Crucial step in cholesterol homeostasis: sterols promote binding of SCAP to INSIG-1, a membrane protein that facilitates retention of SREBPs in ER.

By Tong Yang, P. Espenshade, Michael E. Wright, D. Yabe, Y. Gong, R. Aebersold, J. Goldstein, Michael S. Brown. Cell, 2002

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Fatty acid uptake and lipid storage induced by HIF-1α contribute to cell growth and survival after hypoxia-reoxygenation. (2014, background): “When cells are grown in medium supplemented with 1% lipoprotein-deficient serum (LPDS) instead of full serum, SREBPs are activated due to the alleviation of sterol inhibition (Yang et al., 2002).”
Central leptin regulates total ceramide content and sterol regulatory element binding protein-1C proteolytic maturation in rat white adipose tissue. (2009, background): “Central leptin elicits an almost a 300% increase in INSIG-1 gene expression, the ER anchor of the SCAP-SREBP complex (43).”
Network analysis of the MVA and MEP pathways for isoprenoid synthesis. (2013, background): “The accumulation of HMGR is further regulated at the posttranslational level through a sterolresponsive negative-feedback mechanism that involves Insig1-dependent protein degradation (150).”