Fig. 3.

Cholesterol balance in healthy cells. Both de-novo synthesis from acetyl-CoA produced by glycolysis and exogenous absorption by low-density lipoprotein receptors (LDLR) are major sources of cholesterol for cells. Through [3], the inhibition of proteolytic processing and nuclear import of sterol regulatory element binding proteins (SREBP2), which results in a reduction in activity in the mevalonate pathway, or through its conversion to oxysterols that activate liver X receptors (LXRs), cholesterol can negatively regulate its own levels. By upregulating ABCA1 expression and activating IDOL transcription, an E3 ubiquitin ligase that ubiquitinates LDLR, LXRs reduce cellular cholesterol levels. ER, endoplasmic membrane; SCAP, SREBP cleavage-activating protein.