ライフサイエンスコーパス: PTP

1 PTP activities from thousands of individual cells were m

2 PTP activity can readily be diminished by reactive oxyge

3 PTP inhibition prevents necrosis and rescues regeneratio

4 PTP is sensitive to the PKC inhibitor GF109203X in both

5 PTPs need to undergo oxidative inhibition for activation

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

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

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

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

10 Engineering of the activatable PTPs (actPTPs) is achieved by the introduction of three

11 ium or reactive oxygen species that activate PTP have been proposed.

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

13 2-9895), we showed that ROS production after PTP opening can be sustained when complex III is damaged

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

15 on multiple species delimitation algorithms (PTP, ABGD, Objective Clustering) applied to a dataset co

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

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

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

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

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

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

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

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

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

25 Of the 1325 patients who had a low C-PTP (1285 patients) or moderate C-PTP (40 patients) and

26 These included 315 patients who had a low C-PTP and a d-dimer level of 500 to 999 ng per milliliter

27 A combination of a low C-PTP and a d-dimer level of less than 1000 ng per millili

28 further testing in outpatients with a low C-PTP and a d-dimer level of less than 1000 ng per millili

29 m is considered to be ruled out with a low C-PTP and a d-dimer level of less than 500 ng per millilit

30 ad a low C-PTP (1285 patients) or moderate C-PTP (40 patients) and a negative d-dimer test (i.e., <10

31 1000 ng per milliliter or with a moderate C-PTP and a d-dimer level of less than 500 ng per millilit

32 per milliliter in patients with a moderate C-PTP.

33 s with a low clinical pretest probability (C-PTP) and by a d-dimer level of less than 500 ng per mill

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

35 that a substantial fraction of the classical PTP family will be compatible with the act-engineering a

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

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

38 etime by recruiting leupaxin, which controls PTP-PEST activity and thereby paxillin phosphorylation a

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

40 30 APs at 100 Hz) in cKO over control during PTP.

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

42 after application of phorbol ester or during PTP.

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

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

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

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

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

48 inst Protein Tyrosine Phosphatase 1B enzyme (PTP-1B), overexpressed in type-two diabetes, was investi

49 LPS is mediated by the conserved well-folded PTP domain through multivalent electrostatic interaction

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

51 se results provide a plausible mechanism for PTP inactivation during cell signaling and explain long-

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

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

54 ic assays to confirm loss of ESCRT-II and HD-PTP function.

55 1 were unchanged following loss of EAP20, HD-PTP, or BROX.IMPORTANCE HSV-1 is a pathogen of the human

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

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

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

59 protein sorting 25) and the Bro1 proteins HD-PTP (His domain-containing protein tyrosine phosphatase)

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

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

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

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

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

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

66 etermine the role of classic PKC isoforms in PTP.

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

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

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

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

71 , the first molecule to successfully inhibit PTP activity through degradation has been developed.

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

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

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

75 KIM-PTPs bind and dephosphorylate mitogen-activated protein

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

77 This gene encodes for a receptor-like PTP, PTPRJ (or CD148), which is expressed abundantly in

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

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

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

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

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

83 over 4500-fold preference over 25 mammalian PTPs.

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

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

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

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

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

89 resolve the long-standing mystery of the MMC/PTP and demonstrate that Ca(2+) can transform the energy

90 nit of F-ATP synthase that activates the MMC/PTP, and were inhibited by Mg(2+) and adenine nucleotide

91 ) elicits currents matching those of the MMC/PTP.

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

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

94 c targets for cancers harboring these mutant PTPs.

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

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

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

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

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

100 hances neurotransmitter release and occludes PTP.

101 chemical-biological tool for the control of PTP activity and the study of PTP function.

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

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

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

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

106 o reduce PTP opening either by inhibition of PTP or inhibiting the rise in mitochondrial calcium or r

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

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

109 the control of PTP activity and the study of PTP function.

110 Because SYD-2 is a substrate of PTP-3/LAR PTPR, we speculate a role of this phosphatase

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

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

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

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

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

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

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

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

119 in the selective targeting of SHP2 and other PTP family members.

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

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

122 We propose a position-theta-phase (PTP) model that captures the simultaneous expression of

123 activity of the protein tyrosine phosphatase PTP-PEST, which controls paxillin phosphorylation, requi

124 Protein tyrosine phosphatase (PTP) 4A3 is frequently overexpressed in human solid tumo

125 ach to measure protein tyrosine phosphatase (PTP) activity in individual cells using self-assembled m

126 that classical protein tyrosine phosphatase (PTP) domains from multiple subfamilies can be systematic

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

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

129 dothelial (VE) protein tyrosine phosphatase (PTP) is an endothelial-specific phosphatase that stabili

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

131 he nonreceptor protein-tyrosine phosphatase (PTP) SHP2 is encoded by the proto-oncogene PTPN11 and is

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

133 e non-receptor protein tyrosine phosphatase (PTP) SHP2, encoded by PTPN11, plays an essential role in

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

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 ants lacking receptor tyrosine phosphatases (PTP) Ptp10D and Ptp4E, clear luminal proteins and disass

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

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

140 Protein-tyrosine phosphatases (PTPs) counteract protein tyrosine phosphorylation and co

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

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

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

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

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

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

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

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

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

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

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

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

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

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

155 achannel (MMC)/permeability transition pore (PTP), a key effector of cell death, remains controversia

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

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

158 mitochondrial permeability transition pore (PTP).

159 eatures of the permeability transition pore (PTP).

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

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

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

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

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

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

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

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

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

169 sicle release and post-tetanic potentiation (PTP).

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

171 ive CAD by combining a pre-test probability (PTP) model (Diamond-Forrester approach using sex, age, a

172 alyses were applied: Poisson tree processes (PTP), automatic barcode gap discovery (ABGD), and genera

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

174 ly with Syt1-dependent mechanisms to produce PTP by exerting multiplicative effects on release rates.

175 ole of a previously unidentified gene, PTPN (PTP-like Nucleotidase) in plant drought tolerance.

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

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

178 ubfamilies of both receptor and non-receptor PTPs.

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

180 Strategies to reduce PTP opening either by inhibition of PTP or inhibiting th

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

182 ategy that couples an allosteric, reversible PTP inhibitor with an E3 ligase targeting ligand through

183 uate LLPS of SHP2 mutants, which boosts SHP2 PTP activity.

184 SP-PTP also differentially regulates the expression of appr

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

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

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

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

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

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

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

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

193 expression was significantly reduced and TC-PTP expression was inversely correlated with the increas

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

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

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

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

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

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

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

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

202 We found overexpression of TC-PTP increased epidermal sensitivity to DMBA-induced apop

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

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

205 T3, STAT5, or AKT reversed the effects of TC-PTP overexpression on epidermal survival and proliferati

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

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

208 Mice overexpressing TC-PTP in the epidermis developed significantly reduced num

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

210 T-cell protein tyrosine phosphatase (TC-PTP), encoded by Ptpn2, has been shown to function as a

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

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

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

214 , we generated a novel epidermal-specific TC-PTP-overexpressing (K5HA.Ptpn2) mouse model to show that

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

216 ing (K5HA.Ptpn2) mouse model to show that TC-PTP contributes to the attenuation of chemically induced

217 mous cell carcinomas (SCCs) revealed that TC-PTP expression was significantly reduced and TC-PTP expr

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

219 Our findings demonstrate that TC-PTP is a potential therapeutic target for the prevention

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

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

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

223 uman diseases but also provide evidence that PTP may be regulated by LLPS that can be therapeutically

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

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

226 Lastly, epistatic analysis revealed that PTP-3 is upstream of SYD-2 to regulate its intramolecula

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

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

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

230 We conclude that PTPs and Btk29A regulate WASH activity to balance the en

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

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

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

234 he inner mitochondrial membrane known as the PTP (permeability transition pore) and that opening of t

235 cteristic curves of obstructive CAD: for the PTP model, 72 (95% confidence intervals [CI]: 71 to 74);

236 the identity of the protein(s) that form the PTP and how they are activated by calcium and reactive o

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

238 ton translocation is involved in forming the PTP.

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

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

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

242 adenine nucleotides, which also inhibit the PTP.

243 A major limitation of inhibiting the PTP is the lack of knowledge about the identity of the p

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

245 candidates for the pore-forming unit of the PTP and discuss recent data suggesting that assumption t

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

247 eine residues within a conserved loop of the PTP domain, and the positions of the sensitizing mutatio

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

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

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

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

252 reserve the characteristic properties of the PTP.

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

254 eated to either stimulate OXPHOS or open the PTP.

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

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

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

258 ccurately in the validation cohorts than the PTP model, and markedly increased the area under the rec

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

260 ent data suggesting that assumption that the PTP is formed by a single molecular identity may need to

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

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

263 We use the PTP model to assess the effect of running speed in place

264 We use the PTP model to compare candidate mechanisms of speed modul

265 novel regulator of inflammation in vivo; the PTP-type phosphatase Pez.

266 After lysis and incubation-during which the PTP enzymes act on the peptide substrate-the reaction su

267 lihood of CAD, as compared with 11% with the PTP model.

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

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

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

271 al likelihood (RF-CL) was calculated through PTP and risk factors, while the CACS-weighted clinical l

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

273 gest potential synergy of blocking their two PTP receptors.

274 15,411) and compared with a recently updated PTP table.

275 VE-PTP serves as an adaptor protein that through binding an

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

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

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

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

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

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

282 domain mutant interacting with GEF-H1 in VE-PTP-depleted endothelial cells reduced GEF-H1 activity a

283 Increased VE-PTP expression was dependent on hypoxia-inducible factor

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

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

286 Mechanistically, inhibition of VE-PTP activated endothelial nitric oxide synthase and led

287 In sum, we identify inhibition of VE-PTP as a promising therapeutic target to protect the kid

288 hough studies have focused on the role of VE-PTP in dephosphorylating VE-cadherin in the activated en

289 Genetic deletion of VE-PTP restored TIE2 activity independent of ligand availab

290 activated endothelium, little is known of VE-PTP's role in the quiescent endothelial monolayer.

291 endothelial protein tyrosine phosphatase VE-PTP (also known as PTPRB), which dephosphorylates TIE2,

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

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

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

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

296 We discovered that VE-PTP stabilizes VE-cadherin junctions by reducing the rat

297 Overexpression of the VE-PTP cytosolic domain mutant interacting with GEF-H1 in V

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

299 Thus, VE-PTP stabilizes VE-cadherin junctions and restricts endot

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

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

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