| In Vitro |
GSK-J5 (25 μM) has no effects at inhibiting the LPS-induced response of human primary macrophages derived from healthy volunteers. While GSK-J4 significantly reduced the expression of 16 of 34 LPS-driven cytokines as assessed by PCR array, such as TNF-α[1]. GSK-J5 (30 μM; 6 hours) is the inactive isomer of GSK-J4, has no effect on TNF-α protein production. But neither GSK-J4 nor GSK-J5 directly affects the levels of LPS-induced JMJD3 or of LPS-independent UTX and EZH2[1]. GSK-J5 (30 μM; 1 hour) can not prevent the LPS-induced loss of H3K27me3 associated with the TNFA TSS or block the recruitment of RNA polymerase II to this locus but GSK-J5 can. Finally, GSK-J4, but not GSK-J5, blocks the production of TNF-α by macrophages derived from patients with rheumatoid arthritis[1].
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