Abstract

VOLUME 280 (2005) PAGES 30384–30391 We would like to acknowledge that the controls shown in Fig. 5, B and C, and Fig. 6C have also been used in a previous publication (Bykov, V. J., Issaeva, N., Shilov, A., Hultcrantz, M., Pugacheva, E., Chumakov, P., Bergman, J., Wiman, K. G., and Selivanova, G. (2002) Restoration of the tumor suppressor function to mutant p53 by a low-molecular-weight compound. Nat. Med. 8, 282–288). In Fig. 5, B and C, the control lanes in the gel shift assays, i.e. no treatment and supershift with PAb421 or PAb1801 antibody in the absence of test compound, are the same as those shown in the previous paper. Likewise, in Fig. 6C, the p53 immunostaining and Hoechst staining of untreated control cells is the same as that shown in the previous paper. The reason for this mistake is that we examined the two novel mutant p53-targeting compounds PRIMA-1 and MIRA-1 side by side in several assays and then decided to publish our results in two separate papers. However, it should be noted that these controls can serve equally well as controls for both compounds. Therefore, this does not change the validity of the data nor the conclusions from the experiments.

Highlights

  • Reactivation of mutant p53 and induction of apoptosis in human tumor cells by maleimide analogs

  • The p53 immunostaining and Hoechst staining of untreated control cells is the same as that shown in the previous paper. The reason for this mistake is that we examined the two novel mutant p53-targeting compounds PRIMA-1 and MIRA-1 side by side in several assays and decided to publish our results in two separate papers

  • It should be noted that these controls can serve well as controls for both compounds

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Summary

Introduction

Reactivation of mutant p53 and induction of apoptosis in human tumor cells by maleimide analogs.

Results
Conclusion
Full Text
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