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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Membrane lipid environment of carp brain and liver mitochondrial monoamine oxidase.

Delipidation of carp liver mitochondria by treatment with methyl ethyl ketone (MEK) or Triton X-100 and then perchlorate greatly reduced MAO activities. Treatment with only Triton X-100 resulted in less reduction in activity. The Km values of the remaining activities were similar regardless of these treatments. The sensitivities towards clorgyline and l-deprenyl of the remaining activity in the Triton X-100-treated residue and the phospholipase C-treated carp brain mitochondria were found to be unchanged, but those of the activity remaining in the MEK-treated residue were similarly decreased. No evidence was obtained suggesting conversion of carp MAO to either MAO-A or MAO-B by the modification of the mitochondrial lipid environment by the treatments employed.[1]

References

  1. Membrane lipid environment of carp brain and liver mitochondrial monoamine oxidase. Kinemuchi, H., Sunami, Y., Sudo, M., Suh, Y.H., Arai, Y., Kamijo, K. Comp. Biochem. Physiol. C, Comp. Pharmacol. Toxicol. (1985) [Pubmed]
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