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Literature summary for 2.3.1.21 extracted from

  • Yao, C.H.; Liu, G.Y.; Wang, R.; Moon, S.H.; Gross, R.W.; Patti, G.J.
    Identifying off-target effects of etomoxir reveals that carnitine palmitoyltransferase I is essential for cancer cell proliferation independent of beta-oxidation (2018), PLoS Biol., 16, e2003782 .
    View publication on PubMedView publication on EuropePMC
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Application

Application Comment Organism
medicine when fatty acid oxidation is reduced approximately 90% by pharmacological inhibition of carnitine palmitoyltransferase I CPT1 with low concentrations of etomoxir, the proliferation rate of various cancer cells is unaffected. High concentrations of etomoxir (200 microM) have an off-target effect of inhibiting complex I of the electron transport chain. When fatty acid oxidation is reduced further by genetic knockdown of CPT1, the proliferation rate of these same cells decreases nearly 2fold and cannot be restored by acetate or octanoic acid supplementation. CPT1 knockdowns have altered mitochondrial morphology and impaired mitochondrial coupling, whereas cells in which CPT1 has been approximately 90% inhibited by etomoxir do not. Mitochondria isolated from CPT1 knockdowns show depleted concentrations of complex structural and signaling lipids. Expression of a catalytically dead CPT1 in CPT1 knockdowns does not restore mitochondrial coupling Homo sapiens

Inhibitors

Inhibitors Comment Organism Structure
etomoxir high concentrations of etomoxir (200 microM) have an off-target effect of inhibiting complex I of the electron transport chain. When fatty acid oxidation is reduced approximately 90% by low concentrations of etomoxir, the proliferation rate of various cancer cells is unaffected Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens P50416 isoform CPT1a
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General Information

General Information Comment Organism
physiological function when fatty acid oxidation is reduced by genetic knockdown of CPT1, the proliferation rate of cancer cells decreases nearly 2fold and cannot be restored by acetate or octanoic acid supplementation. CPT1 knockdowns have altered mitochondrial morphology and impaired mitochondrial coupling, whereas cells in which CPT1 has been approximately 90% inhibited by etomoxir do not. Mitochondria isolated from CPT1 knockdowns show depleted concentrations of complex structural and signaling lipids. Expression of a catalytically dead CPT1 in CPT1 knockdowns does not restore mitochondrial coupling Homo sapiens