Trans-repressor BEF-1 Phosphorylation A POTENTIAL CONTROL MECHANISM FOR HUMAN ApoE GENE REGULATION

摘要: Abstract Human apolipoprotein E is a plasma lipoprotein that appears to play an important protective role in the development of atherosclerosis. While little known about regulation apoE, recent studies have shown cytokines repress apoE synthesis both vivo and vitro. Furthermore, we recently endogenous gene negatively regulated by nuclear trans-repressor BEF-1 human HepG2 cell line. In this study demonstrate treatment cells with cytokine interleukin-1 interleukin-6 resulted induction isoform BEF-1, designated B1. The B1 could be blocked protein kinase inhibitor staurosporine, suggesting phosphorylated form BEF-1. As further support, also induced phorbol ester, subsequently inhibited implicating for C-mediated phosphorylation. Quantitation levels isoforms, presence cyclohexamide, provided evidence phosphorylation existing intracellular pool no change total level. Under conditions generated increased isoform, there was concomitant proportional decrease level mRNA. effect did not appear result improved binding regulatory region as DNA affinity identical native Our data suggest modulated differential phosphorylation, possibly through C pathway.