Abstract: Methods for regulation of lipid and cholesterol uptake are described which are based on regulation of the expression or function of the SR-BI HDL receptor. The examples demonstrate that estrogen dramatically downregulates SR-BI under conditions of tremendous upregulation of the LDL-receptor. The examples also demonstrate the upregulation of SR-BI in rat adrenal membranes and other non-placental steroidogenic tissues from animals treated with estrogen, but not in other non-placental non-steroidogenic tissues, including lung, liver, and skin. Examples further demonstrate the uptake of fluorescently labeled HDL into the liver cells of animal, which does not occur when the animals are treated with estrogen. Examples also demonstrate the in vivo effects of SR-BI expression on HDL metabolism, in mice transiently overexpressing hepatic SR-BI following recombinant adenovirus infection. Overexpression of the SR-BI in the hepatic tissue caused a dramatic decrease in cholesterol blood levels.

Abstract: Two fusion proteins are described. One fusion protein comprises a protein having a modular protein domain, wherein the domain is replaced by a single chain antibody. The other fusion protein contains a binding site that binds to a modular protein binding domain, wherein a linear epitope in the binding site that binds to the domain is replaced by at least one copy of an epitope that binds to the single chain antibody. These fusion proteins, and nucleic acid encoding them can be used to screen for specific interaction between two proteins.