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. 2006 May;26(9):3414–3431. doi: 10.1128/MCB.26.9.3414-3431.2006

FIG. 10.

FIG. 10.

PKCδ-dependent activation of topoisomerase IIα in response to DNA damage. (A and B) MOLT-4 cells were pretreated with or without rottlerin for 1 h followed by treatment with ara-C. Nuclear lysates (Nuc. Lysates) were analyzed by decatenation (A) and DNA relaxation (B) assays. DMSO, dimethyl sulfoxide; Cat. KDNA, catenated KDNA; Decat. KDNA, decatenated KDNA. (C) U-937 cells were treated as described above for panel A, and nuclear lysates were analyzed by the decatenation assays. (D) MOLT-4 cells were left untreated or treated with rottlerin for 1 h followed by the treatment with CDDP for the indicated times. Topoisomerase IIα activity was analyzed by decatenation assays. (E) U2-OS cells transfected with scrambled siRNA or PKCδsiRNA2 were left untreated or treated with ara-C for 4 h. Nuclear lysates were analyzed by the decatenation assays. (F) pkcδ+/+ and pkcδ−/− MEFs were left untreated or treated with ara-C for 4 h. Nuclear lysates were analyzed by the decatenation assays.