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. Author manuscript; available in PMC: 2009 Apr 1.
Published in final edited form as: Mol Cancer Ther. 2008 Apr;7(4):905–914. doi: 10.1158/1535-7163.MCT-07-0515

Figure 4.

Figure 4

Effects of proteasome inhibition by ALLN on RA- and UBE1L-mediated repression of PML/RARα domains, respectively. BEAS-2B cells were independently transfected with (A) PML or (B) RARα domain containing expression constructs. Indicated groups were also cotransfected with or without UBE1L. Following transfection, cells in the ALLN treatment groups were incubated with ALLN (100 μmol/L) for 90 additional minutes. RA (1 μmol/L) was then added to the respective RA treatment groups and incubated for 6 additional h. Remaining groups were incubated with the vehicle (DMSO) during this same treatment period. Immunoblot analyses revealed that ALLN inhibited RA-dependent repression of the RARα domain and UBE1L-dependent repression of the PML domain of PML/RARα. Bottom, quantification of each of these signals.