期刊
CELLULAR AND MOLECULAR LIFE SCIENCES
卷 62, 期 16, 页码 1784-1803出版社
BIRKHAUSER VERLAG AG
DOI: 10.1007/s00018-005-5121-4
关键词
metabolic syndrome; obesity; diabetes; structure-based drug design; fatty acid metabolism; protein structure and function; biotin-dependent carboxylases; enzyme catalysis and mechanism
资金
- NIDDK NIH HHS [DK67238] Funding Source: Medline
Acetyl-coenzyme A carboxylases (ACCs) have crucial roles in fatty acid metabolism in most living organisms. Mice deficient in ACC2 have continuous fatty acid oxidation and reduced body fat and body weight, validating this enzyme as a target for drug development against obesity, diabetes and other symptoms of the metabolic syndrome. ACC is a biotin-dependent enzyme and catalyzes the carboxylation of acetyl-CoA to produce malonyl-CoA through its two catalytic activities, biotin carboxylase (BC) and carboxyltransferase (CT). ACC is a multi-subunit enzyme in most prokaryotes, whereas it is a large, multi-domain enzyme in most eukaryotes. The activity of the enzyme can be controlled at the transcriptional level as well as by small molecule modulators and covalent modification. This review will summarize the structural information that is now available for both the BC and CT enzymes, as well as the molecular mechanism of action of potent ACC inhibitors. The current intense research on these enzymes could lead to the development of novel therapies against metabolic syndrome and other diseases.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据