American Society of Hematology

Figure 4

$Figure 4. BCL6 targets involved in multiple pathways are responsive to BCL6 silencing. (A) Seventeen targets representative of the major pathways affected by BCL6 were analyzed in the P3HR1 cell line. The BCL6-bound promoter region identified by ChIP-on-chip in GC B cells was tested for direct binding in P3HR1 by qChIP. All promoters, except JAK3, showed enrichment of at least 2-fold in the BCL6 immunoprecipitated chromatin fraction. (B) BCL6 silencing was obtained by the use of 2 shRNAs delivered by lentiviral infection in P3HR1. Quantitative reverse-transcription PCR analysis showed that the expression of 11 of 17 targets increased more than 2-fold upon BCL6 silencing by at least one of the shRNA. The target induction appeared consistent with the level of BCL6 silencing in all cases, except STAT5A. (C) BCL6 protein expression as detected by immunoblotting upon infection with control and BCL6 shRNAs.$

BCL6 targets involved in multiple pathways are responsive to BCL6 silencing. (A) Seventeen targets representative of the major pathways affected by BCL6 were analyzed in the P3HR1 cell line. The BCL6-bound promoter region identified by ChIP-on-chip in GC B cells was tested for direct binding in P3HR1 by qChIP. All promoters, except JAK3, showed enrichment of at least 2-fold in the BCL6 immunoprecipitated chromatin fraction. (B) BCL6 silencing was obtained by the use of 2 shRNAs delivered by lentiviral infection in P3HR1. Quantitative reverse-transcription PCR analysis showed that the expression of 11 of 17 targets increased more than 2-fold upon BCL6 silencing by at least one of the shRNA. The target induction appeared consistent with the level of BCL6 silencing in all cases, except STAT5A. (C) BCL6 protein expression as detected by immunoblotting upon infection with control and BCL6 shRNAs.

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