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10.1146/annurev-nutr-071813-105541

http://scihub22266oqcxt.onion/10.1146/annurev-nutr-071813-105541
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C5881898!5881898!24819326
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suck abstract from ncbi

pmid24819326      Annu+Rev+Nutr 2014 ; 34 (ä): 1-30
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  • Acyl-CoA Metabolism and Partitioning #MMPMID24819326
  • Grevengoed TJ; Klett EL; Coleman RA
  • Annu Rev Nutr 2014[]; 34 (ä): 1-30 PMID24819326show ga
  • 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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