ライフサイエンスコーパス: PTEN

1 F10A) from its cancerous PTEN mutants (MCF10 PTEN-/-).

2 in cell compartment-specific predominance of Pten.

3 d tumor suppressors, including cyclin D2 and PTEN.

4 B), can partially compensate for the loss of PTEN.

5 by loss of the tumor-suppressing phosphatase PTEN.

6 mal breast cells with wild-type (WT) p53 and PTEN.

7 robust as observed in the setting of loss of PTEN.

8 mour suppressor phosphoinositide phosphatase PTEN.

9 regions of the phosphatase or C2 domains of PTEN.

10 e of normal mammary epithelial cells lacking PTEN.

11 tween PHF8 and PTEN and between PKCalpha and PTEN.

12 TP53 (27%) and PTEN (12%) and DDR gene defects (BRCA2 7%; CDK12 5%; ATM

13 in CTNNB1 (43%), PIK3CA (43%), ARID1A (36%), PTEN (29%), KRAS (26%), TP53 (26%) and SOX8 (19%), a rec

14 xpression, while the original study reported PTEN 3'UTR increased PTENP1 levels (Figure 4A; Poliseno

15 We found PTEN 3'UTR overexpression in DU145 cells did not impact

16 mRNAs (ceRNAs) in DU145 cells did not impact PTEN 3'UTR regulation using a reporter, while the origin

17 RT promoter (51%), TP53 (32%), CTNNB1 (17%), PTEN (8%), AXIN1, ARID2, KMT2D, and TSC2 (each 6%).

18 and tensin homolog deleted on chromosome 10 (PTEN), a negative PI3K regulator that tau controls, as a

19 f beta cells and increased the expression of PTEN, a miR-216a target.

20 Germline mutations in PTEN account for ~10% of cases of autism spectrum disord

21 ather than the lipid phosphatase activity of PTEN accounts for the reversal of the EMT.

22 Notably, siRNA knockdown of both p53 and PTEN activated MEOX1 expression in breast cancer cells,

23 PAR2 activation and explains the changes in PTEN activity.

24 Therefore, non-PTEN aetiologies exist in PTEN wildtype patients.

25 ylation state of PTEN, and the activities of PTEN and Akt measured.

26 a but negative correlations between PHF8 and PTEN and between PKCalpha and PTEN.

27 In conclusion, we identified PTEN and DNA-PK as essential regulators of replication c

28 nd PTEN is prevalent in human disease, where PTEN and FOXA1 are downregulated by allelic loss and sit

29 iRNA that targets the tumor suppressor genes PTEN and FoxO1 and regulates the GBM stem-like cells.

30 uction mechanism and demonstrate that intact PTEN and GSK3beta signaling are essential for effective

31 rvations were in line with downregulation of PTEN and increase in beta cell proliferation in that gro

32 atic sections included staining for insulin, PTEN and Ki67.

33 Prostate organoids lacking PTEN and overexpressing ERG (Pten(-/-) R26-ERG) faithful

34 nate and adaptive immune response, integrin, PTEN and phospholipase C signaling, serotonin and trypto

35 , increased Ki67, PAX8 and Myc and decreased PTEN and RB1 mRNA expression.

36 374b and miR-545 inhibited tumor suppressors PTEN and RIG-I to enhance proto-oncogenic PI3K-AKT signa

37 Although the domain structure of PTEN and the functional impact of a number of its most c

38 ulate the phosphorylation and SUMOylation of PTEN and then correspondingly inactivated the AKT/mTOR s

39 es with mutations to the remaining copies of PTEN and TP53, while the Gleason 7 PTEN-intact tumor is

40 leason 9 tumor harbors single-copy losses of PTEN and TP53.

41 Combined Pten and Trp53 deletion in mouse mesothelium led to none

42 Our findings establish a link between PTEN and WAVE-Arp2/3-regulated actin cytoskeletal dynami

43 Further, depletion of PTEN and/or PTENP1 increased DU145 proliferation compare

44 er A (RhoA); phosphatase and tensin homolog (PTEN); and nuclear factor-kappaB (NF-kappaB).

45 EpCAM, PTEN, and p27 were demonstrated as miR-30e-3p additional

46 uts of mutagenesis experiments for BRCA1 and PTEN, and positively correlate with an independent set o

47 so carried copy-number variations in CDKN2C, PTEN, and REL genes.

48 cells with frequent deficiencies in p53 and PTEN, and that its expression is undetectable in luminal

49 ist peptide and the phosphorylation state of PTEN, and the activities of PTEN and Akt measured.

50 e to rec-TF up to 14 days, resulted in lower PTEN antigen levels, enhanced Akt activity and increased

51 d exposure to TF results in the reduction in PTEN antigen with concurrent increase in Akt activity wh

52 ene level, driver mutations in TP53, MYC and PTEN are enriched in hypoxic tumours, and mutations in P

53 hatase and tensin homolog on chromosome ten (PTEN) are diagnosed with PTEN hamartoma tumor syndrome (

54 nt arrest in response to AZD1775 and defined PTEN as a promising biomarker for efficient WEE1 cancer

55 Mechanistically, we identified PTEN as a putative PRL2 substrate and demonstrated that

56 recapitulate the phenotype seen with loss of PTEN as PI3K signaling is not as robust as observed in t

57 RL2 down-regulates PTEN by dephosphorylating PTEN at Y336, thereby augmenting NEDD4-mediated PTEN ubi

58 vo differential tumor suppressive effects of Pten between these tumors.

59 We conclude that germline disruption of PTEN, both in human and mouse, results in compromised ce

60 te and demonstrated that PRL2 down-regulates PTEN by dephosphorylating PTEN at Y336, thereby augmenti

61 To explore the mechanism of activation of PTEN by TF, the association of "membrane-associated guan

62 espectively, despite both exhibiting loss of Pten/chromosome 19 (chr19) and PI3K/Akt activation with

63 We found depletion of putative PTEN competing endogenous mRNAs (ceRNAs) in DU145 cells

64 engineered murine models with Arid1a and/or Pten conditional deletion in the endometrium.

65 53/p53)- and phosphatase and tensin homolog (PTEN) deficiencies, and combined p53- and PTEN-deficienc

66 c anti-tumor effects on ovarian cancers with PTEN deficiency and KRAS(G12D) mutation.

67 resistance to cisplatin, which is induced by Pten deficiency on the backdrop of Smad4/Apc co-deletion

68 rategy to restore PTEN, thereby obliterating PTEN deficiency-induced malignancies.

69 study, we discovered that combined p53- and PTEN-deficiency in TNBC activates expression of the tran

70 g (PTEN) deficiencies, and combined p53- and PTEN-deficiency is associated with poor prognosis and po

71 orthotopic phosphatase and tensin homologue (PTEN)-deficient glioma mouse models, mRNA-containing exo

72 In this study, we reconstituted PTEN-deficient breast cancer cells with wild-type and mu

73 ies a potential therapeutic approach against Pten-deficient cancers.

74 ivity of NHEJ-DDR proteins in autophagy- and PTEN-deficient cells.

75 delay prostate and skin cancer initiation of Pten-deficient mice.

76 nical observations, BRF1 overexpression in a Pten-deficient mouse (Pten(Delta/Delta) BRF1(Tg)) prosta

77 scription 5B (STAT5B), and STAT6 in p53- and PTEN-deficient TNBC cells.

78 own abolished cell proliferation of p53- and PTEN-deficient TNBC in vitro and inhibited tumor growth

79 High TIP5 expression correlates with primary PTEN-del PCa and this combination strongly associates wi

80 of aggressive primary PCas characterized by PTEN-del, high-TIP5 expression, and a TIP5-regulated gen

81 beta axis promotes migration and invasion of PTEN-deleted endometrial tumor cells.

82 rsely, unleashing PI3K signaling by means of PTEN deletion delayed pericyte maturation.

83 gradation was abolished by cancer-associated PTEN deletion or GSK3beta inactivation.

84 ion gene into the liver coupled with somatic Pten deletion produces spontaneous liver cancers in mice

85 However, how PTEN deletion would impact the epigenome and transcripto

86 lating the immune response, were affected by PTEN deletion.

87 F1 overexpression in a Pten-deficient mouse (Pten(Delta/Delta) BRF1(Tg)) prostate cancer model accele

88 reast cancer cells with wild-type and mutant PTEN, demonstrating that restoration of PTEN expression

89 demonstrates distinct mechanisms involved in PTEN-dependent genome-wide transcriptional control under

90 PTEN dephosphorylates and downregulates Abi1 in breast c

91 We demonstrate that PTEN dephosphorylation of Abi1 at Y213 and S216 results

92 We found PTEN depletion in the prostate cancer cell line DU145 di

93 , defining molecular events underlying PPM1A/PTEN deregulation is necessary to develop expression res

94 Here, we report a Pten derived pro-cancer growth gene fusion Pten-NOLC1 or

95 These suggest that PTEN destabilization occurs mainly via the PKCalpha-Src

96 After 12 weeks, Frmd6/Pten double knockouts presented high-grade prostatic int

97 ctively, these findings suggest that loss of PTEN drives global changes in DNA CpG methylation and tr

98 PPM1A and PTEN emerged as novel suppressors of chronic kidney dise

99 reased under metabolic stress in contrast to PTEN-expressing cells.

100 , introduction of a mimic nanodrug decreased PTEN expression and increased beta cell proliferation.

101 At ~3 weeks of age, with a 50% drop in Pten expression compared with wild-type levels, we obser

102 tant PTEN, demonstrating that restoration of PTEN expression converted cancer cells with mesenchymal

103 TGF-beta1 similarly attenuates PPM1A and PTEN expression in human renal epithelial cells and fibr

104 Using the ESC-GEMM platform to modulate Pten expression in melanocytes in vivo, we highlighted t

105 In this work, we show that loss of PTEN expression is frequent in human sarcomatoid MM and

106 sion is frequent in human sarcomatoid MM and PTEN expression levels are lower in sarcomatoid MM than

107 ent through the activation of STAT3, and low PTEN expression levels have a detrimental impact on pati

108 However, cells with constitutive PTEN expression slow transcription, an evolutionary mech

109 While all PDXs lack PTEN expression, there is no consistent requirement for

110 ion of PHF8 or PKCalpha greatly up-regulated PTEN expression, which could be rescued by ectopic expre

111 Mice with the genotype Amhr2-Cre Pten((fl/fl)) Kras(G12D/+)(G12D mice) had abnormal folli

112 n contrast, mice with the genotype Amhr2-Cre Pten((fl/fl)) Kras(G12V/+) (G12V mice) had normal follic

113 er alleles (LSL-Braf(V600E), LSL-Nras(Q61R), Pten(Flox), and Cdkn2a(Flox)) and regulatory alleles to

114 targeting phosphatase and tensin homologue (PTEN) for proteasomal degradation.

115 or through exposure of cells to TF releases PTEN from MAGI proteins and is concurrent with increases

116 el predicted with high accuracy that loss of PTEN function was indicative of pathogenicity.

117 d that the dual regulation of GR by PI3K and PTEN functions as a rheostat that can be exploited for t

118 n reported as an onco-miRNA that targets the PTEN gene in endometrioid carcinoma, its biological sign

119 Cross-species analyses revealed a PTEN gene signature that identified a group of aggressiv

120 Inactivation of Pten gene through deletions and mutations leading to exc

121 ades of research, it remains unclear how the PTEN genotype is related to clinical outcomes.

122 ereas individual knockdowns of either p53 or PTEN had only minimal effects on MEOX1 expression.

123 on chromosome ten (PTEN) are diagnosed with PTEN hamartoma tumor syndrome (PHTS) and are at high ris

124 tumor suppressor that has been linked to the PTEN hamartoma tumor syndrome.

125 PTEN hamartoma tumour syndrome (PHTS) is an umbrella ter

126 Inactivation of the tumor suppressor PTEN has been shown to induce the EMT, but the underlyin

127 n cancers (e.g. mutations in KRAS or loss of PTEN) have been shown to increase macropinocytosis.

128 ion with an oncogenic insult, illustrated by Pten heterozygosity, elicited lethal metastatic prostate

129 e, we discovered that PRL2 ablation inhibits PTEN heterozygosity-induced tumorigenesis.

130 Although our PTEN immuno-MRM and immuno-MALDI assays can be considere

131 Quantification of the tumor suppressor PTEN in Colo-205 cells by immuno-MRM and immuno-MALDI us

132 Deletion of Pten in Dist-Luminal-C cells resulted in prostatic intra

133 pes indicates a more central involvement for PTEN in immunity than previously recognized.

134 complemented with inactivation of FOXA1 and PTEN in intermediate and luminal mouse urothelium.

135 nues for future studies on the importance of PTEN in maintaining microglia homeostasis.

136 our data provide evidence that dysregulated Pten in microglia has an etiological role in microglial

137 To explore the importance of nuclear PTEN in the development of ASD and macrocephaly, we prev

138 oup and others have reported a novel role of PTEN in the regulation of transcription at the genome-wi

139 Since loss of PPM1A and PTEN in the tubulointerstitium promotes fibrogenesis, de

140 and tensin homolog deleted on chromosome 10 (PTEN) in mural cells.

141 e examined potential mechanisms of FOXA1 and PTEN inactivation in bladder cancer and their contributi

142 elium however, insulin selectively regulates PTEN-induced kinase 1 (PINK-1)-mediated mitophagy and mi

143 91, ubiquitin phosphorylation, a read-out of PTEN-induced kinase 1 (PINK1) activity, and Parkin E3 li

144 Given that PTEN-induced kinase 1 (PINK1) regulates mitochondrial fu

145 involves the E3 ubiquitin ligase Parkin and PTEN-induced kinase 1 (PINK1), which cooperatively initi

146 scovery of the role of the PD familial genes PTEN-induced putative kinase 1 (PINK1) and parkin (PRKN)

147 e been identified and include those encoding PTEN-induced putative kinase 1 (PINK1) and parkin.

148 copies of PTEN and TP53, while the Gleason 7 PTEN-intact tumor is almost entirely ablated.

149 nriched in hypoxic tumours, and mutations in PTEN interact with hypoxia to direct tumour evolutionary

150 evates cellular PTEN levels while lentiviral PTEN introduction increases PPM1A expression.

151 PTEN is a frequently mutated tumor suppressor that has b

152 ntly found reduced in human cancers, but how PTEN is down-regulated is not fully understood.

153 The tumor suppressor PTEN is essential for early development.

154 PTEN is implicated in a wide variety of pathophysiologic

155 Furthermore, CRPC tumors in which Pten is lost are also resistant to eradication by PI3K i

156 tivation and reduced expression of FOXA1 and PTEN is prevalent in human disease, where PTEN and FOXA1

157 f the clinical syndromes typically united by PTEN is reflected by the genetic heterogeneity revealed

158 and tensin homolog located on chromosome 10 (PTEN) is a tumor suppressor gene and one of the most fre

159 Loss of the tumor suppressor, PTEN, is one of the most common findings in prostate can

160 Pathologic analysis revealed Pten/Kdm5b mice displayed mild morphologic changes with

161 At 6 months of age, the prostate weight of Pten/Kdm5b mice was reduced by up to 70% compared with t

162 naling by decreasing P110alpha/P85 levels in Pten/Kdm5b mice.

163 odels of prostate epithelium-specific mutant Pten/Kdm5b.

164 ngs, we performed mechanistic studies in two Pten knock-in murine models, distinct from each other in

165 hypothesis was tested in a prostate-specific PTEN-/- (KO) mouse prostatic adenocarcinoma model throug

166 high PRL2 expression is correlated with low PTEN level with reduced overall patient survival.

167 re, decreases in nuclear but not cytoplasmic Pten levels associated with a reduction in expression of

168 ferent laboratories, the endogenous Colo-205 PTEN levels determined with 2-PIC showed a good correlat

169 Concurrent loss of PPM1A and PTEN levels in aristolochic acid nephropathy further sug

170 1A expression, conversely, elevates cellular PTEN levels while lentiviral PTEN introduction increases

171 The PTEN-like domain has no phosphatase activity, but it can

172 of the Hsc70 "uncoating ATPase." The J- and PTEN-like domain-containing proteins, auxilin 1 (Aux1) a

173 While the role of PTEN lipid-phosphatase activity on PtdIns(3,4,5)P3 and i

174 nse mutations, we show that although loss of PTEN lipid-phosphatase function cooperates with oncogeni

175 yperplasia in prostates, whereas age-matched Pten littermates developed high-grade prostatic intraepi

176 reatment inhibited growth of mutant TP53, WT PTEN LN-229 tumors, and sensitized LN-229 tumors to TMZ

177 en (Pten(m3m4/m3m4)).Cytoplasmic predominant Pten localization results in a phenotype of extreme macr

178 Importantly, deletions of the PTEN locus, which promotes active PI3K signaling, were a

179 vivo studies, we define a critical role for PTEN loss and epigenetic silencing of FOXA1 in heterogen

180 Thus, convergence of PTEN loss and TBK1/IKKepsilon activation on Rab7-S72 pho

181 ticular, we showed that, in prostate cancer, PTEN loss appears to establish an immunosuppressive tumo

182 adherin loss and PI3K pathway activation via PTEN loss in ILC development.

183 ght in understanding tumor pathology and how PTEN loss of function, whether by genetic or non-genetic

184 have a therapeutic benefit for cancers with PTEN loss or PI3K/AKT activation.

185 ndent of the cell of origin, cooperated with Pten loss to drive AR-independent castration-resistant p

186 uncated ASPP2 cooperates with E-cadherin and PTEN loss to drive breast cancer initiation and progress

187 elerated prostate tumorigenesis triggered by Pten loss via the activation of mTOR signaling.

188 g in renal fibroblasts, moreover, results in PTEN loss, while PTEN stable depletion decreases PPM1A e

189 t that can be exploited for the treatment of PTEN loss-driven cancers.

190 tumor onset and progression of a mutant Braf;Pten loss-driven melanoma mouse model.

191 e of tumor tissue integrity in a mutant Braf/Pten loss-driven mouse model for melanoma.

192 indicates that upregulation of Abi1 mediates PTEN loss-induced EMT and CSC activity.

193 ouse model of melanoma driven by BRAF(V600E);PTEN loss.

194 by Pten-loss whereas it is dispensable once Pten-loss mediated transformation is established.

195 tiation of PCa of luminal origin mediated by Pten-loss whereas it is dispensable once Pten-loss media

196 wo additional mouse models of syndromic ASD (Pten(m3m4/m3m4) and Mecp2(tm1.1Bird)).

197 rved enhanced activation of microglia in the Pten(m3m4/m3m4) brain.

198 Transcriptomic analysis of the Pten(m3m4/m3m4) cortex found upregulated gene pathways r

199 n-microglia co-culture experiments, we found Pten(m3m4/m3m4) microglia are more efficient at synaptic

200 ression with enhanced phagocytic capacity in Pten(m3m4/m3m4) microglia, indicating microglial activat

201 direct in vitro assays on Pten wild-type and Pten(m3m4/m3m4) microglia.

202 dence for neuron-microglia cross-talk, where Pten(m3m4/m3m4) neurons elicit enhanced pruning from inn

203 dominantly cytoplasmic localization of Pten (Pten(m3m4/m3m4)).Cytoplasmic predominant Pten localizati

204 These results suggest that PTEN may suppress breast cancer invasion and metastasis

205 o rescue the spheroid formation phenotype of PTEN(-/-) MCF10A cells maintained in suspension.

206 s reduced by up to 70% compared with that of Pten mice.

207 oid modeling and machine learning classifies PTEN missense variants, over 70% of which are currently

208 In the present study, we demonstrate that PTEN modulates genome-wide RNA Polymerase II occupancy i

209 to a lesser extent, likely due to suboptimal PTEN mRNA knockdown using this approach.

210 imilarly, depletion of PTENP1 did not impact PTEN mRNA levels.

211 Pten mutant mice exhibit social behavior deficits, eleva

212 helial cell line (MCF10A) from its cancerous PTEN mutants (MCF10 PTEN-/-).

213 Immunological characterization showed that Pten mutants have increased B-cell proliferation and a p

214 nstitution of PTEN-null embryoid bodies with PTEN mutants that lack only PTEN's lipid phosphatase act

215 ns and oestrogen receptor-negative cancer or PTEN mutation (treated with oral capivasertib 480 mg).

216 We found that PTEN mutations in humans and mice are associated with a

217 gnized as a tumor suppressor, involvement of PTEN mutations in mediating such a diverse range of phen

218 PHTS-associated phenotypes harbour germline PTEN mutations.

219 sposition disorders associated with germline PTEN mutations.

220 Pten-NOLC1 fusion is present in primary human cancer sam

221 Our studies indicate that Pten-NOLC1 gene fusion is a driver for human cancers.

222 Genomic disruption of Pten-NOLC1 induces cancer cell death, while genomic inte

223 The product of Pten-NOLC1 is a nuclear protein that interacts and activ

224 a Pten derived pro-cancer growth gene fusion Pten-NOLC1 originated from a chr10 genome rearrangement

225 Pten-NOLC1 promotes cancer proliferation, growth, invasi

226 ces the survival of animals xenografted with Pten-NOLC1-expressing cancer cells.

227 Interestingly, alternative exon usage by PTEN null cells is increased under metabolic stress in c

228 The glucose-deprived PTEN null cells were found to continue global gene trans

229 Importantly, PTEN null human cancer cells and in vivo murine models a

230 on-induced neuroendocrine differentiation of Pten null prostate adenocarcinoma, corroborates that the

231 This is accomplished by reconstitution of PTEN-null embryoid bodies with PTEN mutants that lack on

232 ant delay in the onset of prostate cancer in Pten-null mice, whereas Kdm5b loss alone caused no morph

233 tumors expressed higher levels of STING, and PTEN-null TNBC cell lines were hyperresponsive to STING

234 PTEN-null TNBC cells expressing a phosphomimetic version

235 Consistent with this data, PTEN-null TNBC tumors expressed higher levels of STING,

236 This emerging role of PTEN on global transcriptional regulation is providing a

237 e established orthotropic Frmd6 and Pten, or Pten only (control) knockout in the ROSA26 mouse prostat

238 Deletion of DNA-PK or PTEN, or inhibition of DNA-PK sensitized recovering BLBC

239 inally, we established orthotropic Frmd6 and Pten, or Pten only (control) knockout in the ROSA26 mous

240 TP53 contexts, whereas other targets such as PTEN, p27, and EpCAM gain relevance and mediate miR-30e-

241 by composite biomarker subgroup for PI3K/AKT/PTEN pathway activation status.

242 xtend cPFS in mCRPC irrespective of PI3K/AKT/PTEN pathway activation status.

243 lts were consistent irrespective of PI3K/AKT/PTEN pathway activation status.

244 nd MS analysis workflows, targeted different PTEN peptides, and were performed in different laborator

245 hat Rab7, a recently identified substrate of PTEN phosphatase activity, is also a substrate of the in

246 proteins and is concurrent with increases in PTEN phosphatase activity.

247 While the loss of the tumor suppressor, PTEN (phosphatase and tensin homolog), is well studied i

248 Tumor suppressor PTEN (phosphatase and tensin homologue deleted on chromo

249 ne (H)3 methylation and deacetylation at the PTEN promoter.

250 ogen deprivation in combination with loss of PTEN promotes the upregulation of CDCP1 and the subseque

251 cells, ceRNA depletion resulted in decreased PTEN protein levels, a result similar to the findings re

252 er(Ex5)) HCT116 cells, we observed increased PTEN protein levels.

253 l characterized, the biological relevance of PTEN protein-phosphatase activity remains undefined.

254 or (GR) levels, which are rescued by loss of PTEN protein-phosphatase activity to restrain cell survi

255 ammary tumorigenesis, the additional loss of PTEN protein-phosphatase activity triggered an extensive

256 n PTEN, the ability of PRL2 to down-regulate PTEN provides a biochemical basis for its oncogenic prop

257 We targeted the PTEN proximal promoter and 5' untranslated region with d

258 th predominantly cytoplasmic localization of Pten (Pten(m3m4/m3m4)).Cytoplasmic predominant Pten loca

259 ganoids lacking PTEN and overexpressing ERG (Pten(-/-) R26-ERG) faithfully recapitulated distinct sta

260 uide RNA (gRNA) achieved potent and specific PTEN repression in human cell line models and neural cel

261 also worked more effectively than shRNAs for Pten repression in rat neural crest-derived PC-12 cells,

262 N results in robust CNS axon regrowth, while PTEN repression with short hairpin RNA (shRNA) improves

263 Conditional genetic deletion of PTEN results in robust CNS axon regrowth, while PTEN rep

264 Germline variation in PTEN results in variable clinical presentations, includi

265 ly PTEN's lipid phosphatase activity or both PTEN's lipid and protein phosphatase activities.

266 yoid bodies with PTEN mutants that lack only PTEN's lipid phosphatase activity or both PTEN's lipid a

267 In this study, we demonstrate that PTEN's protein phosphatase activity is required for epib

268 istochemical analyses of PHF8, PKCalpha, and PTEN showed a positive correlation between PHF8 and PKCa

269 PTEN silencing with CRISPR/dCas9 epigenetic editing may

270 Restoration of PPM1A or PTEN similarly limits SMAD3 phosphorylation and the acti

271 lasia (HG-PIN) and hyperproliferation, while Pten single-knockouts developed only regular PIN lesions

272 lasts, moreover, results in PTEN loss, while PTEN stable depletion decreases PPM1A expression with ac

273 reover, we identified an association between PTEN status and Cav3.1 expression in these cells as a ma

274 ase inhibitor resistance, PIK3CA status, and PTEN status.

275 in (WAVE) regulatory complex (WRC), as a new PTEN substrate.

276 gions (including regions containing TP53 and PTEN) that were identified in patient samples by the TCG

277 ancer susceptibility to subtle reductions in PTEN, the ability of PRL2 to down-regulate PTEN provides

278 vide a novel therapeutic strategy to restore PTEN, thereby obliterating PTEN deficiency-induced malig

279 s with the loss of the tumor suppressor gene PTEN to promote the emergence of metastatic prostate can

280 The PTEN/TP53-deficient tumor demonstrates treatment resista

281 d a combination of four shRNAs targeting the PTEN transcript, a construct previously used in CNS inju

282 employed the CRISPR/dCas9 system to repress PTEN transcription in neural cells.

283 The PTEN tumor suppressor controls cell death and survival b

284 N at Y336, thereby augmenting NEDD4-mediated PTEN ubiquitination and proteasomal degradation.

285 ht guide personalized clinical decisions for PTEN-variant carriers.

286 ith a large, well-curated clinical cohort of PTEN-variant carriers.

287 cterize brain malformations in patients with PTEN variants and assess the relevance of their brain ma

288 y of cortical malformations in patients with PTEN variants and their impact on clinical phenotype are

289 We measured the ability of PTEN variants to rescue the spheroid formation phenotype

290 e clinical significance of cancer-associated PTEN variants.

291 to the clinical outcomes of individuals with PTEN variants.

292 pathogenic phosphatase and tensin homologue (PTEN) variants, but the frequency of cortical malformati

293 nism and demonstrate that tau interacts with PTEN via tau's proline-rich domain.

294 ciated with phosphatase and tension homolog (PTEN) via the PDZ domain to upregulate the phosphorylati

295 erted configuration" (MAGI)1-3 proteins with PTEN was assessed using the proximity ligation assay and

296 ssion of the phosphatase and tensin homolog (PTEN), which is one of the direct targets of miR-216a, w

297 dings were used to direct in vitro assays on Pten wild-type and Pten(m3m4/m3m4) microglia.

298 Therefore, non-PTEN aetiologies exist in PTEN wildtype patients.

299 The interaction of PTEN with all three MAGI proteins was transiently reduce

300 Furthermore, by measuring the association of PTEN with MAGI proteins a mechanism for the induction of