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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 caused by the expression of inactive mutant PTEN protein.
4 nt in ATP show an increased level of nuclear PTEN protein.
9 ate event, although a dose-dependent loss of PTEN protein and function has been implicated in early s
10 ating agent sodium butyrate (NaBT) increased PTEN protein and mRNA expression and induced c-Jun NH2-t
13 sely correlated with the endogenous level of PTEN protein and overexpression of PTEN-blocked Akt phos
14 egulation leads to a decreased expression of PTEN protein and stimulation of PI3K as well as phosphor
15 (DSF-Cu) led to the decreased expression of PTEN protein and the activation of AKT in a dose- and ti
16 stal axonal attenuation of miR-19a increased PTEN proteins and inactivated mTOR in the axons, but did
17 ster reduced phosphatase and tensin homolog (PTEN) proteins and elevated phosphorylated mammalian tar
18 nced nuclear-cytoplasmic localization of the Pten protein, and we developed the Pten(m3m4) model to s
19 and tensin homolog deleted in chromosome 10 (PTEN) protein, and PTEN phosphatase activity in cerebell
20 resulted in the transduction of a functional PTEN protein as evidenced by the upregulation of p27 and
21 nificantly blocked zinc-induced reduction of PTEN protein as well as the increase in Akt phosphorylat
23 nd tissue-specific fashion with the TSC2 and PTEN proteins being coordinately regulated in those tiss
24 dent degradation and diminished abundance of PTEN protein but increased PTEN phosphatase activity.
25 hereas the tumor suppressive activity of the PTEN protein can be altered at multiple levels through a
28 nuclear mislocalization, resulting in rapid PTEN protein degradation, suppression of p53-mediated tr
34 and leukemias, the Jurkat T cell line lacks PTEN protein due to frame-shift mutations in both PTEN a
35 f urothelial carcinoma samples found loss of PTEN protein expression (36.4%, n = 11) and elevation of
37 t when fibroblasts are attached to collagen, PTEN protein expression and activity are inhibited due t
38 rmline PTEN promoter mutations have aberrant PTEN protein expression and an increased frequency of br
40 e investigated the association between tumor PTEN protein expression and disease-free survival (DFS)
41 elated with PTEN mutation status; decreasing PTEN protein expression correlated with increasing CC sc
43 esized that phytoestrogen exposure regulates PTEN protein expression in the breast cancer cell line,
44 suggesting that the mechanism for increased PTEN protein expression is dependent upon transcription.
49 unexpected mechanism by which PD-1 decreases PTEN protein expression while increasing PTEN activity,
50 of p53 expression resulted in a decrease in PTEN protein expression, suggesting that p53 plays a cri
58 y number increases of the gene and decreased PTEN protein function occurring through loss or haploins
63 elic mutated or PTEN wild-type patients lack PTEN protein, implying that additional PTEN inactivation
64 lted in a significant reduction in levels of PTEN protein in a dose- and time-dependent fashion in a
70 tructed different PTEN mutants that targeted PTEN protein into different subcellular compartments.
75 On the basis of experiments with two mutant PTEN proteins, it is shown that PI(4,5)P2 induces this c
77 In general, the inverse correlation between PTEN protein level and Akt phosphorylation was found in
79 zinc treatment results in a reduction of the PTEN protein level in parallel with increased NEDD4-1 ge
80 1 and PRL2 is negatively correlated with the PTEN protein level in the testis and PRL1(+/-)/PRL2(-/-)
81 PTEN and/or PTENP1 resulted in downregulated PTEN protein levels (Figure 2H), downregulation of both
82 hemia and 30-minute reperfusion (I-15/R-30), PTEN protein levels and activity were decreased, and lev
83 ns in MSI- CRCs lead to loss or reduction of PTEN protein levels and contribute to tumor progression.
84 ction-blocking antibodies reduces endogenous PTEN protein levels and inhibits its accumulation at cel
85 evidence that E-cadherin regulates both the PTEN protein levels and its recruitment to cell-cell jun
86 N-targeting miR-19a and miR-21 modulates the PTEN protein levels and the CS and CSL phenotypes, irres
88 th high levels of pAKT and MKRN1 expression, PTEN protein levels are low and correlate with a low 5-y
89 ata indicate that BMP2 exposure can regulate PTEN protein levels by decreasing PTEN's association wit
90 xonal outgrowth and that local modulation of PTEN protein levels by miR-19a likely contributes to the
94 We found that exposure to BMP2 increased PTEN protein levels in a time- and dose-dependent manner
97 to determine whether BMP2 stimulation alters PTEN protein levels in the breast cancer line, MCF-7.
99 sia with and without atypia exhibited higher PTEN protein levels than normal mammary epithelial cells
100 In PHT gastric mucosa 6 h after injury, PTEN protein levels were increased by 2.7-fold; unphosph
113 data suggest that the timing of the loss of PTEN protein plays a critical role in determining the di
116 ormalities mediated the relationship between PTEN protein reductions and reduced cognitive ability.
118 s some light on the mechanisms that regulate PTEN protein stability, which is important to fully eluc
122 activity with siRNA or by expressing active PTEN protein stimulated apoptotic signaling, which reduc
124 was transferred into melanoma cells lacking PTEN protein to express the protein at normal physiologi
125 urthermore, we demonstrate that reduction of PTEN protein to heterozygote levels in human MCF7 cells
126 with an E-cadherin blocking antibody reduced PTEN protein to undetectable levels in wild-type F9 cell
131 and tensin homolog deleted on chromosome 10 (PTEN) protein when compared with CD56(dim) NK cells.
132 t phosphorylation, we examined expression of PTEN protein, which acts as a negative regulator of the
133 , and 60% of these samples had low or absent PTEN protein, which could not be attributed to gene sile
134 ngly, some malignancies exhibit undetectable PTEN protein without mutations or loss of PTEN mRNA.
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