ライフサイエンスコーパス: PTEN

1 defective phosphatase and tensin homologue (PTEN).

2 y loss-of-function mutations or deletions in PTEN.

3 vo growth of melanomas harboring mutant BRAF/PTEN.

4 ance through activating the tumor suppressor PTEN.

5 st ranking prediction (TNRC6B) as a ceRNA of PTEN.

6 egulating expression of the tumor suppressor PTEN.

7 stability and nuclear localization of mutant PTEN.

8 by the phosphatase and tensin homolog DAF-18/PTEN.

9 ically associated with germline mutations in PTEN.

10 es with triple deletions in Trp53, Brca2 and Pten.

11 er cancer in mice with hepatic disruption of Pten.

12 edian PFS was longer in patients with normal PTEN (13.5 v 6.7 months; P = .02), TP53 (13.5 v 7.7 mont

13 gnaling downregulated PD-1/PD-L1 in a Tgfbr1/Pten 2cKO HNSCC mouse model.

14 trating that Abl/Arg cooperate with PI3K/Akt/PTEN, a parallel pathway that is associated with intrins

15 PTEN activity is often lost in prostate cancer.

16 Modulating PTEN activity may have high therapeutic potential to all

17 We propose that rapid alteration of PTEN activity through changes in its phosphorylation sta

18 Overall, our results showed that PTEN acts to prevent the proliferation of a progenitor n

19 ating enzyme E2S (UBE2S) is regulated by the PTEN/Akt pathway and that its degradation depends on the

20 ancers that still retain at least one intact PTEN allele.

21 We found that nuclear PTEN alone is sufficient to regulate soma size.

22 Here we show that PTEN also functions as a PI(3,4)P2 3-phosphatase, both i

23 ted retrospectively for NOTCH1/FBXW7/RAS and PTEN alterations.

24 and tensin homolog deleted on chromosome 10 (PTEN), alters the invasive potential of melanoma cells i

25 TR transport to the membrane, have increased PTEN amounts.

26 tabilizes Bmi-1 and hence inhibits the TP53, PTEN and CDKN1A/CDKN2A pathway.

27 onformation, enhancing polyubiquitination of PTEN and decreasing protein stability.

28 at were doubly mutant in prostate tissue for Pten and Erk5 (prostate DKO) exhibited a markedly increa

29 recurrence associated with combined loss of PTEN and FOXP1-SHQ1 genes.

30 e consider a set of miRNAs known to regulate PTEN and identify high-confidence binding sites for thes

31 ent inhibited AKT phosphorylation, activated PTEN and increased expression of p-eIF2a.

32 reatobiliary IPMN tissue had lower levels of PTEN and increased levels of phosphorylated (activated)

33 2 phosphatase in Mcf10a cytosol, and loss of PTEN and INPP4B, a known PI(3,4)P2 4-phosphatase, leads

34 mutants, with additional mutations in Brca1, Pten and Nf1, all of which are frequently mutated or del

35 quiescence and reveal an interaction between Pten and Notch signalling.

36 ations disrupt intramolecular interaction of PTEN and open its conformation, enhancing polyubiquitina

37 PTEN and PHLPP form a phosphatase network that is polari

38 miR-21 directly targeted the 3'-UTR of PTEN and SMAD7, and negatively regulated their expressio

39 variations and partial copy losses involving PTEN and STK11 showed evidence for having functional rel

40 PTEN and the CF transmembrane conductance regulator (CFT

41 ion factor EIF4A1, the tumor suppressor gene PTEN and the long non-coding RNA NEAT1.

42 PTEN and TP53 are two of the most commonly deleted or mu

43 Postnatal co-deletion of Pten and Trp53 in mouse neural stem cells (NSCs) leads t

44 Codeletion of Pten and Trp53 resulted in fully penetrant medulloblasto

45 Loss of phosphatase and tensin homolog (PTEN) and activation of the PI3K/AKT signaling pathway a

46 er levels of phosphatase and tensin homolog (PTEN), and diminished Akt phosphorylation.

47 ), nuclear localization of XPO1 cargos (p53, PTEN), and increased apoptosis after treatment.

48 on and decreased expression levels of MAGI3, PTEN, and TJP1 in colonic IBD as well as UC mucosa, and

49 ted genes (F11R, MAGI1, MAGI2, MAGI3, PARD3, PTEN, and TJP1) and IBD, Crohn's disease (CD), or ulcera

50 nactivate five tumor suppressor genes (TP53, PTEN, APC, BRCA1, and BRCA2) and activate one oncogene (

51 Since loss of chromosome 10 and PTEN are common events in cancer, this synthetic growth

52 These findings portray PTEN as a node coordinating liver growth with its energy

53 This is the first study to identify PTEN as a potential downstream target of PRMT5 and PRMT5

54 lence (OR 2.7) of thyroid cancer compared to PTEN-associated CS but 50% decreased prevalence (OR 0.54

55 d this interaction was necessary to position PTEN at the membrane.

56 report mutations that block localization of PTEN at the plasma membrane and nucleus without affectin

57 orylation of phosphatase and tensin homolog (PTEN) at residues Ser380/Thr382/383.

58 EN C2 domain mimicked effects of full-length PTEN but a membrane-binding defective mutant of the C2 d

59 Mice with ductal cell-specific disruption of Pten but not control mice developed sporadic, macroscopi

60 ession in the context of loss-of-function of Pten, but alters tumor histopathology and microenvironme

61 Expression of the PTEN C2 domain mimicked effects of full-length PTEN but

62 ased regulation of the tumor suppressor gene PTEN can be modulated by the expression of other miRNA t

63 In quiescent liver, PTEN causes pathological steatosis when lost, whereas it

64 HD-G12S/H50R promotes mono-ubiquitination of PTEN, causing its translocation into the nucleus, upregu

65 ies, we revealed that the miR-144-3p target, PTEN, colocalized with miR-144-3p in the basolateral amy

66 We found that PTEN competes with FBXL2 for IP3R3 binding, and the FBXL

67 vating protein ARHGAP21, we hypothesize that PTEN controls Cdc42 -dependent morphogenic processes thr

68 The tumor suppressor PTEN controls cell proliferation by regulating phosphati

69 Our results show that PTEN controls multicellular assembly through a membrane-

70 PTEN controls three-dimensional (3D) glandular morphogen

71 Our study identified complex PTEN-cooperating tumor suppressor networks in different

72 ice, which was designed for the discovery of Pten-cooperating tumor suppressors.

73 n prostate tumor tissue microarrays, loss of PTEN correlates with increased PTK6 PY342 and poor outco

74 r cell apoptosis and inflammation suggesting PTEN could be a potential therapeutic target for acute k

75 ressor genes phosphatase and tensin homolog (PTEN), cyclin dependent kinase inhibitor 2A (CDKN2A), LK

76 a molecular mechanism for cancer-associated PTEN defects and may lead to a brain cancer treatment th

77 Moreover, it is increasingly evident that PTEN deficiency disrupts the fundamental processes of ge

78 Deregulated AKT kinase activity due to PTEN deficiency in cancer cells contributes to oncogenes

79 responses observed in infected mice because PTEN deficiency or expression of a constitutively active

80 Conversely, PTEN deficiency results in stabilization of CHD1, which

81 Effects of PTEN deficiency were phenocopied by beta-Arrestin1 KD or

82 D1 as a putative synthetic-essential gene in PTEN-deficient cancers.

83 MRE11 is highly unstable in PTEN-deficient cells but stability can be significantly

84 onsistent with reduced MRN complex function, PTEN-deficient cells fail to resect DNA double-strand br

85 encodes an autophagy-regulating factor) in a Pten-deficient context.

86 nd rescued aberrant morphogenic processes of PTEN-deficient cultures.

87 (AKT) inhibitor AZD5363 induced apoptosis in PTEN-deficient DLBCLs irrespective of their molecular su

88 , the AKT inhibitor AZD5363 was effective in PTEN-deficient DLBCLs through downregulation of the onco

89 bit tumor growth in a genetic mouse model of Pten-deficient endometrioid endometrial cancer.

90 rmacokinetic profile and efficacy in a human PTEN-deficient LNCaP prostate carcinoma xenograft tumor

91 crease T-cell infiltration in an established Pten-deficient mouse model of human prostate cancer.

92 PAX2 re-expression in HGSC cells and PTEN-deficient oviductal tumors may have the potential t

93 ors to endometrioid endometrial cancers in a PTEN-deficient setting.

94 ancer-associated gene alteration that causes PTEN degradation has remained futile.

95 hysically separate PTEN from elements of the PTEN degradation machinery.

96 PO11 cargo, UBE2E1, is a limiting factor for PTEN degradation.

97 ects it from cytoplasmic proteins that cause PTEN degradation.

98 Slices containing Pten-deleted neurons showed increased recruitment of neu

99 ortantly, these changes were not confined to Pten-deleted neurons, but involved the entire network, s

100 BMPR2 deletion extended survival relative to Pten deletion alone, establishing its promoting role in

101 We report that fibroblast-specific PTEN deletion greatly restricts mammary ductal elongatio

102 Here, we show that PTEN deletion in HCT116 and DLD1 colon carcinoma cells l

103 In contrast, Pten deletion in mouse organoids does not lead to foldin

104 PTEN deletion increased PI(3,4)P2 levels in a mouse mode

105 Mechanistically, Pten deletion increases Akt phosphorylation, which induc

106 tion or progression in the prostate-specific Pten deletion mouse model for prostate cancer.

107 d that hepatosteatosis resulting from either Pten deletion or transgenic expression of HCV core/NS5A

108 Tumors with combined Foxp1-Shq1 and Pten deletion show increased proliferation and anaplasti

109 ows cells with oncogenic PIK3CA mutations or PTEN deletion to grow using diverse amino acid sources.

110 ssion in prostate epithelium cooperated with Pten deletion to produce a metastasis-prone tumor.

111 ally regenerate following treatments such as Pten deletion, were killed by Sox11 overexpression.

112 In addition, Pten deletion-induced axon regeneration of retinal gangl

113 n of non-alpha-RGCs, which are refractory to Pten deletion-induced regeneration.

114 tumorigenesis specifically in the context of PTEN deletion.

115 tion of Notch1 prevents SC depletion despite Pten deletion.

116 and network effects that occur 1 week after Pten deletion.

117 or Pten(DeltaDuct/DeltaDuct) mice) and used Pten(DeltaDuct/+) and Pten(+/+) mice as controls.

118 In Kras(G12D);Pten(DeltaDuct/+) mice, 70% developed IPMN, predominatel

119 2D);Pten(DeltaDuct/DeltaDuct) and Kras(G12D);Pten(DeltaDuct/+) mice.

120 We also generated Kras(G12D);Pten(DeltaDuct/DeltaDuct) and Kras(G12D);Pten(DeltaDuct/

121 Kras(G12D);Pten(DeltaDuct/DeltaDuct) mice all developed invasive IP

122 tion to detect spontaneous Kras mutations in Pten(DeltaDuct/DeltaDuct) mice and study the effects of

123 Pten(DeltaDuct/DeltaDuct) mice developed IPMNs of severa

124 (Sox9CreER(T2);Pten(flox/flox);R26R(YFP) or Pten(DeltaDuct/DeltaDuct) mice) and used Pten(DeltaDuct/

125 rthermore, we show that CRISPR/Cas9-mediated PTEN depletion rendered PTEN wild-type Hec-1A endometrio

126 inciple that inhibiting IP3R3 degradation in PTEN-deregulated cancers represents a valid therapeutic

127 w that PTEN interacts with DAXX and, in turn PTEN directly regulates oncogene expression by modulatin

128 y inactivating Sleeping Beauty transposon to Pten disruption within the same genome.

129 IL-17 receptor C and Pten double KO mice recapitulated the weak EMT character

130 PTEN down-regulation after hepatectomy promotes the burn

131 PTEN down-regulation may promote beta-oxidation through

132 ly, these findings identify a novel role for PTEN during infection and identify regulation of the PI3

133 campal response to insulin through IRS-1 and PTEN dysregulation and suggest that, in Alzheimer's dise

134 suggest that citrate acts on the IGF-1R-AKT-PTEN-eIF2a pathway.

135 sociation on the chromatin, independently of PTEN enzymatic activity.

136 Loss of the tumor suppressor gene PTEN exerts diverse outcomes on cancer in different deve

137 xpress both low stromal JAG1 and low stromal PTEN exhibit a shorter time to recurrence than those who

138 revealed that unlike GBMDC, PRMT5 regulates PTEN expression and controls Akt and ERk activity in GBM

139 reover, DAXX expression anti-correlates with PTEN expression in GBM patient samples.

140 epithelium of mice with and without stromal PTEN expression.

141 specifically in ductal cells (Sox9CreER(T2);Pten(flox/flox);R26R(YFP) or Pten(DeltaDuct/DeltaDuct) m

142 PTEN that is required to physically separate PTEN from elements of the PTEN degradation machinery.

143 ntial functional associations: these include PTEN, FUBP1, and CDH1.

144 nism by which specific point mutations alter PTEN function is largely unknown.

145 ain, we conditionally inactivated the murine Pten gene in neonatal neural stem/progenitor cells.

146 FICANCE STATEMENT Homozygous deletion of the Pten gene in neuronal subpopulations in the mouse serves

147 Focal CNAs affecting the MYC gene and the PTEN gene were observed only in a minor portion of prima

148 The phosphatase and tensin homologue (PTEN) gene is frequently mutated or lost in human tumour

149 dehydrogenase genes (SDHx) co-occurring with PTEN germline mutations confer a 2-fold increased preval

150 r suppressor phosphatase and tensin homolog (PTEN) has been deactivated.

151 lighted a tumor suppressive role for stromal PTEN, how the adjacent normal epithelium transforms in r

152 Conversely, induced overexpression of PTEN in B cells in uninfected mice led to suppression of

153 By targeting Pten in cerebellar granule cells and activating the AKT1

154 ort a novel chromatin-associated function of PTEN in complex with the histone chaperone DAXX and the

155 PTEN status confirmed a mechanistic role for PTEN in determining the functional outcome of combined p

156 se (PI3K) activity, but the participation of PTEN in host defense against bacterial infection is less

157 Heterozygous loss of function of PTEN in human subjects has a significant effect on T- an

158 ur findings delineate a critical function of Pten in maintaining SC quiescence and reveal an interact

159 By analysing PTEN in malignant glioblastoma primary cells derived fro

160 We demonstrated their synergy with PTEN in preventing invasion in vitro and confirmed their

161 Here, we review the role of PTEN in regulating the key processes in and out of cell

162 a suppression, and reveal a crucial role for PTEN in the early DNA damage signalling cascade, the inh

163 Conditional disruption of Pten in the mouse prostate leads to tumorigenesis and in

164 itory components upstream of mTORC1, TSC1 or PTEN, in mouse SC development, adult homeostasis, and ne

165 Pten inactivation created an abnormal perivascular proli

166 mage induces Phosphatase and Tensin Homolog (PTEN)-induced Putative Kinase 1 (PINK1) and Parkin-depen

167 SIN3B was required for PTEN-induced cellular senescence and prevented progressi

168 iquitin ligase parkin and the protein kinase PTEN-induced kinase 1 (PINK1), respectively.

169 TSC2, associated with altered expression of PTEN-induced putative kinase 1 (PINK1) and PARK2 translo

170 emonstrate for the first time that decreased PTEN-induced putative kinase 1 (PINK1) expression is ass

171 In particular, the PTEN-induced putative kinase 1 (PINK1) p.G411S (c.1231G>

172 and tensin homolog deleted on chromosome 10 (PTEN) induces activation of the phospho-5' adenosine mon

173 PTEN inhibition enhanced tubular cell apoptosis in kidne

174 Furthermore, PTEN inhibition expanded the infiltration of neutrophils

175 e neuronal surface both in vitro and in vivo PTEN inhibition in vivo increases the percentage of TG n

176 PTEN inhibition releases deltaR from this checkpoint and

177 We show that PTEN interacts with DAXX and, in turn PTEN directly regu

178 Introduction of PTEN into a PTEN null prostate cancer cell line leads to

179 at Importin-11 traffics the tumor suppressor PTEN into the nucleus and in so doing protects it from c

180 PTEN is a major PI(3,4)P2 phosphatase in Mcf10a cytosol,

181 PTEN is a PIP3 phosphatase that antagonizes oncogenic PI

182 The Star-PAP-mediated APA of PTEN is essential for DNA damage-induced increase of PTE

183 PTEN is mutated in a subset of children with autism spec

184 rther demonstrate that loss of one allele of PTEN is sufficient to shift isoform dependency from p110

185 Here, we show that PTEN knockdown (KD) impairs beta-Arrestin1 membrane loca

186 Since PTEN lies at the intersection of these two pathways, we

187 Park2 loss and Pten loss also display striking cooperativity to promote

188 We also showed that PTEN loss and activated Kras have synergistic effects in

189 -resistant tumor uniquely harbored biallelic PTEN loss and had reduced expression of two neoantigens

190 revealed that increased AKT activity due to PTEN loss directly phosphorylates WHSC1 at S172, prevent

191 PTEN loss increased the connectivity of all four types o

192 stent with the association of FOXP1-SHQ1 and PTEN loss observed in human cancers.

193 The murine tumours exhibit PTEN loss of function instigated by reduced PTEN mRNA, a

194 r activity in the same genetic background of Pten loss that yields oncogenic activity by ERG.

195 ort that FOXP1-SHQ1 deletion cooperates with PTEN loss to accelerate prostate oncogenesis and that lo

196 normal epithelium transforms in response to PTEN loss was not previously addressed.

197 of AR target genes repressed in tumors with Pten loss, circumventing PI3K-mediated repression of the

198 te tumorigenesis in mice in combination with Pten loss, consistent with the association of FOXP1-SHQ1

199 fferentially-regulated by Pik3ca(H1047R) and Pten loss, suggesting unique roles for these two events

200 tically altered phenotypes in the setting of Pten loss, with early neoplastic lesions (high-grade pro

201 h phosphorylation of p110beta independent of PTEN loss.

202 ssion have been reported in animal models of PTEN loss; however, the full extent of these changes, an

203 response to combined MEK/mTOR inhibition in PTEN-loss contexts and identified JAK1/STAT3 activation

204 Overall, our results show that PTEN-loss is a crucial determinant of synergistic intera

205 ulation and progression-free survival in the PTEN-low (by immunohistochemistry) population.

206 7-0.98; p=0.037) and in the 48 patients with PTEN-low tumours, median progression-free survival was 6

207 ow that Ipo11 loss results in degradation of Pten, lung adenocarcinoma, and neoplasia in mouse prosta

208 Our data indicate that PTEN may provide a potential therapeutic target to ameli

209 a clearance from the CF airway by activating PTEN-mediated anti-bacterial responses and might represe

210 urine cancers (prostate cancers in TRAMP and PTEN mice, pancreatic cancer in KPC mice), we identified

211 taDuct) mice) and used Pten(DeltaDuct/+) and Pten(+/+) mice as controls.

212 of beta-oxidation led to persisting TRAS in Pten(-/-) mice and abrogated hypertrophic liver growth.

213 rom glucose to lipid usage was pronounced in Pten(-/-) mice and correlated with the disappearance of

214 ead to a brain cancer treatment that targets PTEN mono-ubiquitination.

215 ndent degradation of IP3R3 is accelerated in Pten(-/-) mouse embryonic fibroblasts and PTEN-null canc

216 PTEN loss of function instigated by reduced PTEN mRNA, and increased phosphorylated inactivation and

217 promotes the translation of c-MYC, BCL2 and PTEN mRNAs in the human acute myeloid leukemia MOLM-13 c

218 tions (VHL, PBRM1, SETD2, KDM5C, TP53, BAP1, PTEN, MTOR) were associated with the CLEAR score.

219 size and proliferation compared with control Pten-mutant mice, the latter of which exhibited increase

220 AR amplification or copy gain, 34 (43%) had PTEN mutation, 33 (41%) had TP53 mutation, 39 (49%) had

221 The addition of Zc3h13 or Pten mutations altered the gene expression profiles of R

222 ockade in a mesenchymal tumor, we identified PTEN mutations and reduced expression of genes encoding

223 ncer prevalence in patients with co-existent PTEN mutations and SDHx variants.

224 ASD-PTEN mutations display decreased stability, catalytic ac

225 We identified a set of ASD-PTEN mutations displaying altered lipid phosphatase func

226 Thus, the prevalence of PI3-kinase and PTEN mutations in cancer may result in part because they

227 Phosphatase and tensin homolog (PTEN) negatively regulates downstream protein kinase B s

228 co-occurrence relationships among RB1, TP53, PTEN, NKX3-1 and MYC in TCGA of prostate cancer identifi

229 CK2 inhibition restores PTEN nuclear distribution and DNA repair activities and

230 lysine 27 trimethylation (H3K27me3) in both Pten null mouse embryonic fibroblasts (MEFs) and Pten nu

231 null mouse embryonic fibroblasts (MEFs) and Pten null mouse prostate tissues.

232 Introduction of PTEN into a PTEN null prostate cancer cell line leads to dephosphory

233 f a reactive stromal microenvironment in the Pten null prostate cancer model.

234 However, prior to depletion, Pten-null activated SCs can transiently proliferate upon

235 in Pten(-/-) mouse embryonic fibroblasts and PTEN-null cancer cells.

236 Reconstitution of PTEN-null cells with either wild-type PTEN or a catalyti

237 the NOTCH receptor, is downregulated in the PTEN-null fibroblasts leading to a loss in the paracrine

238 troduction of JAGGED-1 expression within the PTEN-null fibroblasts was sufficient to abrogate the obs

239 on inhibiting tumor growth in the BRAF V600E/PTEN-null melanoma mouse model.

240 tion of Whsc1 prevented tumor progression in PTEN-null mice.

241 In a PTEN-null murine PCa model, WHSC1 overexpression in pros

242 SMAD4 constrains progression of Pten-null prostate cancer and serves as a common downstr

243 (TGFBR2) and BMP receptor II (BMPR2) using a Pten-null prostate cancer model.

244 transferase WHSC1 critically drives indolent PTEN-null tumors to become metastatic PCa.

245 rk helps explain the nuclear accumulation of PTEN observed in many healthy tissues and, because Ipo11

246 ion of PTEN-null cells with either wild-type PTEN or a catalytically dead mutant stabilizes IP3R3 and

247 By contrast, loss of Pten or Nf1 increases growth rate in vivo, and reduces s

248 This viral infection-induced PTEN overexpression appears responsible for the suppress

249 This study identifies a novel PTEN pathway in cancer and provides a framework for the

250 and mutations in the tumour suppressor gene PTEN (phosphatase and tensin homolog) are frequent event

251 fy up-regulation of the inositol phosphatase PTEN (phosphatase and tensin homolog) as primarily respo

252 onse to insulin, caused by altered IRS-1 and PTEN (phosphatase and tensin homologue on chromosome 10)

253 rotic fibromas, a cutaneous manifestation of PTEN (phosphatase and tensin homologue) hamartoma-tumor

254 Here we show a function of Pten (phosphatase and tensin homologue) in quiescent SCs

255 tein and modulate, through activation of the PTEN/PI3K/Akt signaling pathway, different molecules inv

256 s/ERK1/2, Src, JAK/STAT, JNK, NF-kappaB, and PTEN/PI3K/AKT.

257 in metastatic cancer included TP53, CDKN2A, PTEN, PIK3CA, and RB1.

258 are more sensitive, whereas tumor cells with PTEN, PIK3CA, PIK3R1 or retinoblastoma (Rb) mutation are

259 Frequent mutations were found in TP53, PTEN, PIK3CA, PPP2R1A, FBXW7, and KRAS, similar to endom

260 These results have demonstrated that PTEN plays a crucial role in the pathogenesis of ischemi

261 PTEN protein expression and BCR surface density may infl

262 in the correlation between loss of IPO11 and PTEN protein in human lung tumors.

263 essential for DNA damage-induced increase of PTEN protein levels.

264 e, using the phosphatase and tensin homolog (PTEN) pseudogene as a model system, that antisense lncRN

265 ts with NOTCH1/FBXW7 (N/F) mutations and RAS/PTEN (R/P) germ line (GL) were classified as oncogenetic

266 In wild-type mice, PTEN reduction occurred after TRAS formation, persisted

267 we define a phosphatase and tensin homolog (PTEN)-regulated checkpoint that retains deltaR in the Go

268 eatures characterizing target recognition by PTEN-regulating miRNAs, we analyze multiple datasets fro

269 lar defects in neurogenesis that may explain PTEN-related macrocephaly and Miller-Dieker lissencephal

270 Furthermore, partial knockdown of Pten rescues the toxicity observed in the NSC34 (G4C2)10

271 MPK activation alone is sufficient to induce PTEN S-nitrosylation in the absence of PARK2 depletion.

272 We employed molecular cloning to examine how PTEN's stability, subcellular localization, and catalyti

273 yostelium cells lacking the tumor suppressor PTEN show strongly impaired migratory activity and adher

274 d development of invasive prostate cancer in Pten single KO mice.

275 We generated mice with disruption of Pten specifically in ductal cells (Sox9CreER(T2);Pten(fl

276 Genetic manipulation of PTEN status confirmed a mechanistic role for PTEN in det

277 these two pathways, we investigated whether PTEN status determines the functional response to combin

278 rapy, chemotherapy-free interval, and tumour PTEN status.

279 Mechanistically, functional PTEN stimulates the GSK3beta-mediated phosphorylation of

280 how that the tyrosine kinase PTK6 (BRK) is a PTEN substrate.

281 ortin-11 (Ipo11) is a transport receptor for PTEN that is required to physically separate PTEN from e

282 n-regulating phosphatase and tensin homolog (PTEN), thereby promoting phosphorylation of Akt, which l

283 chondrial depolarization, and recruitment of PTEN to the immunologic synapse.

284 mbined, these results unveil a novel stromal PTEN-to-JAGGED-1 axis in maintaining the MaSC niche, and

285 ted in a striking decrease of Ezh2 levels in Pten/Trp53 double-null MEFs and in prostate tumors of Pt

286 3 double-null MEFs and in prostate tumors of Pten/Trp53 double-null mutant mice.

287 model of prostate cancer is associated with Pten/Trp53 inactivation and ARF elevation hypothesizing

288 of Skp2 and Ezh2 was found in CRPC tumors of Pten/Trp53 mutant mice, and expression levels of SKP2 an

289 Finally, we demonstrate that PTEN up-regulation is a common mechanism by which infect

290 e also found that p-eIF2a was decreased when PTEN was depleted.

291 tations were in PIK3CA, BRAF, NF1, NRAS, and PTEN We also noted a high burden of NsM in cases with ta

292 Mice with hepatic deletion of PTEN were given tail-vein injections of MAN2A1-FER.

293 noma, including CDKN2A, TP53, NF1, RAC1, and PTEN, were not found among any melanocytic nevi sequence

294 ack the NH2-amino terminal splice variant of PTEN, were unable to eradicate Pseudomonas aeruginosa fr

295 gradation of phosphatase and tensin homolog (PTEN), which impaired intercellular junction formation,

296 atients with melanomas harboring mutant BRAF/PTEN, which often are refractory to current therapies.

297 CRISPR/Cas9-mediated PTEN depletion rendered PTEN wild-type Hec-1A endometrioid endometrial cancer ce

298 Pharmacological inhibition of PTEN with bpV(HOpic) exacerbated renal dysfunction and p

299 xogenous overexpression of a mutated form of PTEN with enhanced phosphatase activity prevented the TG

300 ogical modulation revealed an association of PTEN with TRAS turnover and hypertrophic liver growth.