Lacking cholesterol invariably leads to cell death. Cells acquire cholesterol by uptaking it from the external medium, and by endogenous synthesis from simple precursors. Within the cell, the distribution of cholesterol is highly compartmentalized, with most of the cellular cholesterol concentrated in the plasma membranes. The excess cholesterol is then stored as cholesteryl esters in the form of cytoplasmic lipid droplets. To maintain optimal content of cholesterol within the cells, the LDL uptake process, the endogenous sterol synthesis process, and the sterol esterification process are coordinately regulated.
Cholesterol is a lipid molecule.
It is practically insoluble in water. To follow the fate of cholesterol inside the cells, a somatic cell and molecular genetic approach has been developed in this and other laboratories. Well-characterized mutants can then serve as hosts for cloning genes by functional complementation. The first cleavage occurs within the lumen of the ER, producing an intermediate that contains the SRE-recognition segment but remains to be attached to the ER membrane through the first transmembrane domain. ACAT-1 message and protein are undetectable the mutation is recessive can be complemented by human genomic DNAs.