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Gene Review

Soat2  -  sterol O-acyltransferase 2

Mus musculus

Synonyms: ACAT-2, ACAT2, Acact-2, Acat2, Acyl-coenzyme A:cholesterol acyltransferase 2, ...
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Disease relevance of Soat2


High impact information on Soat2

  • At 30 wk of age, only the control mice had significant atherosclerosis, which was nearly absent in ACAT2(-/-) ApoE(-/-) mice [4].
  • Our results demonstrate the crucial role of ACAT2-derived cholesterol esters in the development of atherosclerosis in mice and suggest that triglyceride-rich apoB-containing lipoproteins are not as atherogenic as those containing cholesterol esters [4].
  • Despite a lower level of ACAT activity, the ACAT1-expressing cells esterified 4-fold more sitosterol than the ACAT2 cells [5].
  • Compared with ACAT1, ACAT2 selectively esterified cholesterol even when sitosterol was loaded into the microsomes [5].
  • This sterol selectivity by ACAT2 may reflect a role in the sorting of dietary sterols during their absorption by the intestine in vivo [5].

Biological context of Soat2


Associations of Soat2 with chemical compounds


Regulatory relationships of Soat2

  • However, it has been found that cholesterol absorption is not completely inhibited in ACAT2-deficient (ACAT2 KO) mice [10].
  • To support this idea, LDL that was modified to decrease its ability to induce net cellular cholesterol efflux stimulated ACAT 2-fold greater than control LDL when matched for lysosomal LDL-cholesterol influx [11].

Other interactions of Soat2


Analytical, diagnostic and therapeutic context of Soat2


  1. Resistance to diet-induced hypercholesterolemia and gallstone formation in ACAT2-deficient mice. Buhman, K.K., Accad, M., Novak, S., Choi, R.S., Wong, J.S., Hamilton, R.L., Turley, S., Farese, R.V. Nat. Med. (2000) [Pubmed]
  2. Acyl-CoA:cholesterol acyltransferase inhibition reduces atherosclerosis in apolipoprotein E-deficient mice. Kusunoki, J., Hansoty, D.K., Aragane, K., Fallon, J.T., Badimon, J.J., Fisher, E.A. Circulation (2001) [Pubmed]
  3. ACBP and cholesterol differentially alter fatty acyl CoA utilization by microsomal ACAT. Chao, H., Zhou, M., McIntosh, A., Schroeder, F., Kier, A.B. J. Lipid Res. (2003) [Pubmed]
  4. Deficiency of acyl CoA:cholesterol acyltransferase 2 prevents atherosclerosis in apolipoprotein E-deficient mice. Willner, E.L., Tow, B., Buhman, K.K., Wilson, M., Sanan, D.A., Rudel, L.L., Farese, R.V. Proc. Natl. Acad. Sci. U.S.A. (2003) [Pubmed]
  5. Compared with Acyl-CoA:cholesterol O-acyltransferase (ACAT) 1 and lecithin:cholesterol acyltransferase, ACAT2 displays the greatest capacity to differentiate cholesterol from sitosterol. Temel, R.E., Gebre, A.K., Parks, J.S., Rudel, L.L. J. Biol. Chem. (2003) [Pubmed]
  6. Acute P-407 administration to mice causes hypercholesterolemia by inducing cholesterolgenesis and down-regulating low-density lipoprotein receptor expression. Leon, C., Wasan, K.M., Sachs-Barrable, K., Johnston, T.P. Pharm. Res. (2006) [Pubmed]
  7. Preferential pharmacological inhibition of macrophage ACAT increases plaque formation in mouse and rabbit models of atherogenesis. Perrey, S., Legendre, C., Matsuura, A., Guffroy, C., Binet, J., Ohbayashi, S., Tanaka, T., Ortuno, J.C., Matsukura, T., Laugel, T., Padovani, P., Bellamy, F., Edgar, A.D. Atherosclerosis (2001) [Pubmed]
  8. Liver-specific inhibition of acyl-coenzyme a:cholesterol acyltransferase 2 with antisense oligonucleotides limits atherosclerosis development in apolipoprotein B100-only low-density lipoprotein receptor-/- mice. Bell, T.A., Brown, J.M., Graham, M.J., Lemonidis, K.M., Crooke, R.M., Rudel, L.L. Arterioscler. Thromb. Vasc. Biol. (2006) [Pubmed]
  9. The aromatase knockout mouse presents with a sexually dimorphic disruption to cholesterol homeostasis. Hewitt, K.N., Boon, W.C., Murata, Y., Jones, M.E., Simpson, E.R. Endocrinology (2003) [Pubmed]
  10. Intestinal cholesterol absorption is substantially reduced in mice deficient in both ABCA1 and ACAT2. Temel, R.E., Lee, R.G., Kelley, K.L., Davis, M.A., Shah, R., Sawyer, J.K., Wilson, M.D., Rudel, L.L. J. Lipid Res. (2005) [Pubmed]
  11. Lipoproteins activate acyl-coenzyme A:cholesterol acyltransferase in macrophages only after cellular cholesterol pools are expanded to a critical threshold level. Xu, X.X., Tabas, I. J. Biol. Chem. (1991) [Pubmed]
  12. Age-related alteration in hepatic acyl-CoA: cholesterol acyltransferase and its relation to LDL receptor and MAPK. Bose, C., Bhuvaneswaran, C., Udupa, K.B. Mech. Ageing Dev. (2005) [Pubmed]
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