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In the remaining cases, p53 function is abrogated by alternative oncogenic events such as hyperactivation of MDM2, the main repressor of p53.
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This strongly implicates the MET pathway in survival signaling upon p53 activation, as none of the cell lines used in this study has ALK translocations or detectable ALK expression (Cancer Cell Line Project, Welcome Trust Sanger Institute).
The key question then becomes: what determines the cellular response to p53 activation?
To test whether HMGB1 retention upon p53 loss was due simply to resumed proliferation, we depleted p53 in cells expressing high levels of p16.
The authors would also like to thank the Review Committee for their valuable contributions and the Affari Project for developing the online version of this document.
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However, the cancer lines we tested were all p53 defective.
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Western blot analyses of p53 and p21waf1 expression in total cell lysates of C8 cells before, or 8 h after, UV treatment.
However, the clinical worth of these drugs is limited a priori by the pleiotropic character of the p53 network.
It has been demonstrated that p53 mutations usually lead to immunopositivity.
It is estimated that 11 million cancer patients worldwide carry tumors expressing wild type p53, creating a unique therapeutic opportunity to harness its tumor suppressive function for selective elimination of cancer cells2.
Isolation and Cloning of Mutant p53 from DU145 Cells.
Current dogma maintains that ATM activates p53 in response to DNA damage by phosphorylating specific serines in both p53 and MDM2, thus preventing their interaction and leading to p53 stabilization44.
Lower damage favored pulsing while monotonic increasing was generated with higher damage.
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Thus, if Fas resistance is, in fact, mediated by some unstable protein factor, it is unlikely to be mutant p53 itself but, rather, it could be one of the proteins induced by the p53 mutants.
Therefore, we hypothesized that SLN pathways may alter cell fate choice by affecting the transactivation of the key p53 target genes mediating each response.
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Second, unlike the SASP, loss of nuclear HMGB1 and HMGB1 secretion required p53 activity.
Molecular and cellular analysis revealed P53 activation, DNA damage and repair, cell cycle arrest and apoptosis in the pathobiology.
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ATM and MET kinases govern cell fate choice upon p53 activation.
Especially, when p53 digital pulses were uncovered, numerous theoretical studies have demonstrated that the number of pulses may tip the balance between survival and death.
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Restoration of p53 function leads to tumour regression in vivo.
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For the sake of conciseness of the Introduction, an overview of p53 modeling results cited in this paragraph is provided in S1 Text.
The results presented here suggest that p53 has a key involvement in preventing the propagation of damaged hESCs when genome is threatened.
In both cases, p53 cooperates with Fas expression.
Boxes inside panels a and b represent Western blots of p53 mutants expression (amount of lysates used were normalized by protein concentration, data not shown).
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Inactivation of both p53 and Fas signaling are frequent events in cancer that play an important role in cancer progression.
We hope that making the results of our screen available to the community will inspire other teams to identify additional strategies to modulate the p53 response for therapeutic purposes and to generate a greater understanding of the p53 network.
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However, we cannot exclude the possibility that p53 immunostaining might be altered by ablative laser resurfacing in a different fashion in facial skin than was demonstrated in this study using forearm skin.
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RITA43, which binds directly to p53 and stabilizes it.
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ATM as a p53 agonist during the DNA damage response37.
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Both p53 and E2F1 are transcription factors involved in the decision process.
Second, small molecule inhibitors are available for both kinases, which could lead us to chemical strategies to modulate the cellular response to p53 activation.
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Is defective p53 the Achilles heel of the tumor?
This is the first report showing that ATM is required for survival upon pharmacological activation of p53 in the absence of exogenously introduced DNA damage.
However, no theoretical studies have been proposed to investigate bimodal p53 induction.
MDM2 or other p53 repressors4.
The majority among p53 mutant tumors express a single mutant allele of p53 (see p53 mutation database).
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Domyati and coworkers24 recently reported a similar approach in examining the effects of tretinoin therapy, superficial chemical peeling, and dermabrasion on p53 immunostaining.
DO1 antibody, and the relative amount of p53 was estimated as the ratios between p53 amounts in the precipitated obtained with Pab1620 or Pab240, and DO1 antibodies.
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Cells were selected in the medium with appropriate antibiotic, and the number of colonies was counted after 2 weeks and were calculated as a percentage of the number of colonies in the case of empty vector.
Thus, as several small molecule activators of p53 enter clinical trials, their efficacy will remain tied to a basic scientific question: what determines the cellular response to p53 activation?
If the repopulating keratinocytes are negative for p53 mutations, the risk of skin cancer development should be reduced.
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There exist three feedback loops: the negative feedback loop between p53 and Mdm2 (red and purple), the positive feedback loop involving p53, Akt, and Mdm2 (blue and purple), and the negative feedback loop between ATM and p53 via Wip1 (green).
This implies that the p53 network is irreducible, but tolerant of small mutations at some ordinary links, and this can be interpreted with evolutionary theory.
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In contrast to cytokine secretion, HMGB1 redistribution required the p53 tumor suppressor, but not its activator ATM.
RAS and the p53 tumor suppressor.
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