Triacsin C is an inhibitor of long fatty acyl CoA synthetase that has been isolated from Streptomyces aureofaciens.[1][2][3] It blocks β-cell apoptosis, induced by fatty acids (lipoapoptosis) in a rat model of obesity. In addition, it blocks the de novo synthesis of triglycerides, diglycerides, and cholesterol esters, thus interfering with lipid metabolism.[4]

Triacsin C
Names
IUPAC name
N-(((2E,4E,7E)-undeca-2,4,7-trienylidene)amino)nitrous amide
Identifiers
3D model (JSmol)
ChEBI
ChemSpider
ECHA InfoCard 100.127.901 Edit this at Wikidata
UNII
  • InChI=1S/C11H17N3O/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15/h4-5,7-11H,2-3,6H2,1H3,(H,13,15)/b5-4+,8-7+,10-9+,12-11+ checkY
    Key: NKTGCVUIESDXPU-YLEPRARLSA-N checkY
  • InChI=1/C11H17N3O/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15/h4-5,7-11H,2-3,6H2,1H3,(H,13,15)/b5-4+,8-7+,10-9+,12-11+
    Key: NKTGCVUIESDXPU-YLEPRARLBF
  • O=NN/N=C/C=C/C=C/C/C=C/CCC
Properties
C11H17N3O
Molar mass 207.277 g·mol−1
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
☒N verify (what is checkY☒N ?)

In addition, triacsin C is a vasodilator.[1]

Inhibition of lipid metabolism reduces/removes lipid droplets from HuH7 cells.[5] In hepatitis C–infected HuH7 cells, this reduction/removal of lipid droplets by triacsin C correlates with a reduction in virion assembly and infectivity.[6]

General chemical description

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Triacsin C belongs to a family of fungal metabolites all having an 11-carbon alkenyl chain with a common N-hydroxytriazene moiety at the terminus. Due to the N-hydroxytriazene group, triacsin C has acidic properties and may be considered a polyunsaturated fatty acid analog.

Triacsin C was discovered by Keizo Yoshida and other Japanese scientists in 1982 in a culture of the microbe Streptomyces aureofaciens.[1] They identified it as a vasodilator.

See also

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References

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  1. ^ a b c Yoshida K, Okamoto M, Umehara K, Iwami M, Kohsaka M, Aoki H, et al. (1982). "Studies on new vasodilators, WS-1228 A and B. I. Discovery, taxonomy, isolation and characterization". J Antibiot (Tokyo). 35 (2): 151–156. doi:10.7164/antibiotics.35.151. PMID 6804425.
  2. ^ Tomoda H, Igarashi K, Omura S (1987). "Inhibition of acyl-CoA synthetase by triacsins". Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism. 921 (3): 595–598. doi:10.1016/0005-2760(87)90088-9. PMID 3117118.
  3. ^ Tomoda H, Igarashi K, Chong JC, Ōmura S (1991). "Evidence for an Essential Role of Long Chain Acyl-CoA Synthetase in Animal Cell Proliferation". The Journal of Biological Chemistry. 266 (7): 4214–4219. doi:10.1016/S0021-9258(20)64309-5. PMID 1999415.
  4. ^ Igal RA, Wang P, Coleman RA (June 1997). "Triacsin C blocks de novo synthesis of glycerolipids and cholesterol esters but not recycling of fatty acid into phospholipid: evidence for functionally separate pools of acyl-CoA". Biochem. J. 324. ( Pt 2) (Pt 2): 529–34. doi:10.1042/bj3240529. PMC 1218462. PMID 9182714.
  5. ^ Fujimoto Y, Itabe H, Kinoshita T, Homma KJ, Onoduka J, More M, et al. (2007). "Involvement of ACSL in local synthesis of neutral lipids in cytoplasmic lipid droplets in human hepatocyte HuH7". Journal of Lipid Research. 48 (6): 1280–1292. doi:10.1194/jlr.M700050-JLR200. PMID 17379924.
  6. ^ Liefhebber JM, Hague CV, Zhang Q, Wakelam MJ, McLauchlan J (2014). "Modulation of Triglyceride and Cholesterol Ester Synthesis Impairs Assembly of Infectious Hepatitis C Virus". The Journal of Biological Chemistry. 289 (31): 21276–21288. doi:10.1074/jbc.M114.582999. PMC 4118089. PMID 24917668.