ライフサイエンスコーパス: PTP1B

1 PTP1B deficiency leads to increased PKM2 total tyrosine

2 PTP1B dephosphorylates PITX1 to weaken its protein stabi

3 PTP1B gene expression and protein abundance were determi

4 PTP1B gene expression was positively related to protein

5 PTP1B gene expression was significantly higher in subjec

6 PTP1B inactivation prevents TrkA exit from soma and caus

7 PTP1B induction by androgen occurred at the mRNA and pro

8 PTP1B inhibited BRK by directly dephosphorylating the Ty

9 PTP1B inhibitors robustly augmented the antiviral effect

10 PTP1B interacts with activated TrkB receptor in mouse br

11 PTP1B is a promising target for treatment of obesity and

12 PTP1B is a ubiquitously expressed tyrosine phosphatase w

13 PTP1B is capable of binding and dephosphorylating IFNAR1

14 PTP1B overexpression impaired the sensitivity of sorafen

15 PTP1B overexpression reduces TrkB phosphorylation and ac

16 PTP1B overexpression resulted in reduction of Akt phosph

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

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

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

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

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

22 related to protein tyrosine phosphatase 1B (PTP1B) and extracellular signal-regulated kinase 1/2 sig

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

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

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

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

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

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

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

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

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

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

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

34 Protein tyrosine phosphatase 1B (PTP1B) is postulated to modulate insulin action by depho

35 role of the protein-tyrosine phosphatase 1B (PTP1B) on the cellular responses to TGF-beta, using for

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

37 ment of the protein tyrosine phosphatase 1B (PTP1B) to a MET/VEGFR2 heterocomplex, thereby suppressin

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

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

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

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

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

43 ling, i.e., protein tyrosine phosphatase 1B (PTP1B), and increased phosphorylation of PTP1B.

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

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

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

47 ormation of protein tyrosine phosphatase 1B (PTP1B).

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

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

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

51 increased inflammation, expression of MMP-9, PTP1B, and aberrant growth factor levels are the main fa

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

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

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

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

56 ibitor series for p38alpha MAP kinase, ACK1, PTP1B, and thrombin.

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

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

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

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

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

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

63 epatocytes isolated from both PTP1B(+/+) and PTP1B(-/-) mice.

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

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

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

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

68 supported the potential interaction between PTP1B and sorafenib.

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

70 ized neonatal hepatocytes isolated from both PTP1B(+/+) and PTP1B(-/-) mice.

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

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

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

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

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

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

77 implicating negative regulation of VEGFR2 by PTP1B.

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

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

80 Briefly, lungs of OVA-challenged PTP1B(-/-) mice had elevated numbers of eosinophils and

81 microscopy revealed that, in OVA-challenged PTP1B(-/-) mice, blood leukocytes rapidly bound to endot

82 ipheral blood, and spleens of OVA-challenged PTP1B(-/-) mice.

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

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

85 B inhibitor, or rosiglitazone that decreased PTP1B levels.

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

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

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

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

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

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

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

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

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

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

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

97 mechanism in which Prx2 or Trx1 facilitates PTP1B oxidation.

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

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

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

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

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

103 Functionally, PTP1B depletion delayed the growth of androgen-dependent

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

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

106 ecycling through perinuclear areas with high PTP1B activity.

107 However, PTP1B was also required for optimal cell migration of an

108 However, PTP1B's function during inflammation in vivo is not know

109 An RNAi-based screen identified PTP1B as a specific regulator of IFNAR1 endocytosis stim

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

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

112 ulator of PTPN1 transcription and implicated PTP1B in a tumor-promoting role in prostate cancer.

113 Importantly, PTP1B inhibition and/or calpain overexpression significa

114 Importantly, PTP1B pharmacological inhibition increased PKM2 Tyr-105

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

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

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

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

119 d at the mRNA and protein levels to increase PTP1B activity.

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

121 ppressed insulin sensitization and increased PTP1B and PTEN.

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

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

124 es the levels of insulin-signaling inhibitor PTP1B.

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

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

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

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

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

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

131 s not observed in cells specifically lacking PTP1B.

132 Likewise, PTP1B deficiency in human or mouse hepatocytes protected

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

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

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

136 LysM PTP1B mice were protected against lipopolysaccharide (LP

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

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

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

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

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

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

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

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

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

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

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

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

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

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

151 etermine the relationship of skeletal muscle PTP1B to whole-body insulin sensitivity.

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

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

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

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

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

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

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

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

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

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

162 mouse with endothelial-specific deletion of PTP1B.

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

164 ibute to the beneficial metabolic effects of PTP1B deficiency.

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

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

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

168 ay was attenuated upon ectopic expression of PTP1B.

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

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

171 by increasing the oxidized inactive form of PTP1B.

172 opes common to oxidized and reduced forms of PTP1B.

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

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

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

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

177 Inhibition of PTP1B led to increased tyrosine phosphorylation of TRKB

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

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

180 treated with a pharmacological inhibitor of PTP1B.

181 ecific, and orally bioavailable inhibitor of PTP1B.

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

183 ization of clinically relevant inhibitors of PTP1B.

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

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

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

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

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

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

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

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

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

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

194 1B (PTP1B), and increased phosphorylation of PTP1B.

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

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

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

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

199 Overexpression and interference RNA of PTP1B were performed in primary human skeletal muscle cu

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

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

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

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

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

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

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

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

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

209 culum and abolished its inhibitory effect on PTP1B.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

228 P14 was essential for control of phosphatase PTP1B activity and phosphorylation of c-Met during liver

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

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

231 c zinc inhibited activity of the phosphatase PTP1B and increased phosphorylation of c-Met, which prom

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

233 cortactin at tyrosine 421 by the phosphatase PTP1B.

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

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

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

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

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

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

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

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

242 found that the protein tyrosine phosphatase PTP1B, a well-established regulator of metabolic signali

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

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

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

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

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

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

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

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

251 rthritis patients have significantly reduced PTP1B expression.

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

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

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

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

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

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

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

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

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

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

262 In summary, PTP1B functions as a critical negative regulator to limi

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

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

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

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

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

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

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

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

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

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

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

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

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

276 It is reported that PTP1B limits cytokine signaling in vitro.

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

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

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

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

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

282 The PTP1B-dependent decline of PITX1 reduced its transcripti

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

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

285 onse elements within the first intron of the PTP1B encoding gene PTPN1, correlating with an AR-mediat

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 In this report, we determined whether PTP1B deficiency affects allergic inflammation in vivo.

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

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

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