|
ACAT-2 DEFICIENT MICE
Background: Acyl CoA:cholesterol acyltransferase (ACAT) catalyzes the formation of cholesterol esters from cholesterol and fatty acids. Cholesterol esterification and the ACAT enzyme have been implicated in a number of important biological processes including cholesterol absorption, lipoprotein (such as LDL) synthesis and secretion, and macrophage foam cell formation in atherosclerotic lesions. 
Description: Scientists at the Gladstone Institutes have created a genetically modified strain of mice carrying a disruption of the mouse ACAT gene. This modification prevents these mice from making the ACAT enzyme. These mice exhibit markedly diminished cholesterol esterification in the adrenal cortical cells and in macrophages. Furthermore, the ACAT-deficient mice offer research advantages over treating mice with pharmaceutical ACAT inhibitors since the ACAT deficiency is complete and specific, avoiding any potential side effects of pharmaceutical agents.
Applications: The Gladstone mice provide a model for examining the role of the ACAT enzyme in macrophage cholesterol ester foam cell formation and in atherosclerosis.
Advantages: The ACAT-deficient mice permit investigations of the effects of blocking the enzymatic action of ACAT without the side effects of pharmaceutical agents.
Gladstone Contact:
Caryl Cachola
Telephone: 415-734-2082  Tell a friend
 Printer friendly version
|
