Acyl-CoA metabolism and partitioning.
Acyl-CoA metabolism and partitioning.
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DOI：
10.1146/annurev-nutr-071813-105541
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发表时间：
2014
影响因子：
8.9
通讯作者：
Coleman RA
中科院分区：
文献类型：
--
作者：
Grevengoed TJ;Klett EL;Coleman RA
长链脂肪酰辅酶A是重要的调节分子和代谢中间体。其合成的第一步是通过13种长链酰基辅酶A合成酶同工型之一激活脂肪酸。这些亚型受到独立调节，并具有不同的组织表达模式和亚细胞位置。它们的酰基辅酶A产物调节代谢酶和信号通路，被氧化以提供细胞能量，并被掺入酰化蛋白质和复杂脂质如三酰甘油、磷脂和胆固醇酯中。它们不同的代谢命运由蛋白质网络决定，该蛋白质网络将酰基辅酶A引导朝向或远离特定的代谢途径，并作为分配的基础。这篇评论评估的证据，酰基辅酶A分区通过审查被认为有助于酰基辅酶A通道，这些蛋白质的损失，代谢的后果，和潜在的作用，适应不良的酰基辅酶A分区代谢疾病和致癌的发病机制的蛋白质的实验数据。
Long-chain fatty acyl-CoAs are critical regulatory molecules and metabolic intermediates. The initial step in their synthesis is the activation of fatty acids by one of 13 long-chain acyl-CoA synthetase isoforms. These isoforms are regulated independently and have different tissue expression patterns and subcellular locations. Their acyl-CoA products regulate metabolic enzymes and signaling pathways, become oxidized to provide cellular energy, and are incorporated into acylated proteins and complex lipids like triacylglycerol, phospholipids, and cholesterol esters. Their differing metabolic fates are determined by a network of proteins that channel the acyl-CoAs towards or away from specific metabolic pathways and serve as the basis for partitioning. This review evaluates the evidence for acyl-CoA partitioning by reviewing experimental data on proteins that are believed to contribute to acyl-CoA channeling, the metabolic consequences of loss of these proteins, and the potential role of maladaptive acyl-CoA partitioning in the pathogenesis of metabolic disease and carcinogenesis.
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影响因子：
6.5
作者：
Bu, So Young;Mashek, Douglas G.
通讯作者：
Mashek, Douglas G.
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4.8
作者：
Caviglia, JM;Li, LO;Lewin, TM
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Lewin, TM
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3.5
作者：
Daikoku, T;Shinohara, Y;Terada, H
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Terada, H
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9.8
作者：
CHEN, MT;KAUFMAN, LN;SHRAGO, E
通讯作者：
SHRAGO, E
影响因子：
4.8
作者：
Bu, So Young;Mashek, Mara T.;Mashek, Douglas G.
通讯作者：
Mashek, Douglas G.