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To determine if the reducing and dominant-negative activity of mER[beta]2 was in part due to differential and ligand-specific co-regulator recruitment, we co-transfected the mER[beta]2 or mER[beta]1expression plasmid with SRC1, SRC2, or SRC3 expression plasmid in HepG2 cells and then treated with [10.sup.-8] M [E.sub.2] (mER[beta]1), [10.sup.-7] M [E.sub.2] (mER[beta]2), or [10.sup.-6] M BPA, BPAF, HPTE or Gen (Figure 4).
Furthermore, miR33 also targets hydroxyacyl-CoA-dehydrogenase (HADBH) [8, 58], sirtuin-6 (SIRT6), and AMP-activated protein kinase subunit-a (AMPKa) [58], while miR-33* targets steroid receptor coactivator 1 (SRC1), SRC3, nuclear transcription factor Y (NFYC), and receptor-interacting protein 140 (RIP140).
Silencing of either VDR, SRC2, or SRC3 resulted in decreases in specific glucosylceramide (GlcCer) species but not other lipids such as cholesterol and free fatty acids.