Figure 3
Figure 3. ChIP-Q-RT-PCR of apoptosis genes asso-ciated with SALL4 binding. Thirty-eight apoptosis genes identified by ChIP-chip were subjected to ChIP-Q-RT-PCR to confirm SALL4 binding by an alternative method. These genes are candidates for SALL4 involvement in leukemogenesis. (A) In NB4 cells, 35 of the 38 genes identified by ChIP-chip were confirmed as bound by SALL4 using ChIP-PCR. (B) Identification of SALL4 binding to apoptosis genes in CD34+ cells sorted from human bone marrow samples. CD34+ cells are likely progenitor cells to the promyelocytic cell line NB4 within these lineages. Identified SALL4 target genes had more than 2-fold enrichment compared with the input control. The position of negative control primers is presented in Figure S1. In Figure 2B, primer neg-2 failed to amplify the experimental DNA but did amplify the input DNA, indicating the absence of DNA template in the experimental group. This is represented by a fold change of less than 0.001.

ChIP-Q-RT-PCR of apoptosis genes asso-ciated with SALL4 binding. Thirty-eight apoptosis genes identified by ChIP-chip were subjected to ChIP-Q-RT-PCR to confirm SALL4 binding by an alternative method. These genes are candidates for SALL4 involvement in leukemogenesis. (A) In NB4 cells, 35 of the 38 genes identified by ChIP-chip were confirmed as bound by SALL4 using ChIP-PCR. (B) Identification of SALL4 binding to apoptosis genes in CD34+ cells sorted from human bone marrow samples. CD34+ cells are likely progenitor cells to the promyelocytic cell line NB4 within these lineages. Identified SALL4 target genes had more than 2-fold enrichment compared with the input control. The position of negative control primers is presented in Figure S1. In Figure 2B, primer neg-2 failed to amplify the experimental DNA but did amplify the input DNA, indicating the absence of DNA template in the experimental group. This is represented by a fold change of less than 0.001.

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