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. 2011 May;2(5):593–596. doi: 10.1177/1947601911420139

Figure 1.

Figure 1.

LIF is a direct transcriptional target of STAT5. (A) LIF expression is increased in M07e cells after activation of the JAK2-STAT5 pathway with IL-3. This was prevented by the addition of a specific STAT5 inhibitor (SI). Untreated control cells (RQ = 1) were used to normalize expression values. (B) Chromatin immunoprecipitation shows increased binding of STAT5 to a specific DNA motif in LIF promoter in IL-3–treated M07e cells (IP IL-3) compared to nonstimulated cells (IP Ctrl). Quantitative qPCR assays (bottom) confirm increased binding to a motif (G1) located 740 bp upstream of the transcription start site (TSS) but not to another putative binding motif (G2) located 154 bp upstream of the TSS. Input DNA (RQ = 1) was used to normalize values. An agarose gel of the PCR products (only for motif G1) is shown at the top. (C) LIF expression is increased in cell lines carrying the V617F activating mutation of JAK2 (HEL and SET-2) compared to cell line M07 and to peripheral blood from a healthy control (P < 0.05). (D) Treatment of JAK2-mutated cell lines HEL and SET-2 with a specific STAT5 inhibitor reduces the basal expression levels of LIF and OSM without affecting the expression of the STAT3-regulated gene CEBPD. For each gene, results show fold inhibition compared to untreated cells (RQ = 1).