Role of c-MYC, STAT6, and PPARγ on the induction of c-MYC–sensitive M2 markers. Bioinformatic analysis identified candidate binding sites for c-MYC (CACGTG E-box sequence; ●) and STAT6 (TTCN_3-4GAA sequence; ○) in the putative promoter region of SCARB1 (c-MYC sites: −198/−202 and −765/−770; A); ALOX15 (c-MYC sites: +295/+301 and −1318/−1323; B); STAT6 (c-MYC sites: −273/−279, −798/−803, −1198/−1203, −1873/−1878; C); PPARγ (c-MYC sites: −224/−229; D); and CD209 (STAT6 sites: −408/−417, −1521/−1540, −1585/−1594; (E). No c-MYC- or STAT6-binding sites were identified in PCSK5 (F). ChIP experiments performed with an anti–c-MYC Ab (closed bars) and an isotypic control (open bars) on the promoter region of indicated genes from unstimulated (M0) and IL-4–stimulated macrophages (M2) confirmed c-MYC binding in the putative promoter region of SCARB1, ALOX15, STAT6, and PPARγ (A- D). No evidence for c-MYC binding in the promoter region of CD209 (E) or PCSK5 (F) was detected. Results are shown as means ± SD of n = 3 independent experiments. To evaluate the role of c-MYC, STAT6, and PPARγ on the induction of the alternative activation genes, the c-MYC inhibitor 10058-F4 (60μM), the JAK2/3 inhibitor AG490 (10μM), and the PPARγ antagonist GW9662 (10μM) or their respective vehicles were added to macrophage cultures during polarization with IL-4 (M2). After 24 hours, expression levels of SCARB1, ALOX15, STAT6, PPARγ, CD209, and PCSK5 (panels G through L, respectively) were evaluated by Q-PCR. Results are shown as means ± SD of n = 3 independent experiments.