Mapping of a Serine-Rich Domain Essential for the Transcriptional, Antiapoptotic, and Transforming Activities of the v-Rel Oncoprotein

Volume 19, no. 1, p. 307–316, 1999. Since publication of this article, we found anomalies in Table 2 and Fig. 6. A secondary mutation was found in the JD214-D10 vector listed in Table 2 that is likely to be responsible for the transformation-defective phenotype observed in spleen cells. This unintentional mutation occurred during subcloning into JD214. Similarly, JD214-A10, also listed in Table 2, was found to contain a frameshift mutation. Investigation also revealed that mutants A6.7 and A6.7.10 were not tested in spleen transformation assays, contrary to what was reported in Table 2, and that the protective activity of mutant A6.7.10 (Fig. 6B) was derived from cell clones different from those shown in Fig. 6A. In light of these anomalies, we withdraw the data in Table 2 and Fig. 6 derived from these mutants. These mistakes do not affect the other figures in the paper and do not alter the main conclusion that the transcriptional activity of v-Rel correlates with cell transformation and protection from tumor necrosis factor alpha-induced cell death. We apologize for any confusion that these errors may have caused.