Liu, Yan published the artcileIdentification of a hormone response element that mediates suppression of APOF by LXR and PPARα agonists, Synthetic Route of 637-07-0, the publication is Biochimica et Biophysica Acta, Molecular and Cell Biology of Lipids (2020), 1865(3), 158583, database is CAplus and MEDLINE.
Here we show in human liver C3A cells that APOF mRNA levels are reduced by agonists of LXR and PPARα nuclear receptors. This neg. regulation requires co-incubation with the RXR agonist, retinoic acid. Bioinformatic anal. of the ∼2 kb sequence upstream of the APOF promoter identified one potential LXR and 4 potential PPARα binding sites clustered between nucleotides -2007 and -1961. ChIP anal. confirmed agonist-dependent binding of LXRα, PPARα, and RXRα to this hormone response element complex (HREc). A luciferase reporter containing the 2 kb 5′ APOF sequence was neg. regulated by LXR and PPARα ligands as seen in cells. This regulation was maintained in constructs lacking the ∼1700 nucleotides between the HREc and the APOF proximal promoter. Mutations of the HREc that disrupted LXRα and PPARα binding led to the loss of reporter construct inhibition by agonists of these nuclear receptors. siRNA knockdown studies showed that APOF gene regulation by LXRα or PPARα agonists did not require an interaction between these two nuclear receptors. Thus, APOF is subject to neg. regulation by agonist-activated LXR or PPARα nuclear receptors binding to a regulatory element ∼1900 bases 5′ to the APOF promoter. High fat, cholesterol-enriched diets likely reduce APOF gene expression via these receptors interacting at this regulatory site.
Biochimica et Biophysica Acta, Molecular and Cell Biology of Lipids published new progress about 637-07-0. 637-07-0 belongs to chlorides-buliding-blocks, auxiliary class Inhibitor,Cell Cycle,PPAR, name is Ethyl 2-(4-chlorophenoxy)-2-methylpropanoate, and the molecular formula is C12H15ClO3, Synthetic Route of 637-07-0.
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