Literature summary for 2.3.1.85 extracted from

Razani, B.; Zhang, H.; Schulze, P.C.; Schilling, J.D.; Verbsky, J.; Lodhi, I.J.; Topkara, V.K.; Feng, C.; Coleman, T.; Kovacs, A.; Kelly, D.P.; Saffitz, J.E.; Dorn, G.W.; Nichols, C.G.; Semenkovich, C.F.
Fatty acid synthase modulates homeostatic responses to myocardial stress (2011), J. Biol. Chem., 286, 30949-30961.

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Organism

Organism	UniProt	Comment	Textmining
Mus musculus	-	-	-

General Information

General Information	Comment	Organism
physiological function	mice with fatty acid synthase knockout in the myocardium, FASKard, develop normally, manifest normal resting heart function, and have normal cardiac PPARalpha signaling as well as fatty acid oxidation. Mutant mice decompensate with stress. Most die within 1 h of transverse aortic constriction, probably due to arrhythmia. Voltage clamp measurements of FASKard cardiomyocytes show hyperactivation of L-type calcium channel current that can not be reversed with palmitate supplementation.Ca2+/calmodulin-dependent protein kinase II but not protein kinase A signaling is activated in FASKard hearts, and knockdown of fatty acid synthase in cultured cells activates Ca2+/calmodulin-dependent protein kinase II. In addition to being intolerant of the stress of acute pressure, FASKard hearts are also intolerant of the stress of aging, reflected as persistent CaMKII hyperactivation, progression to dilatation, and premature death by 1 year of age. Ca2+/calmodulin-dependent protein kinase II signaling appears to be pathogenic in FASKard hearts	Mus musculus

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Release 2023.1 (January 2023)