Figure 7.
Figure 7. ChIP assays of RNA Pol II binding to the cyclin D1 promoter and IgH regulatory regions. (A) Pol II bound to the cyclin D1 promoter in the cyclin D1+ MCL cell lines Granta (G), NCEB-1 (N). Pol II also bound to IgH regulatory regions (Eμ, HS4, HS3) in Granta, NCEB-1, and Manca (M) cells, which contain chromosomal translocation involving IgH regulatory elements. Myeloid HL60 cells were used as a negative control. (B) MCF7, a cyclin D1+ breast cancer cell line, demonstrated Pol II binding in the cyclin D1 promoter region but not the IgH regulatory elements. EBV-immortalized human B cells, LCL1 and LCL2, showed Pol II binding in the Eμ intronic enhancer region. K562 was used as a negative control. (C) Normal human CD4+ T cells (NT) and activated T-cell clone (D160) showed no Pol II binding in either region. Granta (G) and NCEB-1 (N) were used as positive controls.

ChIP assays of RNA Pol II binding to the cyclin D1 promoter and IgH regulatory regions. (A) Pol II bound to the cyclin D1 promoter in the cyclin D1+ MCL cell lines Granta (G), NCEB-1 (N). Pol II also bound to IgH regulatory regions (Eμ, HS4, HS3) in Granta, NCEB-1, and Manca (M) cells, which contain chromosomal translocation involving IgH regulatory elements. Myeloid HL60 cells were used as a negative control. (B) MCF7, a cyclin D1+ breast cancer cell line, demonstrated Pol II binding in the cyclin D1 promoter region but not the IgH regulatory elements. EBV-immortalized human B cells, LCL1 and LCL2, showed Pol II binding in the Eμ intronic enhancer region. K562 was used as a negative control. (C) Normal human CD4+ T cells (NT) and activated T-cell clone (D160) showed no Pol II binding in either region. Granta (G) and NCEB-1 (N) were used as positive controls.

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