ライフサイエンスコーパス: PTP

1 PTP activity can readily be diminished by reactive oxyge

2 PTP inhibition prevents necrosis and rescues regeneratio

3 PTP is sensitive to the PKC inhibitor GF109203X in both

4 stance of a protein tyrosine phosphatase-1B (PTP-1B).

5 rc and protein tyrosine phosphatase type 1D (PTP-1D) coimmunoprecipitate with WNK4.

6 Specifically, the activity of SHP-2, PTP-1beta, and PTP-PEST was enhanced by LKB1-expressing

7 so show that 2 mum GF109203 does not abolish PTP even though it inhibits the PDBu-dependent phosphory

8 PKC inhibitor GF109203X nearly abolished PTP in both control and cKO.

9 enhancement of PTP in cKO, without affecting PTP in control.

10 2-9895), we showed that ROS production after PTP opening can be sustained when complex III is damaged

11 ch damage could lead to ROS production after PTP opening has occurred.

12 ndings of this study suggest that allosteric PTP inhibitors may help reinvigorate drug development ef

13 tor type protein tyrosine phosphatase alpha (PTP-alpha encoded by PTPRA) has emerged as a key regulat

14 AK) with protein-tyrosine phosphatase-alpha (PTP-alpha) in IL-1 signaling.

15 dation protection is critical when analyzing PTPs, for example, in drug screening.

16 cally, the activity of SHP-2, PTP-1beta, and PTP-PEST was enhanced by LKB1-expressing cells.

17 s subject to I/R expressed IL-34, c-FMS, and PTP-zeta in TECs during AKI that increased with advancin

18 beta8 integrin and PTP-PEST form protein complexes at the leading edge of m

19 f SFKs and that the association of c-Src and PTP-1D with WNK4 at Tyr(1092) and Tyr(1143) plays an imp

20 We then estimated D from both tautp and PTP(t) from theories assuming one-dimensional diffusive

21 te how the combinatorial effects of PTKs and PTPs may be integrated to regulate signaling, with both

22 ing phenylene (P) and thiophene (T) units as PTP and TPT.

23 phosphorylation of RhoGDI1 by integrin-bound PTP-PEST promotes RhoGDI1 release from the membrane and

24 hopeptide that is hydrolyzed specifically by PTPs.

25 In the present work, we report that T-cell PTP (TC-PTP) activity is stimulated during the initial r

26 n tyrosine phosphatase SH2 domain-containing PTP (SHP2), have been shown to develop SLE, suggesting a

27 n, and protein oligomerization, that control PTP activity.

28 however, the spEPSC amplitude in cKO during PTP was significantly larger than in control.

29 30 APs at 100 Hz) in cKO over control during PTP.

30 synaptic currents (spEPSCs) increased during PTP in both control and cKO; however, the spEPSC amplitu

31 after application of phorbol ester or during PTP.

32 target protein for the action of PKC during PTP.

33 rm enhancement of transmitter release during PTP.

34 We found an increase in RRPtrain during PTP in both control and cKO, but no significant changes

35 ired-pulse ratios (PPRs) and RRP size during PTP.

36 The varying effects of either PTP on podosome organization in osteoclasts are caused b

37 n contrast, P-LTF was unaffected when either PTP or HSD was evoked in the presence of either rapamyci

38 mum of the PKC inhibitor GF109203 eliminates PTP and the PKC activator PDBu enhances neurotransmitter

39 ), we report that cKO synapses show enhanced PTP compared to control.

40 rotein crucial for SV regeneration, enhances PTP in cKO over control.

41 acking protein tyrosine phosphatase epsilon (PTP epsilon) are mildly osteopetrotic.

42 ble epithelial cells (which were assayed for PTP activity immediately after collection by bronchial b

43 at allostery might provide a way forward for PTP inhibitor development.

44 tes of Munc18-1 are critically important for PTP, which identifies the presynaptic target protein for

45 C isoforms alpha and beta are necessary for PTP, and the expression of PKCbeta in PKCalphabeta doubl

46 tinct responses will enable novel routes for PTP-selective drug design, important for managing diseas

47 HD-PTP is a tumour suppressor phosphatase that controls end

48 ver, the molecular mechanisms that enable HD-PTP to regulate ESCRT function are unknown.

49 t of UBPY by STAM2 displaces ESCRT-0 from HD-PTP, deubiquitinates EGFR, and releases ESCRT-0 from car

50 ure of the entire ESCRT binding region of HD-PTP using small angle X-ray scattering and hydrodynamic

51 rationalise the functional cooperation of HD-PTP with ESCRT-0, ESCRT-I and ESCRT-III and support a mo

52 HMP4B, which binds an overlapping site on HD-PTP Bro1.

53 receptor-type tyrosine phosphatase PTPN23/HD-PTP.

54 We show that HD-PTP adopts an open and extended conformation, optimal fo

55 We demonstrate that the HD-PTP open conformation is functionally competent for bind

56 ncerted recruitment of CHMP4B and UBPY to HD-PTP and the engagement of UBPY by STAM2 displaces ESCRT-

57 phosphorylation of the previously identified PTP-zeta downstream effectors focal adhesion kinase and

58 Mice genetically deficient in PTP-alpha (Ptpra(-/-)) were protected from pulmonary fib

59 les (SVs), but the role of SV endocytosis in PTP is unknown.

60 any synapses, but the role of endocytosis in PTP is unknown.

61 any synapses, but the role of endocytosis in PTP is unknown.

62 etermine the role of classic PKC isoforms in PTP.

63 al studies have implicated this mechanism in PTP at hippocampal synapses, but the results are controv

64 or identification of new allosteric sites in PTP, and given the basis of this method in thermodynamic

65 e formation by alamethicin or Ca(2+)-induced PTP opening.

66 ced by either alamethicin or calcium-induced PTP opening.

67 raplegia 7 (SPG7) in Ca(2+)- and ROS-induced PTP opening using RNAi-based screening.

68 t if complex III is damaged during ischemia, PTP opening may result in succinate/malate-fueled ROS pr

69 d biochemical and molecular study of all KIM-PTP family members to determine their H2O2 oxidation pro

70 ntical 3D structures and sequences, each KIM-PTP family member has a unique oxidation profile.

71 KIM-PTPs bind and dephosphorylate mitogen-activated protein

72 summary, despite being closely related, KIM-PTPs significantly differ in oxidation profiles.

73 f osteoclasts, are unchanged in mice lacking PTP alpha.

74 tent and selective inhibitors to control LMW-PTP activity.

75 ibit greater than 50-fold preference for LMW-PTP over a large panel of PTPs.

76 report the discovery of a novel class of LMW-PTP inhibitors derived from sulfophenyl acetic amide (SP

77 lar weight protein tyrosine phosphatase (LMW-PTP) is a regulator of a number of signaling pathways an

78 a striking conformational change in the LMW-PTP active site, leading to the formation of a previousl

79 than 5-fold selectivity against 20 mammalian PTPs.

80 ng of human cancer genomes reveals that many PTPs are frequently mutated in a variety of cancers.

81 lowing dicarboxylate efflux from the matrix, PTP opening during reperfusion may activate sustained RO

82 1,2-naphthoquinone (91%, 88%, and 87% median PTP inhibition, respectively).

83 Thus, two similar PKC isoforms mediate PTP in distinctly different ways.

84 mes are not the calcium sensors that mediate PTP at the CA3 to CA1 synapse.

85 s do not serve as calcium sensors to mediate PTP.

86 ritically, our understanding of ROS-mediated PTP oxidation is not yet sufficient to predict the molec

87 hat although protein kinase C (PKC) mediates PTP at the calyx of Held synapse in the auditory brainst

88 PKCbeta are both present, PKCgamma mediates PTP by increasing p and partially suppressing PKCbeta ac

89 ctional studies indicate that most of mutant PTPs are tumor suppressor genes.

90 ates and corresponding kinases of the mutant PTPs may provide novel therapeutic targets for cancers h

91 c targets for cancers harboring these mutant PTPs.

92 T) appears to be the most frequently mutated PTP in human cancers.

93 Among these mutated PTPs, PTP receptor T (PTPRT) appears to be the most freq

94 latory mechanisms are integral to the myriad PTP-mediated biochemical events and reinforce the concep

95 All four biradicals TTT-NN, TPT-NN, PTP-NN, and PPP-NN were investigated by EPR and optical

96 for radical precursors of 3, 5, 6, PPP-NNSi, PTP-NNSi, and final biradicals of TTT-NN, TPT-NN, and PP

97 hances neurotransmitter release and occludes PTP.

98 TC-2153 represents a novel class of PTP inhibitors based upon a cyclic polysulfide pharmacop

99 ng this sequence to the catalytic domains of PTP alpha enables them to function in osteoclasts.

100 phosphatase normally limits the duration of PTP, and that PTP is initiated by the action of a 'conve

101 e increase contributes to the enhancement of PTP in cKO over control and an altered endocytosis affec

102 , but selectively blocked the enhancement of PTP in cKO, without affecting PTP in control.

103 and cKO, and it abolishes the enhancement of PTP in cKO.

104 e increase contributes to the enhancement of PTP in dynamin-1 cKO, and this change depends on strong

105 from podosomes, and the nonreceptor form of PTP epsilon (cyt-PTPe), which is present in these struct

106 A leading hypothesis for the mechanism of PTP is that tetanic stimulation elevates presynaptic cal

107 st PTP, to study the molecular mechanisms of PTP.

108 phenylcarbamoyl moiety at the 5 position of PTP nucleus with a thiourea functionality to evaluate th

109 technique for the ex vivo quantification of PTP activity in small, heterogeneous, human cells and ti

110 ) outer mitochondrial membrane regulation of PTP activity occurs though a mechanism that does not req

111 Here we compare the role of PTP epsilon with that of the closely related PTP alpha i

112 ought to determine more directly the role of PTP-alpha in pulmonary fibrosis.

113 tion have enhanced oxidation/inactivation of PTPs and STAT1 signaling compared with NOD mice that do

114 Inactivation of PTPs with sodium orthovanadate in human and rodent islet

115 d visualization of oxidized intermediates of PTPs inside cells during signaling, and provide support

116 preference for LMW-PTP over a large panel of PTPs.

117 icient to predict the molecular responses of PTPs to oxidative stress.

118 striatum and highlight the potential role of PTPs and specifically STEP in the effects of cocaine.

119 arized, this mechanism is self-limiting once PTP opens during reperfusion.

120 ry efforts made in targeting these oncogenic PTPs as compelling candidates for cancer therapy.

121 ry brainstem before and after hearing onset, PTP is produced primarily by an increased probability of

122 In contrast, OXPHOS inhibition or PTP opening increased synthasome disassembly in WT, but

123 lanine decreased the association of c-Src or PTP-1D with WNK4, respectively.

124 as developed that integrates synchronous pan-PTP oxidation with ROS-independent mechanisms.

125 I IPPI containing a plastid transit peptide (PTP) at its amino terminus.

126 measurement of protein tyrosine phosphatase (PTP) activity in single human airway epithelial cells (h

127 a nonreceptor protein tyrosine phosphatase (PTP) encoded by the PTPN11 gene involved in cell growth

128 member of the protein tyrosine phosphatase (PTP) family.

129 Ks and induces protein-tyrosine phosphatase (PTP) inactivation.

130 ied reversible protein tyrosine phosphatase (PTP) oxidation as the primary redox regulatory mechanism

131 ch encodes the protein tyrosine phosphatase (PTP) SHP2, are implicated in CHD and cause Noonan syndro

132 t comprised of protein tyrosine phosphatase (PTP)-PEST and the extracellular matrix (ECM) adhesion re

133 teraction with protein-tyrosine phosphatase (PTP)-PEST.

134 Protein tyrosine phosphatase (PTP)sigma (PTPRS) was shown previously to be associated

135 Protein tyrosine phosphatases (PTP) are exciting and novel targets for cancer drug disc

136 monstrated in protein tyrosine phosphatases (PTP) by creation of single alanine mutations in the cata

137 Protein tyrosine phosphatases (PTPs) are enzymes that remove phosphate from tyrosine re

138 transduction.Protein-tyrosine phosphatases (PTPs) are thought to be major targets of receptor-activa

139 dation of three split-tyrosine phosphatases (PTPs) attached to FKBP and FRB, where catalytic activity

140 Receptor protein tyrosine phosphatases (PTPs) counterbalance RTK signaling; however, the functio

141 g activity of protein tyrosine phosphatases (PTPs) ensures robust yet diverse responses to extracellu

142 gnificance of protein tyrosine phosphatases (PTPs) in cellular signaling and disease biology has hist

143 of classical protein-tyrosine phosphatases (PTPs) in three-dimensional mammary epithelial cell morph

144 IM) family of protein-tyrosine phosphatases (PTPs) includes hematopoietic protein-tyrosine phosphatas

145 vented by the protein tyrosine phosphatases (PTPs) inhibitor sodium orthovanadate (Na3VO4).

146 depletion of protein tyrosine phosphatases (PTPs) resulted in the recovery of receptor phosphorylati

147 ll known that protein tyrosine phosphatases (PTPs) that become oxidized due to exposure to reactive o

148 activation of protein tyrosine phosphatases (PTPs) through the oxidation and reduction of their activ

149 regulated by protein tyrosine phosphatases (PTPs) to prevent excessive activation.

150 itors against protein-tyrosine phosphatases (PTPs), nearly all of it unsuccessful.

151 ogenic of all protein-tyrosine phosphatases (PTPs), play a critical role in metastatic progression of

152 regulated by protein tyrosine phosphatases (PTPs).

153 es (PTKs) and protein tyrosine phosphatases (PTPs).

154 ed breathing behavior if the constituent Por-PTP linker is nonmetalated.

155 mitochondrial permeability transition pore (PTP) abruptly opens, resulting in mitochondrial membrane

156 g those of the permeability transition pore (PTP) of mammals.

157 ) that induces permeability transition pore (PTP) opening and damages the heart during ischemia/reper

158 mitochondrial permeability transition pore (PTP) opening is accelerated in MICU1-deficient hepatocyt

159 , known as the permeability transition pore (PTP), in the inner membrane.

160 , known as the permeability transition pore (PTP), in the inner membranes of mitochondria can be trig

161 mitochondrial permeability transition pore (PTP), which has been associated with cell death in many

162 eatures of the permeability transition pore (PTP).

163 mitochondrial permeability transition pore (PTP).

164 t ceases when permeability transition pores (PTP) open during reperfusion.

165 Posttetanic potentiation (PTP) is a widely observed form of short-term plasticity

166 ength either after posttetanic potentiation (PTP) or through activation of the phospholipase-C-diacyl

167 mulation leads to post-tetanic potentiation (PTP) at many types of synapses.

168 mulation leads to post-tetanic potentiation (PTP) at many types of synapses.

169 Post-tetanic potentiation (PTP) is a widespread form of short-term synaptic plastic

170 Post-tetanic potentiation (PTP) is a widespread form of synaptic plasticity that la

171 Post-tetanic potentiation (PTP) is attributed mainly to an increase in release prob

172 KEY POINTS: Post-tetanic potentiation (PTP) is attributed mainly to an increase in release prob

173 Ca(2+) sensor for post-tetanic potentiation (PTP), a form of plasticity thought to underlie short-ter

174 nd uniquely large post-tetanic potentiation (PTP).

175 t of release like post-tetanic potentiation (PTP).

176 duced by tetanus [post-tetanic potentiation (PTP)] or low-frequency stimulation [homosynaptic depress

177 vely regulate ROS levels in order to prevent PTP inhibition has yet to be investigated.

178 f T1D patients in the Pathway to Prevention (PTP) Study of the Type 1 Diabetes TrialNet.

179 the PKCbeta C2 domain specifically prevents PTP without impairing other PKCbeta-dependent forms of s

180 g growth factor-mediated cellular processes, PTPs are usually perceived as the negative regulators of

181 ressed PKCgamma overrides PKCbeta to produce PTP by increasing p.

182 set, PKCgamma is absent and PKCbeta produces PTP by increasing RRP.

183 Among these mutated PTPs, PTP receptor T (PTPRT) appears to be the most frequently

184 ized bronchial epithelial cells showed rapid PTP-mediated dephosphorylation of the substrate (2.2 pmo

185 We found that a receptor PTP, PTPsigma, was substantially overexpressed in mouse

186 ignaling; however, the functions of receptor PTPs in HSCs remain incompletely understood.

187 ponding allosteric domains of other receptor PTPs.

188 nd synthetic ligands of TSPO do not regulate PTP activity through TSPO, 3) outer mitochondrial membra

189 PTP epsilon with that of the closely related PTP alpha in osteoclasts.

190 d had >100-fold selectivity over six related PTPs.

191 Remarkably, PTP switched mossy fiber synapses into full detonators f

192 in PKCalphabeta double knockout mice rescues PTP.

193 arge CNS model synapse that expresses robust PTP, to study the molecular mechanisms of PTP.

194 SP-PTP also differentially regulates the expression of appr

195 g cells infected with GAS mutants lacking SP-PTP displayed increased Ser-/Thr-/Tyr-phosphorylation.

196 henotypic analysis of GAS mutants lacking SP-PTP revealed that the phosphatase activity per se positi

197 osphorylation in GAS and the relevance of SP-PTP as an important therapeutic target.

198 on, and the physiological significance of SP-PTP is, therefore, questionable.

199 ed virulence, a GAS mutant overexpressing SP-PTP is hypervirulent.

200 ntains one encoding tyrosine phosphatase (SP-PTP).

201 Here, we demonstrate that SP-PTP possesses dual phosphatase specificity for Tyr- and

202 ctivity of user defined split-PTKs and split-PTPs.

203 TC-PTP deficiency also resulted in a significant increase i

204 TC-PTP is therefore shown to be required to safeguard the d

205 Finally, TC-PTP knockout mice showed a shortened latency of tumorige

206 nded with increased cell proliferation in TC-PTP-deficient keratinocytes following UVB irradiation.

207 Novel genetic strategies used to modulate TC-PTP expression demonstrate that depletion of TC-PTP expr

208 Loss of TC-PTP also reduced UVB-induced apoptosis.

209 n of STAT3 or AKT reversed the effects of TC-PTP deficiency on apoptosis and proliferation.

210 expression demonstrate that depletion of TC-PTP expression heightens the phosphorylation of STAT fam

211 upon UVB exposure, and overexpression of TC-PTP in keratinocyte cell lines further increased its act

212 ing with these results, overexpression of TC-PTP in keratinocyte cell lines yielded a decrease in pho

213 tpn2(fl/fl)) mice, we demonstrate loss of TC-PTP led to a desensitization to tumor initiator 7,12-dim

214 atinocytes, confirming that the effect of TC-PTP on cell viability is mediated by STAT3 dephosphoryla

215 indicate that UVB-mediated activation of TC-PTP plays an important role in the STAT3-dependent regul

216 tion between TC45 (the nuclear isoform of TC-PTP) and STAT3 specifically.

217 Treatment of TC-PTP-deficient keratinocytes with the STAT3 inhibitor STA

218 e significantly increased in epidermis of TC-PTP-deficient mice compared to control mice following TP

219 fied T cell protein tyrosine phosphatase (TC-PTP), also known as PTPN2, as a negative regulator of IL

220 ing, T-cell protein tyrosine phosphatase (TC-PTP), and the E3 ubiquitin ligase component UV-damaged D

221 e of T-cell protein tyrosine phosphatase (TC-PTP), encoded by Ptpn2, in chemically-induced skin carci

222 present work, we report that T-cell PTP (TC-PTP) activity is stimulated during the initial response

223 Using epidermal specific TC-PTP knockout (K14Cre.Ptpn2(fl/fl)) mice, we demonstrate

224 We demonstrate that TC-PTP activity was increased upon UVB exposure, and overex

225 Our findings reveal that TC-PTP has potential as a novel target for the prevention o

226 Furthermore, these results suggest that TC-PTP may be a novel potential target for the prevention o

227 Our results show that TC-PTP-deficient keratinocyte cell lines expressed a signif

228 UVB exposure in comparison with untreated TC-PTP-deficient keratinocytes, confirming that the effect

229 ormally limits the duration of PTP, and that PTP is initiated by the action of a 'conventional' PKC i

230 through integrin-mediated signaling and that PTP-alpha promotes fibroblast expression of matrix metal

231 We conclude that PTP-alpha promotes profibrotic signaling pathways in fib

232 Here, we demonstrate that PTP non-receptor type 12 (PTPN12) protects cells against

233 We find that PTP is unchanged in PKC triple knock-out (TKO) mice in w

234 a molecular genetic approach and found that PTP was unaffected when all calcium-dependent PKC isozym

235 We previously reported that PTP-alpha regulates cellular responses to cytokines and

236 Previous studies suggest that PTP results primarily from a protein kinase C (PKC)-depe

237 It follows, therefore, that PTP malfunction can actively contribute to a host of hum

238 emical events and reinforce the concept that PTPs are indispensable and specific modulators of cellul

239 We conclude that PTPs alpha and epsilon play distinct roles in osteoclast

240 However, mounting evidence indicate that PTPs do not always antagonize the activity of PTKs in re

241 The PTP is an inner membrane channel that forms from F-ATPas

242 The PTP study examines risk factors for T1D and disease prog

243 ic candidates have been proposed to form the PTP complex, however, the core component is unknown.

244 ton translocation is involved in forming the PTP.

245 lvement of the subunit b and the OSCP in the PTP by generating clonal cells, HAP1-Deltab and HAP1-Del

246 gate the involvement of the c-subunit in the PTP, we generated a clonal cell, HAP1-A12, from near-hap

247 reviously from possible participation in the PTP; thus, the only subunits of ATP synthase that could

248 These findings indicate that the mCrC is the PTP of D. melanogaster and that the signature conductanc

249 We show (i) that like the PTP, the mCrC is affected by the sense of rotation of F-

250 al protein, SPG7, as a core component of the PTP at the OMM and IMM contact site.

251 ecific, orally bioavailable inhibitor of the PTP oncoprotein SHP2 with in vivo activity, suggests tha

252 PRL) are infamously oncogenic members of the PTP superfamily.

253 sess the role of TSPO in the function of the PTP through the generation of mice in which the Tspo gen

254 o role in the regulation or structure of the PTP, 2) endogenous and synthetic ligands of TSPO do not

255 hat stimulation of OXPHOS, inhibition of the PTP, or deletion of CypD increased high order synthasome

256 After the removal of the PTP, the recombinant truncated AaIPPI1 isomerized isopen

257 reserve the characteristic properties of the PTP.

258 reserve the characteristic properties of the PTP; therefore, the membrane domain of subunit b does no

259 logical processes through its actions on the PTP.

260 eated to either stimulate OXPHOS or open the PTP.

261 herefore, the c-subunit does not provide the PTP.

262 We conclude that CypD not only regulates the PTP, but also regulates the dynamics of synthasome assem

263 e the subunits ATP6 and ATP8, but retain the PTP.

264 Biochemical analyses revealed that the PTP is a heterooligomeric complex composed of VDAC, SPG7

265 main of subunit b does not contribute to the PTP, and the OSCP does not provide the site of interacti

266 In contrast to the PTP, the mCrC of Drosophila is not permeable to sucrose

267 locked by pretreatment of the cells with the PTP inhibitors pervanadate, Zn(2+), and 1,2-naphthoquino

268 The PTPs, YopH and PTP1B, have very different catalytic rate

269 Although the PTPs have been considered undruggable, the findings of t

270 We also discuss how disruption of these PTP regulatory mechanisms can cause human diseases and h

271 n, mutation, or other dysregulation of these PTPs has been positively correlated with cancer initiati

272 he distribution of individual transit times, PTP(t).

273 dergo inner membrane permeabilization due to PTP opening.

274 e (76%, 69%, and 100% inhibition relative to PTP activity in untreated controls, respectively).

275 formation) display a striking resistance to PTP opening.

276 gest potential synergy of blocking their two PTP receptors.

277 Osteoclasts express the receptor-type PTP alpha (RPTPa), which is absent from podosomes, and t

278 increases Ezh2 recruitment to claudin-5, VE-PTP, and vWf promoters, causing gene downregulation.

279 binding to promoter regions of claudin-5, VE-PTP, and vWf.

280 tion of clinical safety and efficacy of a VE-PTP inhibitor and Tie2 activator.

281 alleled decreased levels of claudin-5 and VE-PTP.

282 Intraocular injection of an anti-VE-PTP antibody previously shown to activate TIE2 suppresse

283 fic deletion of Hif2a exhibited decreased VE-PTP expression and increased VE-cadherin phosphorylation

284 Moreover, activation of HIF2alpha/VE-PTP signaling via PHD2 inhibition has the potential to p

285 HIF2alpha activation increased VE-PTP expression, decreased VE-cadherin phosphorylation, p

286 HIF2alpha-induced VE-PTP expression enhanced dephosphorylation of VE-cadherin

287 urthermore, a small-molecule inhibitor of VE-PTP catalytic activity (AKB-9778) activated TIE2, enhanc

288 EC-specific protein tyrosine phosphatase (VE-PTP) and Src homology phosphatase 2 (SHP2), both of whic

289 endothelial protein tyrosine phosphatase (VE-PTP) is a HIF2alpha target.

290 endothelial-protein tyrosine phosphatase (VE-PTP) that promotes Tie2 activation and reduces vascular

291 endothelial-protein tyrosine phosphatase (VE-PTP), and von Willebrand factor (vWf).

292 endothelial-protein tyrosine phosphatase (VE-PTP), which negatively regulates TIE2 activation, is upr

293 These data support targeting VE-PTP to stabilize retinal and choroidal blood vessels and

294 helial barrier integrity, in part through VE-PTP expression and the resultant VE-cadherin dephosphory

295 We tested whether PTP could convert mossy fiber synapses from subdetonator

296 However, whether PTPs can actively regulate ROS levels in order to preven

297 gether our data provide a mechanism by which PTP inactivation induces signaling in pancreatic islets

298 us SFK effect on WNK4 by decreasing the WNK4-PTP-1D association because inhibition of SFK enabled SGK

299 These results show that the yeast PTP originates from F-ATP synthase and indicate that dim

300 receptor, protein-tyrosine phosphatase zeta (PTP-zeta) were upregulated in the kidney after I/R.