcineurin phosphatase inhibitors, cyclosporine (CsA) and tacrolimu

112 of the distribution of cells containing the phosphatase inhibitor, DARPP-32, we raised the possibili

113 Phosphatase inhibitors decreased CYP2E1 mRNA levels by g

114 and C, and okadaic acid (a serine/threonine phosphatase inhibitor) decreased the current contributed

115 ngly increased by phorbol esters and protein phosphatase inhibitors, demonstrating modulation of the

116 kinase inhibitor genistein nor the tyrosine phosphatase inhibitor dephostatin prevented inhibition b

117 and were further stimulated by the tyrosine phosphatase inhibitor dephostatin.

118 Okadaic acid, a phosphatase inhibitor, did not affect H2O2-stimulated PK

119 ty of Arix, treatment of cultured cells with phosphatase inhibitors diminishes transcriptional activa

120 his response is known to be dependent on the phosphatase inhibitor dopamine- and cAMP-regulated phosp

121 n blocker) or okadaic acid (serine/threonine phosphatase inhibitor) dramatically enhanced ERK2 and ML

122 rylation was inhibited by the PP2A-selective phosphatase inhibitor endothall.

123 In addition, bpV, a tyrosine phosphatase inhibitor, facilitated the ability of subthr

124 proof of concept, we screened 84 kinase and phosphatase inhibitors for their ability to induce diffe

125 lopment of phototropic curvatures by protein phosphatase inhibitors further suggests that this post-t

126 d response is observed in cells treated with phosphatase inhibitors, further validating our model.

127 ining the effect of the competitive alkaline phosphatase inhibitor glycerol phosphate (GP), the ecto-

128 Treatment of cells with serine and threonine phosphatase inhibitors had no effect on ankyrin/AE1 comp

129 oxovanadate (PVN), a potent protein tyrosine phosphatase inhibitor, had no effect on the basal Ca(2+)

130 inhibitor, and calyculin A, a cell-permeable phosphatase inhibitor, had no effect on the stability of

131 lions of U.S. dollars per year, not a single phosphatase inhibitor has yet been approved for clinical

132 r to the kinase world, substrate-competitive phosphatase inhibitors have been developed but were not

133 Tyr-modified alphaII spectrin by vanadate, a phosphatase inhibitor, implies a dynamic balance between

134 SSG as a clinically usable protein tyrosine phosphatase inhibitor in cancer treatment and provide in

135 The addition of phosphatase inhibitors in combination with immunodepleti

136 nhibition of SDF-1alpha-induced migration by phosphatase inhibitors in CXCR4-transfected pre-B lympho

137 Use of phosphatase inhibitors in mpkCCD14 cells, co-IP with pho

138 ylation at Ser(19), followed by microcystin (phosphatase inhibitor) in the absence of Ca(2+), which i

139 he analysis of the effect of okadaic acid, a phosphatase inhibitor, in rice cell suspension cultures

140 usion of bpV(phen), a potent phosphotyrosine phosphatase inhibitor, in the recording chamber prior to

141 Sublethal dosage of salubrinal, an eIF2alpha phosphatase inhibitor, increased P-eIF2alpha and reduced

142 Okadaic acid (a phosphatase inhibitor) increases, while B56 expression r

143 We find that treatment of cells with strong phosphatase inhibitors interferes with the genome-wide d

144 btle changes in similar compounds can turn a phosphatase inhibitor into an activator.

145 tment of lymphocytes with a protein tyrosine phosphatase inhibitor is able to block the antiapoptotic

146 embranes obtained in the presence of protein phosphatase inhibitors is readily recognized by phosphoa

147 TTM) is a highly potent and specific protein phosphatase inhibitor isolated from Streptomyces spirove

148 and adenosine 3',5'-monophosphate-regulated phosphatase inhibitor known as "DARPP-32" is present in

149 w that treatment with calyculin A, a protein phosphatase inhibitor, leads to a marked increase of HDA

150 The effect of protein phosphatase inhibitors, light, and overexpression of PP2

151 abolished by intracellular dialysis with the phosphatase inhibitor microcystin, suggesting involvemen

152 The phosphatase inhibitor microcystin-LR blocked rescue of m

153 ne/threonine phosphatases on the immobilized phosphatase inhibitor microcystin-LR identified histone

154 A protein phosphatase inhibitor, microcystin LR, also induced cont

155 The serine/threonine protein phosphatase inhibitor, microcystin, inhibited the desens

156 nvergent asymmetric synthesis of the protein phosphatase inhibitor motuporin 1a is described.

157 a phosphatase (VH1) that is sensitive to the phosphatase inhibitor Na(3)VO(4) but not to okadaic acid

158 f PLD2 were further enhanced by the tyrosine phosphatase inhibitor, Na(3)VO(4).

159 tin AG 1478) and potentiated by the tyrosine phosphatase inhibitor Na3VO4.

160 re lysed in the presence of serine/threonine phosphatase inhibitor, NaF, the PKA-enhancing effect of

161 preconditioning tumor cells with the protein phosphatase inhibitor nitric oxide (NO) by altering the

162 Neither phosphatase inhibitors nor nonhydrolyzable nucleotide an

163 RAS, an Src homology 2 domain-containing Tyr phosphatase inhibitor (NSC 87877), or the MEK inhibitor

164 monstrated that i.c.v. administration of the phosphatase inhibitor okadaic acid (3 pmol/mouse; a dose

165 Co-treatment with the protein phosphatase inhibitor okadaic acid (OA) synergistically

166 spects those associated with addition of the phosphatase inhibitor okadaic acid (OA); moreover, OA al

167 Similarly, the protein phosphatase inhibitor okadaic acid also caused an accumu

168 In addition, the phosphatase inhibitor okadaic acid and the Ca2+/calmodul

169 Applying the phosphatase inhibitor okadaic acid causes vesicles to di

170 Phosphorylation by cAMP or the phosphatase inhibitor okadaic acid desensitized I(Ca) to

171 The protein phosphatase inhibitor okadaic acid did not prevent the c

172 a parallel preparation was treated with the phosphatase inhibitor okadaic acid during the terminal s

173 In contrast, the PP2A-specific phosphatase inhibitor okadaic acid promoted increased Ak

174 otic cells or cells treated with the protein phosphatase inhibitor okadaic acid remains active when d

175 s inhibition of PP2A activity by the protein phosphatase inhibitor okadaic acid stabilizes the Pim pr

176 The phosphatase inhibitor okadaic acid, but not PP2B inhibit

177 '-tetraacetic acid (BAPTA), prolonged by the phosphatase inhibitor okadaic acid, but unaffected by th

178 of micromolar concentrations of the protein phosphatase inhibitor okadaic acid, implicating PDGF-ind

179 LC neurons was absent in the presence of the phosphatase inhibitor okadaic acid, indicating that deph

180 was inhibited by treatment of cells with the phosphatase inhibitor okadaic acid, the ability of artem

181 of the NMDA receptor and is occluded by the phosphatase inhibitor okadaic acid.

182 active cAMP analog Sp-cAMP, and the protein phosphatase inhibitor okadaic acid.

183 orylation in cultured cells with the protein phosphatase inhibitor okadaic acid.

184 channels by ATP removal was inhibited by the phosphatase inhibitor okadaic acid.

185 and tartrate or the protein serine/threonine phosphatase inhibitor okadaic acid.

186 phosphorylation was prevented by the protein phosphatase inhibitor okadaic acid.

187 pette and not affected by treatment with the phosphatase inhibitor okadaic acid.

188 eotidase inhibitor ARL 67156, or the protein phosphatase inhibitor okadaic acid.

189 The phosphatase inhibitors okadaic acid and calyculin A acce

190 to the nonspecific serine/threonine protein phosphatase inhibitors okadaic acid and calyculin A at v

191 Neutrophil exposure to the Ser/Thr phosphatase inhibitors okadaic acid and calyculin A indu

192 ith insulin-like growth factor-1 or with the phosphatase inhibitors okadaic acid and calyculin A, but

193 erythrine chloride, but was activated by the phosphatase inhibitors okadaic acid and calyculin A.

194 ults from incubation of hepatocytes with the phosphatase inhibitors okadaic acid and calyculin A.

195 nuclear import and export, we found that the phosphatase inhibitors okadaic acid and microcystin inhi

196 is resistant to the classic serine/threonine phosphatase inhibitors okadaic acid and microcystin, but

197 The protein phosphatase inhibitors okadaic acid and nodularin enhanc

198 ating human adrenal NCI-H295A cells with the phosphatase inhibitors okadaic acid, fostriecin, and can

199 INAD was partially suppressed by the protein phosphatase inhibitors okadaic acid, microcystin, and pr

200 Treatment of cells with the general Ser/Thr phosphatase inhibitor (okadaic acid) lead to activation

201 Pre-incubation with phosphatase inhibitors (okadaic acid and cyclosporine A)

202 In addition, the phosphatase inhibitor, okadaic acid, prevents degradatio

203 This was blocked by the PP1/PP2A phosphatase inhibitor, okadaic acid.

204 of adenosine triphosphate or the nonspecific phosphatase inhibitor, okadaic acid.

205 nhibitor geldanamycin negated the effects of phosphatase inhibitors on HRI maturation/activation.

206 Protein-tyrosine phosphatase inhibitors or expression of a dominant negat

207 odies, antisense ribonucleotides, ribozymes, phosphatase inhibitors or SH2/SH3-directed agents).

208 ity is maintained by PKC activators, protein phosphatase inhibitors, or pseudo-phosphorylation by sub

209 MAP kinase inhibitor PD98,059 (20 microM) or phosphatase inhibitor orthovanadate (30 microM) complete

210 icrocystin, but is inhibited by the tyrosine phosphatase inhibitor orthovanadate and is particularly

211 Treatment of the cells with the tyrosine phosphatase inhibitor orthovanadate in the presence of i

212 CCR5 L1.2 transfectants or T-cells with the phosphatase inhibitor orthovanadate markedly abolished M

213 and incubation of the mutant cells with the phosphatase inhibitor orthovanadate resulted in strong c

214 Using tyrosine kinase (B44) and a tyrosine phosphatase inhibitor (orthovanadate), changes in both C

215 GCs treated with different phosphatase inhibitors permitted elimination of both Ser

216 normal human keratinocytes with the tyrosine phosphatase inhibitor peroxovanadate, directly and rever

217 ine was also mimicked by the phosphotyrosine phosphatase inhibitor pervanadate (PVN).

218 TRANCE sheddases is induced by the tyrosine phosphatase inhibitor pervanadate but not by phorbol est

219 The protein phosphatase inhibitor pervanadate reproduces the alterat

220 t of choriocarcinoma cells with the tyrosine phosphatase inhibitor pervanadate significantly enhanced

221 rosine phosphorylated in the presence of the phosphatase inhibitor, pervanadate, and recruits SHP-1 a

222 diated responses, whereas a protein tyrosine phosphatase inhibitor, pervanadate, caused depression.

223 Moreover, treatment of WT intestine with the phosphatase inhibitor, pervanadate, removed E-cadherin a

224 ematopoietic cells treated with the tyrosine phosphatase inhibitor, pervanadate.

225 tment of adipocytes with the phosphotyrosine phosphatase inhibitor phenylarsine oxide also enhanced i

226 from the phas promoter, nor did the tyrosine phosphatase inhibitors phenylarsine oxide and sodium ort

227 the periphery and inhibited by the tyrosine phosphatase inhibitor, phenylarsine oxide.

228 CPI-17, a myosin phosphatase inhibitor phosphoprotein, is phosphorylated

229 phorylation and C-kinase-potentiated protein phosphatase inhibitor phosphorylation.

230 Eight transcripts encoding phosphatase inhibitor Pip-1 protein, heat shock protein

231 Moreover, treatment with the phosphotyrosine-phosphatase inhibitor potassium bisperoxo(1,10-phenanthr

232 ing protein MYPT1 and increase in the myosin phosphatase inhibitor protein CPI-17.

233 estigated protein kinase C (PKC)-potentiated phosphatase inhibitor protein of 17 kDa (CPI-17) and myo

234 MEFs were treated with pervanadate (a global phosphatase inhibitor), pTyr(576)/pTyr(577)-FAK accounte

235 A protein phosphatase inhibitor reduced nicotine-induced upregulat

236 Phenylarsine oxide, a tyrosine phosphatase inhibitor, reduced the base-line activity of

237 Okadaic acid, a potent phosphatase inhibitor, reduced the level of dephosphoryl

238 Enhancement of Cav1 phosphorylation using a phosphatase inhibitor reduces Cdc42-regulated pinocytosi

239 Many of the more potent Cdc25 phosphatase inhibitors reported to date are quinones, wh

240 imicked or prevented by a tyrosine kinase or phosphatase inhibitor, respectively.

241 ase SHP-1, and treatment of the cells with a phosphatase inhibitor restored STAT1 tyrosine phosphoryl

242 with 70 micromol/L orthovanadate, a tyrosine phosphatase inhibitor, resulted in both increased tyrosi

243 Pervanadate, a general tyrosine phosphatase inhibitor, revealed marked phosphatase regul

244 response to calyculin A, indicating that the phosphatase inhibitor's effects depend upon an opposing

245 The protein phosphatase 1 a (PP1a)-specific phosphatase inhibitor Salubrinal (SAL) synergized with T

246 T signaling module by the specific eIF2alpha phosphatase inhibitor, salubrinal, induces resistance ag

247 The phosphatase inhibitor Sds23 acts upstream of PP6 to regu

248 esence of PKC inhibitors, activators, and/or phosphatase inhibitors shows that activity at each regio

249 PI 3-kinase, RAFTK/Pyk2 and tyrosine phosphatase inhibitors significantly blocked CXCL12-indu

250 bitors sensitize ovine PT cells and tyrosine phosphatase inhibitors significantly blunt adenylate cyc

251 Incubation without phosphatase inhibitors significantly increased tau immun

252 The tyrosine phosphatase inhibitor sodium orthovanadate ablated the i

253 Inhibition of MKP-1 using either the phosphatase inhibitor sodium orthovanadate or antisense

254 tion, whereas administration of the tyrosine phosphatase inhibitor sodium orthovanadate prior to etha

255 ylation of Cps2D even in the presence of the phosphatase inhibitor sodium orthovanadate.

256 d PP2 (200 nm), and mimicked by the tyrosine phosphatase inhibitor sodium vanadate (100 microm).

257 s with LPA, to activate Rho, or the tyrosine phosphatase inhibitor sodium vanadate increased the leve

258 Protein-tyrosine-phosphatase inhibitors sodium orthovanadate and dephosta

259 Phosphatase inhibitor (sodium pyrophosphate) decreases R

260 or to induce apoptosis in the presence of a phosphatase inhibitor, sodium orthovanadate, or antisens

261 a combination of TPA and a protein-tyrosine phosphatase inhibitor, sodium orthovanadate.

262 Conversely, the phosphotyrosine phosphatase inhibitor, sodium vanadate, or expression of

263 Of interest, addition of the tyrosine phosphatase inhibitor, sodium vanadate, selectively repr

264 horylated under basal conditions and Ser/Thr phosphatase inhibitors stimulate basal exchange activity

265 of erythroid cells with serine and threonine phosphatase inhibitors stimulated the hyperphosphorylati

266 phores, calmodulin antagonists, and tyrosine phosphatase inhibitors stimulated the release of both li

267 Tyrosine phosphatase inhibitor studies revealed that p38 promotes

268 rm were incubated in the presence of Ser/Thr phosphatase inhibitors such as okadaic acid and calyculi

269 t of cells with insulin and protein tyrosine phosphatase inhibitors such as vanadate and pervanadate

270 Results using specific protein phosphatase inhibitors suggested that protein phosphatas

271 ll surface after exposure of cells to ATP or phosphatase inhibitor, suggesting that loss of transport

272 1-P, but not 2dR, was blocked by an alkaline phosphatase inhibitor, suggesting that the actions of dR

273 vity or by the addition of a specific PIP(3) phosphatase inhibitor, suggesting that the induction of

274 Nup358/RanBP2 and Nup153 are not affected by phosphatase inhibitors, suggesting that transport inhibi

275 Sensitivity to a panel of phosphatase inhibitors suggests involvement of the phosp

276 daic acid (OA), a serine/threonine PP2A-like phosphatase inhibitor, suppresses sympathoadrenal lineag

277 eatment with calyculin A, a serine/threonine phosphatase inhibitor that elevates MLC phosphorylation,

278 DARPP-32 is a dual-function protein kinase/phosphatase inhibitor that is involved in striatal signa

279 Moreover, phosphatase inhibitors that increased phosphorylation of

280 cific feature of CSF arrest, and we also use phosphatase inhibitors to demonstrate an additional mode

281 Addition of phosphatase inhibitors to enzyme extracts from unstresse

282 The inability of known phosphatase inhibitors to inhibit the Nterm-phos constit

283 d with okadaic acid (OA), a serine/threonine phosphatase inhibitor, to induce tau phosphorylation and

284 e addition of ammonium metavanadate (AMV), a phosphatase inhibitor, to PIA (PIA-AMV) induced mucoidy

285 hen suppression of NMDARs was prevented with phosphatase inhibitors, tolerance of anoxia was lost.

286 basipetal transport was increased in rcn1 or phosphatase inhibitor-treated seedlings but showed norma

287 Increased auxin transport in rcn1 or phosphatase inhibitor-treated seedlings did not require

288 reatment with exogenous H(2)O(2) or with the phosphatase inhibitor vanadate abrogates the inhibition

289 n low concentrations of the protein-tyrosine phosphatase inhibitor vanadate are added with IFN-alpha.

290 The phosphatase inhibitor vanadate reduced these effects.

291 However, the phosphatase inhibitor vanadate reversed the inhibitory e

292 sphatase, which in turn, was reversed by the phosphatase inhibitor vanadate.

293 detected in cells treated with the tyrosine phosphatase inhibitor vanadate.

294 A library of 84 known kinase and phosphatase inhibitors was screened.

295 auopathy model, okadaic acid (OA), a protein phosphatase inhibitor, was microinfused into the right l

296 Using phosphatase inhibitors, we detected multiple phosphoryla

297 mice, and the impairment could be rescued by phosphatase inhibitors, which also restored Arc translat

298 Increasing interest in specific phosphatase inhibitors would allow PTPL1 to be evaluated

299 Because selective Cdc25 phosphatase inhibitors would be valuable biological tool

300 table, potent and selective protein tyrosine phosphatase inhibitor, would be neuroprotective after a