ライフサイエンスコーパス: PTP1B

1 PTP1B (protein-tyrosine phosphatase nonreceptor type 1,

2 PTP1B deficiency leads to increased PKM2 total tyrosine

3 PTP1B dephosphorylates PITX1 to weaken its protein stabi

4 PTP1B has a mobile so-called WPD loop (named for its thr

5 PTP1B inactivation prevents TrkA exit from soma and caus

6 PTP1B inhibited BRK by directly dephosphorylating the Ty

7 PTP1B inhibitors robustly augmented the antiviral effect

8 PTP1B interacts with activated TrkB receptor in mouse br

9 PTP1B is a ubiquitously expressed tyrosine phosphatase w

10 PTP1B overexpression impaired the sensitivity of sorafen

11 PTP1B overexpression reduces TrkB phosphorylation and ac

12 PTP1B overexpression resulted in reduction of Akt phosph

13 PTP1B was markedly up-regulated in the glomerulus, notab

14 PTP1B(-/-) cells showed elevated NF-kappaB activation in

15 and computational data on WT-PTP1B and >/=10 PTP1B variants in multiple states, we discovered a funda

16 to inhibit protein-tyrosine phosphatase 1B (PTP1B) activity, which acts to suppress apoptosis and st

17 ain via the protein tyrosine phosphatase 1B (PTP1B) and alpha- and beta-catenins.

18 sion of the protein-tyrosine phosphatase 1B (PTP1B) and in wild-type and PTP1B-deficient mice chronic

19 hosphatases protein tyrosine phosphatase 1B (PTP1B) and phosphatase and tensin homolog (PTEN) were fo

20 identified protein tyrosine phosphatase 1B (PTP1B) as a major target of H-RAS(V12)-induced ROS.

21 Protein tyrosine phosphatase 1B (PTP1B) counteracts leptin signaling and is a therapeutic

22 Neuronal protein-tyrosine phosphatase 1B (PTP1B) deficiency in mice results in enhanced leptin sig

23 sed hepatic protein-tyrosine phosphatase 1B (PTP1B) expression and enhanced PTP1B and IR interactions

24 (SOCS1) or protein-tyrosine phosphatase 1B (PTP1B) in this process.

25 Protein-tyrosine phosphatase 1B (PTP1B) is a physiological regulator of glucose homeostas

26 Protein tyrosine phosphatase 1B (PTP1B) is a ubiquitously expressed nonreceptor protein-t

27 Protein tyrosine phosphatase 1B (PTP1B) is a validated therapeutic target for the treatme

28 hibition of protein tyrosine phosphatase 1B (PTP1B) is associated with reduced cardiac dysfunction in

29 Protein tyrosine phosphatase 1B (PTP1B) is implicated in inflammatory signaling, but its

30 Protein-tyrosine phosphatase 1B (PTP1B) is the canonical enzyme for investigating how dis

31 Protein-tyrosine phosphatase 1B (PTP1B) regulates food intake (FI) and energy expenditure

32 trated that protein-tyrosine phosphatase 1B (PTP1B) was underexpressed in a panel of ovarian carcinom

33 onnected in Protein Tyrosine Phosphatase 1B (PTP1B), a drug target for diabetes and cancer that catal

34 action with protein tyrosine phosphatase 1B (PTP1B), an ER-associated protein tyrosine phosphatase in

35 gulation of protein tyrosine phosphatase 1B (PTP1B), an inhibitory phosphatase for EGFR.

36 (S-NO) and protein-tyrosine phosphatase 1B (PTP1B), and Akt phosphorylation at Ser(473) and inhibite

37 rate protein phosphotyrosine phosphatase 1B (PTP1B), and the relevance of this pathway to VEGF-induce

38 tivates the protein-tyrosine phosphatase 1B (PTP1B), and this could suppress many signaling pathways

39 to control protein tyrosine phosphatase 1B (PTP1B)-an important regulator of receptor tyrosine kinas

40 tivation of protein tyrosine phosphatase 1B (PTP1B).

41 nduction of protein-tyrosine phosphatase 1B (PTP1B).

42 the enzyme protein tyrosine phosphatase 1B (PTP1B).

43 Protein tyrosine phosphatase-1B (PTP1B) negatively regulates insulin and leptin signaling

44 MMP-9, and protein tyrosine phosphatase-1B (PTP1B), which negatively regulates the signaling of insu

45 eport that protein tyrosine phosphatases 1B (PTP1B) directly dephosphorylated PITX1 at Y160, Y175, an

46 mpaired hypothalamic leptin signaling, and a PTP1B inhibitor normalized PTP1B activity and restored l

47 ates copper, which enhanced its potency as a PTP1B inhibitor.

48 sulin signaling were prevented by suramin, a PTP1B inhibitor, or rosiglitazone that decreased PTP1B l

49 ; targeting the PITX1-p120RasGAP axis with a PTP1B inhibitor may provide a new therapy for patients w

50 conducted in the presence of reduced active PTP1B, which enriches antibodies to epitopes unique to t

51 We showed that calnexin and PTP1B form UBC9-dependent complexes, revealing a previou

52 hosphorylated SRC and its regulators CSK and PTP1B (PTPN1) was conducted in 30 synovial sarcomas.

53 not induce death, phosphorylation of JNK and PTP1B expression and enzymatic activity were increased.

54 F stimulation, complexes containing Mena and PTP1B are recruited to the EGFR, causing receptor dephos

55 Both silencing of PTP1B and PTP1B inhibitor up-regulated the PITX1-p120RasGAP axis t

56 Shc recruited tyrosine phosphatases SHP2 and PTP1B to Jak3 and thereby dephosphorylated Jak3.

57 phosphatase 1B (PTP1B) and in wild-type and PTP1B-deficient mice chronically treated with APAP.

58 PTP1B, mouse hepatocytes from wild-type and PTP1B-deficient mice, and a mouse model of chronic APAP

59 The PTPs, YopH and PTP1B, have very different catalytic rates; however, we

60 supported the potential interaction between PTP1B and sorafenib.

61 Here we investigated interactions between PTP1B and the peroxiredoxin 2 (Prx2)/thioredoxin 1 (Trx1

62 tivation, which can be completely blocked by PTP1B overexpression.

63 TrkA receptors are then dephosphorylated by PTP1B, an ER-resident protein tyrosine phosphatase, prio

64 This was due to dephosphorylation by PTP1B of IGF-1R beta-subunit and BRK/PTK6, an SRC-like p

65 ctor receptor (EGFR), which is influenced by PTP1B.

66 in hepatocytes, which is in part mediated by PTP1B.

67 R2 phosphorylation, which can be restored by PTP1B siRNA.

68 implicating negative regulation of VEGFR2 by PTP1B.

69 ata for the first time demonstrate a calpain/PTP1B/VEGFR2 negative feedback loop in the regulation of

70 These data implicate calpain/PTP1B negative feedback regulation of VEGFR2, in additio

71 In contrast, PTP1B potentiated SRC activity, but not by dephosphoryla

72 hepatocellular carcinoma, directly decreased PTP1B activity and promoted the expression of PITX1 and

73 B inhibitor, or rosiglitazone that decreased PTP1B levels.

74 eceptor kinase B (TrkB) receptor is a direct PTP1B substrate and implicate PTP1B in the regulation of

75 interference RNA transfection downregulated PTP1B expression and enhanced Akt phosphorylation in sub

76 with neuronal ablation of LMO4 have elevated PTP1B activity and impaired hypothalamic leptin signalin

77 Therefore, the elevated PTP1B that accompanies disruption of MECP2 function in R

78 onstrated that the PTPN1 gene, which encodes PTP1B, was a target of MECP2 and that disruption of MECP

79 a whole-brain deletion of the gene encoding PTP1B (Ptpn1) are lean, leptin-hypersensitive, and resis

80 protein tyrosine phosphatase Ptpn1 (encoding PTP1B) enables a highly invasive disease.

81 n of endothelial dysfunction, by endothelial PTP1B deficiency, is sufficient to reduce cardiac dysfun

82 Investigation of the role of endothelial PTP1B in these effects may provide direct evidence of th

83 osphatase 1B (PTP1B) expression and enhanced PTP1B and IR interactions, which contributed to the decr

84 s opens up exciting opportunities to exploit PTP1B inhibitors as anxiolytics.

85 When Mena(INV) is expressed, PTP1B recruitment to the EGFR is impaired, providing a m

86 mechanism in which Prx2 or Trx1 facilitates PTP1B oxidation.

87 s recognized that dynamics are essential for PTP1B function, the data collected thus far have not res

88 These data reveal an important role for PTP1B as a negative regulator of BRK and IGF-1Rbeta sign

89 Our results establish a novel role for PTP1B in regulating insulin action in the VMH and sugges

90 esults establish a tumor suppressor role for PTP1B in the myeloid lineage cells, with evidence that i

91 Aortic discs isolated from PTP1B siRNA-transfected mice also had augmented endothel

92 Interestingly, spleen leukocytes from PTP1B(-/-) mice exhibited an increased chemotaxis, chemo

93 Zip14 KO mice showed greater hepatic PTP1B activity during ER stress.

94 e endosomes where it is switched-off by high PTP1B activity.

95 ecycling through perinuclear areas with high PTP1B activity.

96 We then identified PTP1B, a ubiquitously expressed phosphatase, as the targ

97 or is a direct PTP1B substrate and implicate PTP1B in the regulation of the central brain-derived neu

98 Importantly, PTP1B inhibition and/or calpain overexpression significa

99 Importantly, PTP1B pharmacological inhibition increased PKM2 Tyr-105

100 In PTP1B and VHR, two new allosteric clusters were identifi

101 elp explain previously observed increases in PTP1B oxidation and PDGF receptor phosphorylation in Trx

102 lterations in islet alpha/beta cell ratio in PTP1B(-/-) mice.

103 d by overexpression or Ca/A23187 resulted in PTP1B cleavage, which can be blocked by ALLN.

104 ted LMO4, less oxidized PTP1B, and increased PTP1B activity in the hypothalamus.

105 ppressed insulin sensitization and increased PTP1B and PTEN.

106 ed PTP1B is an effective strategy to inhibit PTP1B function; it is possible that this approach may be

107 kt phosphorylation at Ser(473) and inhibited PTP1B activity.

108 NO also inhibits PTP1B activity, thereby enhancing insulin signaling.

109 found that LIM domain only 4 (LMO4) inhibits PTP1B activity by increasing the oxidized inactive form

110 hosphorylating SRC itself directly; instead, PTP1B regulated the interaction between CBP/PAG and CSK.

111 ere used to examine the mechanisms involving PTP1B in the effects of APAP on glucose homeostasis and

112 n signaling in VMH neurons from mice lacking PTP1B in SF-1 neurons.

113 LysM-PTP1B(-/-) mice lacking PTP1B in the innate myeloid cell lineage displayed a dys

114 s not observed in cells specifically lacking PTP1B.

115 Likewise, PTP1B deficiency in human or mouse hepatocytes protected

116 Modulation of local PTP1B and/or calpain activities may prove beneficial in

117 nction in hematopoietic cells, Tie2-Cre/LoxP-PTP1B mice were lethally irradiated and reconstituted wi

118 etion of PTP1B was obtained by crossing LoxP-PTP1B with Tie2-Cre mice.

119 LysM PTP1B mice were protected against lipopolysaccharide (LP

120 effects of macrophage PTP1B deficiency; LysM PTP1B mice exhibited improved glucose and insulin tolera

121 HF-fed LysM PTP1B mice had increased basal and LPS-induced IL-10 lev

122 IL-10-induced STAT3 phosphorylation in LysM PTP1B BMDMs.

123 yeloid-cell (LysM) PTP1B knockout mice (LysM PTP1B).

124 In vitro, LPS-treated LysM PTP1B bone marrow-derived macrophages (BMDMs) displayed

125 le-body metabolism using myeloid-cell (LysM) PTP1B knockout mice (LysM PTP1B).

126 LysM-PTP1B(-/-) mice lacking PTP1B in the innate myeloid cell

127 to equally beneficial effects of macrophage PTP1B deficiency; LysM PTP1B mice exhibited improved glu

128 We assessed the role of macrophage PTP1B in inflammation and whole-body metabolism using my

129 es suggest caution when targeting macrophage PTP1B, due to its potential anti-inflammatory role.

130 yr-105 and Tyr-148 as key sites that mediate PTP1B-PKM2 interaction.

131 nate, potently facilitates H(2)O(2)-mediated PTP1B inactivation in the presence of thioredoxin reduct

132 is important for the recruitment of the Mena-PTP1B complex to the EGFR.

133 In mice, PTP1B deletion reduces axonal TrkA levels and attenuates

134 These data show that skeletal muscle PTP1B gene expression is increased in African American s

135 Our studies implicate myeloid PTP1B in negative regulation of STAT3/IL-10-mediated sig

136 ed inflammation in the hippocampus, neuronal PTP1B ablation did not.

137 nitive decline and demonstrate that neuronal PTP1B hastens neurodegeneration and cognitive decline in

138 signaling, and a PTP1B inhibitor normalized PTP1B activity and restored leptin control of circulatin

139 dentify pyruvate kinase M2 (PKM2) as a novel PTP1B substrate in adipocytes.

140 One of these novel PTP1B variants, a splice variant lacking exon 6 (PTP1BDe

141 Importantly, neuron-targeted ablation of PTP1B also prevented cognitive decline and neuron loss b

142 Neuronal ablation of PTP1B did not affect cerebral amyloid levels or plaque n

143 with trodusquemine or selective ablation of PTP1B in neurons prevents hippocampal neuron loss and sp

144 intestinal epithelium through activation of PTP1B and subsequent suppression of intestinal tumorigen

145 ingly, that small changes in the activity of PTP1B can cause large shifts in the phosphorylation stat

146 sibility that COP1 modulates the activity of PTP1B, the major insulin receptor tyrosine phosphatase.

147 atase activity as well as the association of PTP1B with IRbeta.

148 are essential for the allosteric control of PTP1B activity.

149 amic unity throughout the catalytic cycle of PTP1B.

150 hat global or myeloid-specific deficiency of PTP1B in mice decreases lifespan.

151 onstrate that myeloid-specific deficiency of PTP1B is sufficient to promote the development of acute

152 Endothelial deletion of PTP1B was obtained by crossing LoxP-PTP1B with Tie2-Cre

153 mouse with endothelial-specific deletion of PTP1B.

154 also in the adjacent alpha-helical domain of PTP1B.

155 The protective effect of PTP1B inhibition or ablation coincides with the restorat

156 brain contribute to the metabolic effects of PTP1B deficiency remains unclear.

157 ibute to the beneficial metabolic effects of PTP1B deficiency.

158 ale to investigate the anticancer effects of PTP1B inhibitors currently being studied clinically for

159 Furthermore, high expression of PTP1B was significantly associated with poor tumor diffe

160 tissue from 155 patients, the expression of PTP1B was significantly in tumor parts higher than nontu

161 ay was attenuated upon ectopic expression of PTP1B.

162 levels directly correlate with the extent of PTP1B oxidation.

163 on of the sulfenic acid intermediate form of PTP1B by TrxR1 and is therefore distinct from the previo

164 that covalently capture the oxidized form of PTP1B generated in cells during insulin signaling events

165 by increasing the oxidized inactive form of PTP1B.

166 opes common to oxidized and reduced forms of PTP1B.

167 s a consequence of oxidative inactivation of PTP1B and inhibition of miRNA-mediated gene silencing.

168 Inactivation of PTP1B was necessary and sufficient to induce premature s

169 umor samples, we further found inhibition of PTP1B activity and up-regulation of the PITX1-p120RasGAP

170 Pharmacological inhibition of PTP1B ameliorated the effects of MECP2 disruption in mou

171 Inhibition of PTP1B led to increased tyrosine phosphorylation of TRKB

172 Pharmacological inhibition of PTP1B may have therapeutic potential in the treatment of

173 Intriguingly, while systemic inhibition of PTP1B reduced inflammation in the hippocampus, neuronal

174 Conversely, inhibition of PTP1B with a small molecular inhibitor, MSI-1436, increa

175 , we show that pharmacological inhibition of PTP1B with trodusquemine or selective ablation of PTP1B

176 ession could be ameliorated by inhibition of PTP1B.

177 ecific, and orally bioavailable inhibitor of PTP1B.

178 treated with a pharmacological inhibitor of PTP1B.

179 gy and identified as effective inhibitors of PTP1B in vitro.

180 In addition, lack of PTP1B promoted an altered NADPH oxidase (NOX) expression

181 tion was associated with increased levels of PTP1B in RTT models.

182 e, activity, and subcellular localization of PTP1B, affords changes in activity that match those elic

183 nine mutations in the catalytic acid loop of PTP1B and VHR.

184 Genetic or pharmacologic modulation of PTP1B activity regulated IFN1 signaling in a manner depe

185 ween K8 and a "substrate-trapping" mutant of PTP1B (D181A).

186 Overexpression of PTP1B inhibited VEGF-induced VEGFR2 and Akt phosphorylat

187 Prostate-specific overexpression of PTP1B was not sufficient to initiate prostate cancer, ar

188 In fact, EGF-induced cellular oxidation of PTP1B was completely dependent on the presence of bicarb

189 uce reactive oxygen species and oxidation of PTP1B, may be controlled by several other putative mecha

190 xnrd1(-/-)) displayed increased oxidation of PTP1B, whereas SHP2 oxidation was unchanged.

191 ntly capture the sulfenyl amide "oxoform" of PTP1B generated during insulin signaling events.

192 ion of individual PTPs, with a preference of PTP1B over SHP2 activation.

193 study of Ile, Leu, and Val (ILV) residues of PTP1B, which, because of its substantially increased sen

194 Restoration of PTP1B expression led to enhanced activation of BAD, one

195 Stable restoration of PTP1B in those cancer cell lines substantially decreased

196 contribution of calnexin to the retention of PTP1B at the ER membrane.

197 The current study addresses the role of PTP1B in podocyte injury and proteinuria.

198 We next examined a potential role of PTP1B in VEGF-induced angiogenesis.

199 However, the significance of PTP1B in AD pathology remains unclear.

200 Both silencing of PTP1B and PTP1B inhibitor up-regulated the PITX1-p120Ras

201 ndings identify PKM2 as a novel substrate of PTP1B and provide new insights into the regulation of ad

202 We identified PAG as a substrate of PTP1B, and dephosphorylation abolished recruitment of th

203 argonaute 2 (AGO2) as a direct substrate of PTP1B.

204 e observed that RNAi-mediated suppression of PTP1B resulted in opposing effects on the activity of BR

205 findings support the preclinical testing of PTP1B inhibitors for prostate cancer treatment.

206 the effects of high-fat diet consumption on PTP1B expression and NF-kappaB activation.

207 culum and abolished its inhibitory effect on PTP1B.

208 majority of tumors; dysregulation of CSK or PTP1B was excluded as the reason for the activation of t

209 The sulfenyl amide residue found in oxidized PTP1B presents a unique electrophilic sulfur center that

210 d had less palmitoylated LMO4, less oxidized PTP1B, and increased PTP1B activity in the hypothalamus.

211 Covalent capture of oxidized PTP1B could permanently disable the intracellular pool o

212 vs illustrate that stabilization of oxidized PTP1B is an effective strategy to inhibit PTP1B function

213 e, we employed a dipeptide model of oxidized PTP1B to investigate the nucleophilic capture of the sul

214 described reactivation of end-point oxidized PTP1B, which requires both Trx1 and TrxR1.

215 R1 substrate TRP14 also reactivated oxidized PTP1B, but not SHP2.

216 Trx1 reduced oxidized PTP1B in vitro but failed to reactivate oxidized SHP2.

217 Furthermore, in vivo-oxidized PTP1B was reduced by exogenously added Trx system compon

218 Furthermore, panc-PTP1B KO mice exhibited enhanced cerulein- and arginine-

219 necrosis factor-alpha were increased in panc-PTP1B KO mice compared with controls.

220 and lipase were significantly higher in panc-PTP1B KO mice compared with controls.

221 in AP, we used pancreas PTP1B knockout (panc-PTP1B KO) mice and determined the effects of pancreatic

222 nced features of AP in cerulein-treated panc-PTP1B KO mice compared with controls.

223 TP1B may have a role in AP, we used pancreas PTP1B knockout (panc-PTP1B KO) mice and determined the e

224 findings reveal a novel role for pancreatic PTP1B in cerulein- and arginine-induced acute pancreatit

225 ice and determined the effects of pancreatic PTP1B deficiency on cerulein- and arginine-induced acute

226 nd asked whether activation of a phosphatase PTP1B participates in the disease process.

227 chemotaxis via dysregulation of phosphatase PTP1B and more recently in haptotaxis via interaction wi

228 017) report that the ER-resident phosphatase PTP1B is required to prime TrkA for axonal transport.

229 yrosine 421 is suppressed by the phosphatase PTP1B, and that PTP1B localization to the invadopodium i

230 cortactin at tyrosine 421 by the phosphatase PTP1B.

231 constitutively with the tyrosine phosphatase PTP1B and mediates a novel negative feedback mechanism t

232 identified the protein tyrosine phosphatase PTP1B as a therapeutic candidate for treatment of RTT.

233 unction for the protein tyrosine phosphatase PTP1B in myeloid lineage cells, with evidence that its g

234 hibition of the protein-tyrosine phosphatase PTP1B increased K8 Tyr-267 phosphorylation, decreased so

235 Protein tyrosine phosphatase PTP1B is a critical regulator of signaling pathways cont

236 The protein-tyrosine phosphatase PTP1B is a negative regulator of insulin and leptin sign

237 reveal that the protein tyrosine phosphatase PTP1B is upregulated in patients with RTT and in murine

238 Recently, the protein tyrosine phosphatase PTP1B was identified as a novel regulator of stress-indu

239 ng sites where the ER-localized phosphatase, PTP1B, interacts with endocytosed EGFR before the recept

240 Deletion of the phosphatases PTP1B and TCPTP enhanced insulin and leptin signaling in

241 EGF signaling, protein tyrosine phosphatases PTP1B and TC-PTP, and VE-cadherin.

242 In cultured mouse podocytes, PTP1B knockdown and/or pretreatment with the PTP1B inhib

243 This study presents PTP1B as a mechanism-based therapeutic target for RTT, v

244 Instead, these proteins prevented PTP1B inactivation by H2O2 Intriguingly, we discovered t

245 increased in zinc content and proliferation; PTP1B was inhibited and phosphorylation of c-Met increas

246 iscovered that TrxR1/NADPH directly protects PTP1B from inactivation when present during the H2O2 exp

247 rthritis patients have significantly reduced PTP1B expression.

248 vated the NFkappaB pathway, and up-regulated PTP1B and PTEN, these effects being mediated by LTB4 rec

249 patocytes, Huh7 hepatoma cells with silenced PTP1B, mouse hepatocytes from wild-type and PTP1B-defici

250 The use of a specific PTP1B inhibitor also protected against lipopolysaccharid

251 evelopment have produced potent and specific PTP1B inhibitors, but these inhibitors lack oral bioavai

252 Mice with a B cell-specific PTP1B deficiency show increased T cell-dependent immune

253 of which were inhibited by podocyte-specific PTP1B knockout and the PTP1B inhibitor.

254 In contrast, podocyte-specific PTP1B transgenic male mice developed spontaneous protein

255 Moreover, podocyte-specific PTP1B transgenic mice showed increased glomerular expres

256 ort that DPM-1001, an analog of the specific PTP1B inhibitor trodusquemine (MSI-1436), is a potent, s

257 Specifically, PTP1B counteracts p38 mitogen-activated protein kinase (

258 In summary, PTP1B up-regulation in podocytes induces a migratory res

259 sically interacted with PTP1B and suppressed PTP1B phosphatase activity as well as the association of

260 ive picture on how the validated drug target PTP1B functions.

261 ctively, our data indicate that by targeting PTP1B, miR-744 plays a feed-forward role in regulating t

262 s and provide strong evidence that targeting PTP1B has potential as a viable therapeutic strategy for

263 ur preclinical study suggests that targeting PTP1B may be a new strategy to intervene in the progress

264 sed-bicyclic triazolo-thiadiazoles targeting PTP1B and its analogs could be the therapeutic drug-seed

265 uppressed by the phosphatase PTP1B, and that PTP1B localization to the invadopodium is reduced by Men

266 aken together, our findings demonstrate that PTP1B is a novel physiological regulator of TrkB and tha

267 We demonstrated that PTP1B was a negative regulator of tyrosine phosphorylati

268 We discovered that PTP1B exhibits dynamics at three distinct time scales.

269 We have found that PTP1B deficiency conferred resistance to TGF-beta suppre

270 Using purified proteins, we also found that PTP1B is relatively insensitive to inactivation by H2O2

271 We show here that PTP1B negatively regulates CD40, B cell activating facto

272 orafenib in vitro and in vivo, implying that PTP1B has a significant effect on sorafenib-induced apop

273 We report that PTP1B protein expression was increased in the early phas

274 Thus, these data show that PTP1B activity is not controlled by a single functional

275 Furthermore, our data show that PTP1B uses conformational and dynamic allostery to regul

276 Second, we showed that PTP1B (13)C-methyl group side chain fast time-scale dyna

277 In summary, our results suggest that PTP1B deficiency confers resistance to TGF-beta through

278 Our data suggest that PTP1B plays an important role in the control of B cell a

279 but much milder, phenotype, suggesting that PTP1B also acts in other neurons to regulate metabolism.

280 f the PITX1-p120RasGAP axis, suggesting that PTP1B inhibitor may be effective for the treatment of he

281 The PTP1B-dependent decline of PITX1 reduced its transcripti

282 by podocyte-specific PTP1B knockout and the PTP1B inhibitor.

283 s hepatic insulin signaling by enhancing the PTP1B/IR interaction that is induced by ER stress, indic

284 2 cytokine levels were elevated early in the PTP1B(-/-) mice.

285 ce, while inhibited ER stress normalized the PTP1B expression and restored insulin signaling in the C

286 Podocyte-specific ablation of the PTP1B gene ameliorated proteinuria induced by lipopolysa

287 PTP1B knockdown and/or pretreatment with the PTP1B inhibitor blunted lipopolysaccharide-induced cell

288 In peripheral tissues, PTP1B regulates insulin signaling, but its effects on CN

289 TEN targets PTK6, with efficiency similar to PTP1B, a phosphatase that directly dephosphorylates PTK6

290 Here, we report the expression of truncated PTP1B mRNA variants identified in cHL cell lines and pri

291 Thus, unleashed PTP1B activity attributable to loss of LMO4 palmitoylati

292 ce of these findings in the context of using PTP1B inhibitors to increase the therapeutic efficacy of

293 and increased K8 filament bundling, whereas PTP1B overexpression had the opposite effects.

294 on of downstream signaling pathways, whereas PTP1B inhibition augments TrkB signaling.

295 To investigate whether PTP1B may have a role in AP, we used pancreas PTP1B knoc

296 on in bovine aortic endothelial cells, while PTP1B siRNA increased both, implicating negative regulat

297 (+)-granatumine A, a limonoid alkaloid with PTP1B inhibitory activity, in ten steps.

298 dicated that COP1 physically interacted with PTP1B and suppressed PTP1B phosphatase activity as well

299 Endothelial cells transfected with PTP1B siRNA showed faster wound closure in response to V

300 ew experimental and computational data on WT-PTP1B and >/=10 PTP1B variants in multiple states, we di