In this article (Cancer Res 2007;67:9490–500), which was published in the October 1, 2007 issue of Cancer Research (1), the corresponding author informed us that the same Mcl-1 Western blots were inadvertently duplicated in Fig. 4C and Fig. 3C. The corrected versions of both figures, and their corrected legends, appear below.

Figure 3C.

C, both U937/EV and U937/Mcl-1 cells were exposed to sorafenib (7.5 μg), TRAIL (75 ng/mL), or their combination for the indicated time intervals, and at the end cells were pelleted, lysed, and 30 μg of protein were separated by SDS-PAGE, blotted, and probed with the corresponding anti–Mcl-1 and tubulin (to ensure equivalent loading and transfer) antibodies. The results of a representative study are shown; two additional experiments yielded similar results.

Figure 3C.

C, both U937/EV and U937/Mcl-1 cells were exposed to sorafenib (7.5 μg), TRAIL (75 ng/mL), or their combination for the indicated time intervals, and at the end cells were pelleted, lysed, and 30 μg of protein were separated by SDS-PAGE, blotted, and probed with the corresponding anti–Mcl-1 and tubulin (to ensure equivalent loading and transfer) antibodies. The results of a representative study are shown; two additional experiments yielded similar results.

Close modal
Figure 4C.

C, expression levels of Mcl-1 were determined in whole lysates of U/casp8DN and U/EV cells exposed to sorafenib (7.5 μmol/L), TRAIL (75 ng/mL), or the combination (S24→T) as indicated; blots were subsequently stripped and probed with a tubulin antibody to ensure equivalent loading and transfer. Analysis of conformational change in Bax and Bak was done using extracts from the same cells; lysates were prepared, immunoprecipitated with either anti–Bak-Ab1– or anti–Bax-6A7–specific antibodies, followed by immunoblotting with anti-Bak or anti-Bax antibodies, respectively, as described in Materials and Methods. Each lane was loaded with 30 μg of protein; IgG controls confirm equivalent loading and transfer. The results of a representative study are shown; two additional experiments yielded similar results.

Figure 4C.

C, expression levels of Mcl-1 were determined in whole lysates of U/casp8DN and U/EV cells exposed to sorafenib (7.5 μmol/L), TRAIL (75 ng/mL), or the combination (S24→T) as indicated; blots were subsequently stripped and probed with a tubulin antibody to ensure equivalent loading and transfer. Analysis of conformational change in Bax and Bak was done using extracts from the same cells; lysates were prepared, immunoprecipitated with either anti–Bak-Ab1– or anti–Bax-6A7–specific antibodies, followed by immunoblotting with anti-Bak or anti-Bax antibodies, respectively, as described in Materials and Methods. Each lane was loaded with 30 μg of protein; IgG controls confirm equivalent loading and transfer. The results of a representative study are shown; two additional experiments yielded similar results.

Close modal

The online version of the article has been corrected and no longer matches the print. The authors regret this error.

1.
Rosato
RR
,
Almenara
JA
,
Coe
S
,
Grant
S
. 
The multikinase inhibitor sorafenib potentiates TRAIL lethality in human leukemia cells in association with Mcl-1 and cFLIPL down-regulation
.
Cancer Res
2007
;
67
:
9490
500
.