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. Author manuscript; available in PMC: 2010 Apr 1.
Published in final edited form as: J Immunol. 2009 Apr 1;182(7):4167–4174. doi: 10.4049/jimmunol.0802976

FIGURE 4.

FIGURE 4

CREM regulates gene expression by a chromatin-dependent mechanism. a, U937 cells were stimulated with LPS for 0, 6, and 24 h and cells were harvested for ChIP analysis with Abs against CREM, acetylated histone 4, and an isotypic control, subsequently semiquantitative PCR with primers specific for the CD86 promoter was performed and the products were run on a 1.5% agarose gel (n = 3 experiments). b, −21 CRE mutated (M) or nonmutated (WT) CD86 promoter luciferase constructs were tranfected into U937 cells and subsequently treated with the HDAC inhibitor SAHA. Luciferase activity after treatment with SAHA was measured 24 h later and values were normalized to nontreated transfected cells. Number shows fold increase of luciferase after treatment with SAHA (n = 3 experiments).