Chemistry:Triacsin C
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| IUPAC name
N-(((2E,4E,7E)-undeca-2,4,7-trienylidene)amino)nitrous amide
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3D model (JSmol)
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| 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). | |
 verify (what is   ?)
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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]
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
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
- Fatty acid degradation
- Fatty acyl CoA synthetase
References
- ↑ 1.0 1.1 1.2 "Studies on new vasodilators, WS-1228 A and B. I. Discovery, taxonomy, isolation and characterization". J Antibiot (Tokyo) 35 (2): 151–156. 1982. doi:10.7164/antibiotics.35.151. PMID 6804425.
- ↑ "Inhibition of acyl-CoA synthetase by triacsins". Biochimica et Biophysica Acta 921 (3): 595-598. 1987. doi:10.1016/0005-2760(87)90088-9. PMID 3117118.
- ↑ "Evidence for an Essential Role of Long Chain Acyl-CoA Synthetase in Animal Cell Proliferation". The Journal of Biological Chemistry 266 (7): 4214-4219. 1991. doi:10.1016/S0021-9258(20)64309-5. PMID 1999415.
- ↑ "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. June 1997. doi:10.1042/bj3240529. PMID 9182714. PMC 1218462. http://www.biochemj.org/bj/324/0529/bj3240529.htm.
- ↑ "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. 2007. doi:10.1194/jlr.M700050-JLR200. PMID 17379924.
- ↑ "Modulation of Triglyceride and Cholesterol Ester Synthesis Impairs Assembly of Infectious Hepatitis C Virus". The Journal of Biological Chemistry 289 (31): 21276-21288. 2014. doi:10.1074/jbc.M114.582999. PMID 24917668.
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