Background: ZFP57 is a maternal-zygotic effect gene that maintains genomic imprinting in mouse embryos. Results: KAP1 facilitates the interaction between ZFP57 and DNA methyltransferases. The KRAB box of ZFP57 is required for maintaining DNA methylation imprint in ES cells. Conclusion: ZFP57 recruits DNA methyltransferases and maintains DNA methylation imprint through KRAB box-mediated interaction.Significance: This work implies that ZFP57 recruits DNA methyltransferases via KAP1 to maintain DNA methylation imprint.
TLR activation by multiple pathways leads to triglyceride accumulation in macrophages that could contribute to the accelerated atherosclerosis seen in chronic infections and inflammatory diseases.
Objective-Toll-like receptors (TLRs) recognize pathogens and mediate signaling pathways important for host defense.Recent studies implicate TLR polymorphisms in atherosclerosis risk in humans. Adipocyte fatty acid-binding protein (aP2) is present in macrophages and has an important role in atherosclerotic plaque development. We investigated aP2 expression in RAW 264.7 cells treated with lipopolysaccharide (LPS) and other TLR agonists and assessed lipid accumulation in these activated murine macrophages. Methods and Results-Stimulation with LPS, a TLR4 ligand, resulted in a 56-fold increase in aP2 mRNA expression, and zymosan, a TLR2 ligand, induced an Ϸ1500-fold increase. Polyinosine: polycytidylic acid (poly I:C), a TLR3 ligand, led to a 9-fold increase. Levels of aP2 protein were significantly increased in LPS or zymosan-treated macrophages compared with control or poly I:C-treated cells. In addition, the cholesteryl ester content of LPS or zymosan-treated macrophages was Ϸ5-fold greater in the presence of low-density lipoprotein, and triglyceride content was Ϸ2-fold greater in the absence of exogenous lipid than control or poly I:C-treated cells.
Conclusions-Expression
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