GSK J5 HCl

GSK-J5 hydrochloride is a cell-permeable ester derivative of GSK J2 (HY-15648A), inactive. GSK-J5 hydrochloride is also an isomer of GSK-J4 (HY-15648B) and often used as a negative group[1].

Research Areas >> Cancer

Signaling Pathways >> Epigenetics >> Histone Demethylase

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].

[1]. Laurens Kruidenier, et al. A selective jumonji H3K27 demethylase inhibitor modulates the proinflammatory macrophage response. Nature. 2012 Aug 16;488(7411):404-8.