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1 prostate tumors correlates with loss of the PTEN protein.
2 of transcript and relatively high levels of PTEN protein.
3 KO phenotypes are caused by dysregulation of PTEN protein.
4 caused by the expression of inactive mutant PTEN protein.
5 nt in ATP show an increased level of nuclear PTEN protein.
10 ate event, although a dose-dependent loss of PTEN protein and function has been implicated in early s
11 ating agent sodium butyrate (NaBT) increased PTEN protein and mRNA expression and induced c-Jun NH2-t
14 sely correlated with the endogenous level of PTEN protein and overexpression of PTEN-blocked Akt phos
15 egulation leads to a decreased expression of PTEN protein and stimulation of PI3K as well as phosphor
16 (DSF-Cu) led to the decreased expression of PTEN protein and the activation of AKT in a dose- and ti
17 stal axonal attenuation of miR-19a increased PTEN proteins and inactivated mTOR in the axons, but did
18 ster reduced phosphatase and tensin homolog (PTEN) proteins and elevated phosphorylated mammalian tar
19 nced nuclear-cytoplasmic localization of the Pten protein, and we developed the Pten(m3m4) model to s
20 and tensin homolog deleted in chromosome 10 (PTEN) protein, and PTEN phosphatase activity in cerebell
21 resulted in the transduction of a functional PTEN protein as evidenced by the upregulation of p27 and
22 nificantly blocked zinc-induced reduction of PTEN protein as well as the increase in Akt phosphorylat
23 sm involves truncation of the 403 amino acid PTEN protein at amino acid 68 by the Y68 frame shift, le
25 nd tissue-specific fashion with the TSC2 and PTEN proteins being coordinately regulated in those tiss
26 dent degradation and diminished abundance of PTEN protein but increased PTEN phosphatase activity.
27 hereas the tumor suppressive activity of the PTEN protein can be altered at multiple levels through a
30 tivation and phosphatase and tensin homolog (PTEN) protein deactivation predicted axon growth across
31 nuclear mislocalization, resulting in rapid PTEN protein degradation, suppression of p53-mediated tr
37 and leukemias, the Jurkat T cell line lacks PTEN protein due to frame-shift mutations in both PTEN a
38 f urothelial carcinoma samples found loss of PTEN protein expression (36.4%, n = 11) and elevation of
40 t when fibroblasts are attached to collagen, PTEN protein expression and activity are inhibited due t
41 rmline PTEN promoter mutations have aberrant PTEN protein expression and an increased frequency of br
43 e investigated the association between tumor PTEN protein expression and disease-free survival (DFS)
44 n and poor overall survival, whereas lack of PTEN protein expression associated with lower progressio
45 elated with PTEN mutation status; decreasing PTEN protein expression correlated with increasing CC sc
47 esized that phytoestrogen exposure regulates PTEN protein expression in the breast cancer cell line,
48 suggesting that the mechanism for increased PTEN protein expression is dependent upon transcription.
49 of eight melanoma samples with focal loss of PTEN protein expression to understand the features and m
54 ritic arborization, and spine density, while PTEN protein expression was significantly increased in F
55 unexpected mechanism by which PD-1 decreases PTEN protein expression while increasing PTEN activity,
56 of p53 expression resulted in a decrease in PTEN protein expression, suggesting that p53 plays a cri
57 or PTENP1 depletion in DU145 cells decreased PTEN protein expression, which was similar to the origin
65 y number increases of the gene and decreased PTEN protein function occurring through loss or haploins
71 elic mutated or PTEN wild-type patients lack PTEN protein, implying that additional PTEN inactivation
72 lted in a significant reduction in levels of PTEN protein in a dose- and time-dependent fashion in a
79 tructed different PTEN mutants that targeted PTEN protein into different subcellular compartments.
85 On the basis of experiments with two mutant PTEN proteins, it is shown that PI(4,5)P2 induces this c
87 In general, the inverse correlation between PTEN protein level and Akt phosphorylation was found in
89 zinc treatment results in a reduction of the PTEN protein level in parallel with increased NEDD4-1 ge
90 1 and PRL2 is negatively correlated with the PTEN protein level in the testis and PRL1(+/-)/PRL2(-/-)
91 PTEN and/or PTENP1 resulted in downregulated PTEN protein levels (Figure 2H), downregulation of both
92 hemia and 30-minute reperfusion (I-15/R-30), PTEN protein levels and activity were decreased, and lev
93 ns in MSI- CRCs lead to loss or reduction of PTEN protein levels and contribute to tumor progression.
94 ction-blocking antibodies reduces endogenous PTEN protein levels and inhibits its accumulation at cel
95 evidence that E-cadherin regulates both the PTEN protein levels and its recruitment to cell-cell jun
97 N-targeting miR-19a and miR-21 modulates the PTEN protein levels and the CS and CSL phenotypes, irres
99 th high levels of pAKT and MKRN1 expression, PTEN protein levels are low and correlate with a low 5-y
101 ata indicate that BMP2 exposure can regulate PTEN protein levels by decreasing PTEN's association wit
102 xonal outgrowth and that local modulation of PTEN protein levels by miR-19a likely contributes to the
106 We found that exposure to BMP2 increased PTEN protein levels in a time- and dose-dependent manner
110 to determine whether BMP2 stimulation alters PTEN protein levels in the breast cancer line, MCF-7.
113 sia with and without atypia exhibited higher PTEN protein levels than normal mammary epithelial cells
114 In PHT gastric mucosa 6 h after injury, PTEN protein levels were increased by 2.7-fold; unphosph
117 cells, ceRNA depletion resulted in decreased PTEN protein levels, a result similar to the findings re
126 vation identified tumors more likely to have PTEN protein loss (p = 4 x 10(-37)) and metabolically pe
130 o its lipid phosphatase activity, a role for PTEN protein phosphatase activity in cell cycle regulati
131 K1 autophosphorylation in its activation and PTEN protein phosphatase activity in governing glycolysi
132 the Y68 frame shift, leading to the loss of PTEN protein phosphatase and lipid phosphatase activitie
133 l characterized, the biological relevance of PTEN protein-phosphatase activity remains undefined.
134 or (GR) levels, which are rescued by loss of PTEN protein-phosphatase activity to restrain cell survi
135 ammary tumorigenesis, the additional loss of PTEN protein-phosphatase activity triggered an extensive
136 data suggest that the timing of the loss of PTEN protein plays a critical role in determining the di
139 ormalities mediated the relationship between PTEN protein reductions and reduced cognitive ability.
141 s some light on the mechanisms that regulate PTEN protein stability, which is important to fully eluc
145 activity with siRNA or by expressing active PTEN protein stimulated apoptotic signaling, which reduc
147 was transferred into melanoma cells lacking PTEN protein to express the protein at normal physiologi
148 urthermore, we demonstrate that reduction of PTEN protein to heterozygote levels in human MCF7 cells
149 with an E-cadherin blocking antibody reduced PTEN protein to undetectable levels in wild-type F9 cell
155 and tensin homolog deleted on chromosome 10 (PTEN) protein when compared with CD56(dim) NK cells.
156 t phosphorylation, we examined expression of PTEN protein, which acts as a negative regulator of the
157 , and 60% of these samples had low or absent PTEN protein, which could not be attributed to gene sile
158 ngly, some malignancies exhibit undetectable PTEN protein without mutations or loss of PTEN mRNA.