Fumonisin toxicity and sphingolipid biosynthesis.

@article{Merrill1996FumonisinTA,
  title={Fumonisin toxicity and sphingolipid biosynthesis.},
  author={Alfred H. Merrill and Elaine Ying Wang and Teresa R Vales and Elizabeth R. Smith and Joseph J Schroeder and David S. Menaldino and Christian Alexander and Heidi M. Crane and Jiang Xia and Dennis C Liotta and Filmore I. Meredith and Ronald T. Riley},
  journal={Advances in experimental medicine and biology},
  year={1996},
  volume={392},
  pages={297-306}
}
Fumonisins are inhibitors of sphinganine (sphingosine) N-acyltransferase (ceramide synthase) in vitro, and exhibit competitive-type inhibition with respect to both substrates of this enzyme (sphinganine and fatty acyl-CoA). Removal of the tricarballylic acids from fumonisin B1 reduces the potency by at least 10 fold; and fumonisin A1 (which is acetylated on the amino group) is essentially inactive. Studies with diverse types of cells (hepatocytes, neurons, kidney cells, fibroblasts, macrophages… CONTINUE READING

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Some of the sphinganine is metabolized to the 1-phosphate and degraded to hexadecanal and ethanolamine phosphate , which is incorporated into phosphatidylethanolamine .
Removal of the tricarballylic acids from fumonisin B1 reduces the potency by at least 10 fold ; and fumonisin A1 ( which is acetylated on the amino group ) is essentially inactive .
Removal of the tricarballylic acids from fumonisin B1 reduces the potency by at least 10 fold ; and fumonisin A1 ( which is acetylated on the amino group ) is essentially inactive .
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