Bremer J, Woldegiorgis G, Schalinske K, Shrago E
Biochim Biophys Acta. 1985 Jan 9;833(1):9-16. doi: 10.1016/0005-2760(85)90247-4.
Extraction of rat liver mitochondria twice with 0.5% Triton X-100 in a salt-free medium leaves less than 10% of the carnitine palmitoyltransferase membrane bound. The remaining membrane-bound enzyme is inhibited virtually completely by 10 microM malonyl-CoA. Preincubation of the extracted membranes with palmitoyl-CoA and salts (KCI) for several minutes activates the enzyme and makes it increasingly insensitive to malonyl-CoA. Addition of malonyl-CoA to the preincubation reverses this desensitization. In albumin-containing media salts also decrease the binding of palmitoyl-CoA to albumin and stimulate carnitine palmitoyltransferase by increasing substrate availability in free solution. The reverse reaction shows accelerated desensitization by palmitoylcarnitine and resensitization by malonyl-CoA.
在无盐培养基中用0.5% Triton X-100对大鼠肝脏线粒体进行两次提取后，膜结合的肉碱棕榈酰转移酶含量不到10%。剩余的膜结合酶几乎完全被10微摩尔丙二酸单酰辅酶A抑制。将提取的膜与棕榈酰辅酶A和盐（氯化钾）预孵育几分钟可激活该酶，并使其对丙二酸单酰辅酶A的敏感性降低。在预孵育中加入丙二酸单酰辅酶A可逆转这种脱敏作用。在含白蛋白的培养基中，盐也会降低棕榈酰辅酶A与白蛋白的结合，并通过增加游离溶液中底物的可用性来刺激肉碱棕榈酰转移酶。逆反应显示，棕榈酰肉碱可加速脱敏，丙二酸单酰辅酶A可使其重新敏感。
