SCL regulates the expression of survival genes in progenitors. (A) Strategy used to identify genes controlled by SCL and Kit in human CD34⁺ TF-1 cells. (B) Schematic diagram representing our approach to analyze microarray data. We performed a paired comparison between TF-1 cells stimulated with either SF or GM-CSF and TF-1 cells harboring either the empty vector or the ΔbSCL under SF treatment. Nineteen survival genes were found to be coregulated by SCL and Kit signaling. (C) Relative expression levels for the 19 genes modulated by SCL and Kit. Ratio of gene expression levels of control cells (MSCV) stimulated with SF over GM-CSF, and of ΔbSCL-expressing cells over control cells, both stimulated with SF. ^a, ChIP-Seq peaks identified by Wilson et al³⁵  with anti-SCL, LMO2, or GATA-1 antibodies; ^b, ChIP-Seq peaks identified by Kassouf et al²⁷  with anti-SCL. (D) TF-1 cells harboring either the empty vector or ΔbSCL were treated with GM-CSF or SF (upper panel), or TF-1 cells expressing SCL were treated with GM-CSF (lower panel). Api-5 mRNA levels were assessed by semiquantitative RT-PCR. Data shown are the means ± SD of n experiments. (E) SCL occupies several loci by ChIP. E boxes within the proximal promoters of the indicated genes are shown (left panel). TF-1 cell chromatin extracts were subjected to immunoprecipitation with SCL antibody or with species-matched control immunoglobulin G (right panel). Fold enrichments were calculated as described in “Materials and methods.”