Figure 5
Figure 5. KLF4 regulates expression of candidate target genes. (A) Forced KLF4 expression reduces c-Myc and augments p21CIP expression. BCR-ABL–transformed cells were infected with MIC-KLF4 and magnetically sorted after 24 hours. Parental cells were left untreated or treated with imatinib for 4 hours. Lysates were immunoblotted with indicated antibodies. Representative blot from 3 experiments is shown. (B) Restoration of c-Myc does not rescue depletion by KLF4. v-Abl cells were double infected as in Figure 4B and maintenance of cells expressing both markers was measured from 24 to 48 hours. (+) indicates empty vector. (C, D) Compiled Oncomine expression data for p21CIP and cyclin D2 with normal lymphoid tissue compared with the indicated B-cell malignancies (*P < .05, **P < .01).

KLF4 regulates expression of candidate target genes. (A) Forced KLF4 expression reduces c-Myc and augments p21CIP expression. BCR-ABL–transformed cells were infected with MIC-KLF4 and magnetically sorted after 24 hours. Parental cells were left untreated or treated with imatinib for 4 hours. Lysates were immunoblotted with indicated antibodies. Representative blot from 3 experiments is shown. (B) Restoration of c-Myc does not rescue depletion by KLF4. v-Abl cells were double infected as in Figure 4B and maintenance of cells expressing both markers was measured from 24 to 48 hours. (+) indicates empty vector. (C, D) Compiled Oncomine expression data for p21CIP and cyclin D2 with normal lymphoid tissue compared with the indicated B-cell malignancies (*P < .05, **P < .01).

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