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1 (+) or without (-) etomoxir (an inhibitor of carnitine palmitoyltransferase I).
2 tty acid oxidation through the inhibition of carnitine palmitoyltransferase I, a mitochondrial compon
3 lated to the role of ACC-beta in controlling carnitine palmitoyltransferase I activity and fatty acid
4 tic expression of enzymes of fat catabolism (carnitine palmitoyltransferase-I, acyl-CoA oxidase, and
6 uscle suppress the activity of mitochondrial carnitine palmitoyltransferase I and thus fatty acid oxi
7 ndrial (medium-chain acyl-CoA dehydrogenase, carnitine palmitoyltransferase I) and extramitochondrial
8 me for fatty acid oxidation in mitochondria, carnitine palmitoyltransferase I; and by reduction of su
10 s were transduced with adenoviruses encoding carnitine palmitoyltransferase I (CPT I) isoforms or bet
11 nd an inhibitor of the two known isoforms of carnitine palmitoyltransferase I (CPT I), which control
16 oxidase], and mitochondrial differentiation [carnitine palmitoyltransferase I (CPT-I) isoforms] were
18 FAO by pretreatment of fasting rats with the carnitine palmitoyltransferase-I (CPT-I) inhibitor reduc
19 ent, endogenous, and allosteric inhibitor of carnitine palmitoyltransferase-I (CPT-I), a key enzyme f
20 sequence coverage for the membrane proteins carnitine palmitoyltransferase-I (CPT-I), long-chain acy
22 d by the outer mitochondrial membrane enzyme carnitine palmitoyltransferase I (CPTI) and inhibited by
24 ut distinct carnitine palmitoyltransferases: carnitine palmitoyltransferase I (CPTI), which is malony
25 oncentration of malonyl-CoA, an inhibitor of carnitine palmitoyltransferase I, have been linked to th
26 idative responses to fasting are maintained; carnitine palmitoyltransferase-I induction and glucose l
30 N-terminal amino acid residues of rat liver carnitine palmitoyltransferase I (L-CPTI) are essential
31 N-terminal amino acid residues of rat liver carnitine palmitoyltransferase I (L-CPTI) on malonyl-CoA
32 n catalytic activity in the liver isoform of carnitine palmitoyltransferase I (L-CPTI), we separately
33 t in the heart, but the liver isoform (liver carnitine palmitoyltransferase I [L-CPT1]) is elevated i
34 xidative flux, the expression of muscle-type carnitine palmitoyltransferase I (M-CPT I) was character
35 n the expression of the gene encoding muscle carnitine palmitoyltransferase I (M-CPT I), an enzyme in
36 induced accumulation of mRNA encoding muscle carnitine palmitoyltransferase I (M-CPT I), an enzyme th
39 activated receptor alpha target, muscle-type carnitine palmitoyltransferase I, providing a second mec
40 chain free fatty acids into mitochondria via carnitine palmitoyltransferase I relative to overall oxi
41 tricarboxylic acid cycle rates, flux through carnitine palmitoyltransferase I was 23% lower in hypert
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