IndraLab
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"The tumor-suppressive role of miR-34a was confirmed by Luan et al. who also found that miR-34a levels reflect the status of tumor suppressor p53, and that miR-34a could activate the p53 signaling cascade of p53 expression independently, possibly through targeting of SIRT1 [XREF_BIBR]."
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"While transfection with empty vector and subsequent forskolin treatment again showed significant downregulation of p53 protein, p53 overexpression completely abrogated forskolin induced downregulation of p53 and showed no significant difference in p53 protein levels between forskolin stimulation and vehicle control."
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"13 These phenotypes seen in HPV16E6 expressing human cells have been reproduced using other means to inactivate p53 including expression of dominant negative p53 alleles and RNAi mediated depletion of p53 protein expression, XREF_BIBR - XREF_BIBR demonstrating that the phenotypes are likely derived from the effects of HPV16E6 on p53."
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"Expression of exogenous Plk1 and p53 in p53 deficient lung carcinoma H1299 cells greatly decreased the p53 mediated transcription from the p53 responsive p21 (WAF1), MDM2, and BAX promoters, whereas the kinase deficient mutant form of Plk1 failed to reduce the transcriptional activity of p53."
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"Similarly, Kuenzi et al., have reported increased p53-ser15 phosphorylation but decreased expression of p53 in fungal alkaloid, militarinone A treated N2a cells XREF_BIBR, indicating the activation of p53 by increased phosphorylation at ser15 might reduce p53 level in curcumin treated N2a cells."
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"Expression of exogenous Plk1 and p53 in lung carcinoma H1299 cells deficient in p53 greatly decreased the p53 mediated transcription of the p53 responsive p21, MDM2, and BAX promoters, whereas the kinase deficient mutant Plk1 failed to reduce the transcriptional activity of p53 [XREF_BIBR], suggesting that Plk1 mediated negative regulation of p53 might be a fundamental mechanism for the role of Plk1 in oncogenesis."
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"Compared with the EGFP control, overexpression of either RSL1D1-NT or RSL1D1-CT significantly increased the levels of p53 protein (Fig. 7E) by inhibition of p53 ubiquitination (Fig. 7F) in HCT116 cells, consistent with the increased level of p53 protein (Fig. 2B) and decreased p53 ubiquitination (Fig. 3A) in RSL1D1-downregulated cells."
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"Therapeutic strategies in mutant p53 cells include attempts to decrease mutant p53 expression, prevent mutant p53 from binding to target proteins, target downstream signalling molecules, restore the normal folding of the mutant protein or viral delivery of wildtype p53 or perhaps family members (summarised and discussed in [81,82,83])."
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"Given that depletion of mutant p53 and RUNX2 reduces the expression level of RUNX2 and mutant p53, respectively, it is likely that there exists a positive auto-regulatory feedback loop between mutant p53 and RUNX2, and this regulatory system might contribute to the low sensitivity of MiaPaCa-2 cells against SAHA."
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"Interestingly MDA-MB-231, has high levels of a mutant p53 and phospholipase D (PLD) activity, which provides a survival signal in these cells when deprived of serum growth factors (Hui et al., 2006), however in our results, mutant p53 levels is suppressed by all these three extracts.5
Conclusion."
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"The loss or mutation of p53 in many cancers leads to impaired cell cycle regulation, genomic instability, and the inhibition of apoptosis The protein levels of p53 in the per1 silenced cells tended to be lower than those in the control cells, indicating that per1 regulated p53 expression, and this activity may at least partially contribute to the apoptosis of per1 silenced cells."
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"The Chk signal transducers induce cell cycle arrest by phosphorylation of two critical effectors : inhibitory phosphorylation of the Cdc25 phosphatase results in CDK inactivation, while the activating phosphorylation of the p53 tumor suppressor stabilizes p53 and increases transcription of p53 target genes, including the cyclin dependent kinase inhibitor p21/CIP1/WAF-1."
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"We show that the C-terminal sequence of PEPD binds to the PRD in p53, which allows PEPD to accomplish two important tasks : (1) to prevent nuclear p53 phosphorylation in its transactivation domain andto reduce free nuclear p53 level, leading to inhibition of p53 trans-activation and trans-suppression activities, and (2) to prevent mitochondrial translocation of nuclear and cytosolic p53 by preventing p53 from binding to MDM2 (Figs."
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"Since a basal level of p53 is required for antioxidant activities in normal cell growth, the p53 and RPA complex formation may serve to mask this p53 domain and prevent the above-basal levels of free p53 from interrupting normal cellular functions, complementing the MDM2 function of sequestering and inactivating p53."
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"It is postulated that this hydroxylation on K382 of p53 negatively regulates the p53 pathway by antagonizing the acetylation (enhancer of p53 transcription) of this site, thereby promoting the interaction of p53 with its negative regulator double minute X human homolog (MDMX) and downregulating transcriptional activity of p53."