INT28215
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
We have found that p53 protein accumulated in a dose- and time-dependent manner after Dx treatment, while p21 expression increased over time with low but decreased with high Dx doses. | |||||||||||||||
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We then studied expression of p53 and p21, cell-cycle kinetics and apoptosis. | |||||||||||||||
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While these investigators also showed that p21 levels were reduced in Pkd1 knockout mice, there has to our knowledge been no published study examining the function of p21 in human tissues or in non-knockout animal models of this disease. | |||||||||||||||
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Expression of p21 in cortical homogenates from control and cystic Han:SPRD animals was assessed by immunoblotting (Fig. 3). | |||||||||||||||
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Antisense p21 ODN transfection of MDCK cells at 400 and 600 nM showed increased cell proliferation as compared to cells transfected with scrambled control ODN (Fig. 5b). | |||||||||||||||
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Consistent with this finding, our data indicate reduced expression of p21 in cystic kidneys from male, but not female, Han:SPRD rats. | |||||||||||||||
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However, our finding that p21 is decreased in ADPKD, while in agreement with earlier studies showing that PKD1-deficient cells express lower p21, is not in complete concordance with the mTOR inhibitor data. | |||||||||||||||
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Our present findings that ADPKD, which is characterized by increased RTE cell growth, may in fact be a disease which results from diminished p21 expression in affected tissues are consistent with recent data showing that polycystin-1 induces p21 [9] and causes resistance to apoptosis [23]. | |||||||||||||||
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In this study, we examine the expression of p21 in human tissue as well as in rat tissues. | |||||||||||||||
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In contrast, renal p21 expression in cystic females did not differ from that seen in noncystic control females. | |||||||||||||||
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Renal expression of p21 was significantly attenuated in cystic male rats, as compared with noncystic controls (p < 0.01). | |||||||||||||||
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To clarify the basis for cell killing during prostate cancer radiotherapy, we determined the IR-induced expression of several apoptotic- (bax, bcl-2, survivin and PARP) and G1-cell cycle checkpoint- (p53 and p21(WAF1/Cip1)) related proteins, in both normal (PrEC-epithelial and PrSC-stromal) and malignant (LNCaP, DU-145 and PC-3; all epithelial) prostate cells. | |||||||||||||||
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We observed that IR-induced bax and p21(WAF1/Cip1) protein expression were attenuated selectively in normal stromal and epithelial cell cultures, yet maintained their p53-dependency in malignant cell lines. | |||||||||||||||
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Terminal growth arrest was dose-responsive at 96 h following irradiation and associated with long-term expression of both p21(WAF1/Cip1) and p16(INK4a) genes. | |||||||||||||||
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Terminal growth arrest was dose-responsive at 96 h following irradiation and associated with long-term expression of both p21(WAF1/Cip1) and p16(INK4a) genes. | |||||||||||||||
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Inhibition of PKCbeta(1)-mediated overexpression of p21(waf1/cip1) partially reduced the anti-apoptotic effect of PKCbeta(1). | |||||||||||||||
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We observed that IR-induced bax and p21(WAF1/Cip1) protein expression were attenuated selectively in normal stromal and epithelial cell cultures, yet maintained their p53-dependency in malignant cell lines. | |||||||||||||||
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To clarify the basis for cell killing during prostate cancer radiotherapy, we determined the IR-induced expression of several apoptotic- (bax, bcl-2, survivin and PARP) and G1-cell cycle checkpoint- (p53 and p21(WAF1/Cip1)) related proteins, in both normal (PrEC-epithelial and PrSC-stromal) and malignant (LNCaP, DU-145 and PC-3; all epithelial) prostate cells. | |||||||||||||||
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The expression of COX-1 and COX-2. and of two cyclin dependent kinase inhibitors, p21Cip1 and p27Kip1, was analysed by Western blotting and RT-PCR. | |||||||||||||||
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Higher concentrations of indomethacin and dexamethasone also up-regulated p21Cip1/Waf1 expression in hBMSCs, and so did celecoxib on D1-cells. | |||||||||||||||
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