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. Author manuscript; available in PMC: 2021 Jul 28.
Published in final edited form as: J Cancer Res Clin Oncol. 2019 Apr 2;145(6):1437–1448. doi: 10.1007/s00432-019-02909-z

Fig. 3.

Fig. 3

Rel-B regulates CDK6, CCND3 and BCL2 expression in U-H01 HL cell line. a Single-locus ChIP confirmed the ChIP-Seq results and showed Rel-B binding enrichment on CDK6 (a-1), CCND3 (a-2) and BCL2 (a-3) gene promoters. Error bars represents the mean and SD. Three independent experiments were performed in triplicates. A representative assay is shown. b A significant decrease in CDK6, CCND3 and BCL2 protein level was observed in U-H01 cells following Rel-B depletion (b1) meanwhile their levels did not change upon cRel downregulation by a specific shRNA (b2). c The transcriptional control of the CDK6, CCND3 and BCL2 genes by Rel-B as assessed by Qt-PCR, showed decreased mRNA levels in response to Rel-B depletion via a specific shRNA. Error bars mean SD. Three independent experiments were performed in triplicates. This is a representative assay (c1–c4). Single-locus ChIP shows cRel enrichment on these promoters in GCB-Like BJAB (d) and ABC-Like HBL-1 cell lines. Error bars mean SD. Three independent experiments were performed in triplicates. This is a representative assay (e). Results shown in A, B and C were performed in L1236 HL cell line in supplementary Fig. 1 (SF1)