BCL6 de-repression induces the fasting transcriptome and protects from steatosis (ChIP-Seq I)

Here, we find that the B cell lymphoma 6 (BCL6) repressor is enriched upon feeding and converges genome-wide with PPARs to opposingly control lipid metabolism. Overall design: Identification of BCL6, PPARa, PPARd, and H3K27ac binding sites in fasted and fed livers.

本研究发现，B细胞淋巴瘤6（BCL6）阻遏蛋白在进食后表达富集，并可在全基因组范围内与过氧化物酶体增殖物激活受体（PPARs）发生结合位点趋同，进而反向调控脂质代谢。整体实验设计：在禁食与进食状态的肝脏组织中，鉴定BCL6、PPARα、PPARδ以及组蛋白H3第27位赖氨酸乙酰化修饰（H3K27ac）的结合位点。