EC Number   |
Natural Substrates |
|---|
   2.3.1.43 | more |
enzyme deficiency can cause corneal opacity, proteinuria, anemia, and kidney failure |
| 2.3.1.43 | more |
enzyme forms higher aggregates with HDL and apolipoprotein A-I in plasma, esterification of cholesterol and binding to cholesteryl ester transfer protein are required for reverse cholesterol transport from peripheral cells to plasma |
| 2.3.1.43 | more |
a frameshift mutation of the LCAT gene is associated with renal failure with proteinuria, corneal opacity, and anemia in familial LCAT deficiency |
| 2.3.1.43 | more |
key enzyme in reverse cholesterol transport |
| 2.3.1.43 | more |
LCAT adds cholesteryl ester to LDL in mice and is important in remodeling VLDL to LDL, LCAT deficiency significantly decreases the cholesteryl ester percentage and significantly increases the phospholipid percentage of LDL, overview |
| 2.3.1.43 | more |
the activity and fatty acid specificity of LCAT may be altered during the inflammatory response |
| 2.3.1.43 | more |
the enzyme is involved in development of atherosclerosis |
| 2.3.1.43 | more |
the enzyme is responsible for the cholesterol transport, controlling the flow of cholesterol from peripheral tissues to the liver |
| 2.3.1.43 | more |
the rare enzyme genetic disorder, familial LCAT deficiency, leads to altered plasma lipid and lipoprotein levels, corneal opacities and proteinuria with renal failure, phenotype analysis, overview |
| 2.3.1.43 | more |
about 75% of plasma LCAT is associated with HDL |
