Literature summary for 2.7.1.107 extracted from

Harada, M.; Takeishi, Y.; Arimoto, T.; Niizeki, T.; Kitahara, T.; Goto, K.; Walsh, R.A.; Kubota, I.
Diacylglycerol kinase zeta attenuates pressure overload-induced cardiac hypertrophy (2007), Circ. J., 71, 276-282.

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Application

Application	Comment	Organism
medicine	creation of thoracic transverse aortic constriction in transgenic mice with cardiac-specific overexpression of diacylglycerol kinase zeta and wild-type mice. Increases in heart weight at 4 weeks after thoracic transverse aortic constriction are attenuated in diacylglycerol kinase zeta transgenic mice compared with wild-type mice. Increases in interventricular septal thickness, dilatation of the left ventricular cavity, and decreases in left ventricular systolic function in wild-type mice are observed at 4 weeks after surgery and are attenuated in diacylglycerol kinase zetatransgenic mice. Contrary to wild-type, cardiac fibrosis and gene induction of type I and type III collagens, but not transforming growth factor are blocked in diacylglycerol kinase zeta transgenic mice	Mus musculus

Protein Variants

Protein Variants	Comment	Organism
additional information	creation of thoracic transverse aortic constriction in transgenic mice with cardiac-specific overexpression of diacylglycerol kinase zeta and wild-type mice. Increases in heart weight at 4 weeks after thoracic transverse aortic constriction are attenuated in diacylglycerol kinase zeta transgenic mice compared with wild-type mice. Increases in interventricular septal thickness, dilatation of the left ventricular cavity, and decreases in left ventricular systolic function in wild-type mice are observed at 4 weeks after surgery and are attenuated in diacylglycerol kinase zetatransgenic mice. Contrary to wild-type, cardiac fibrosis and gene induction of type I and type III collagens, but not transforming growth factor are blocked in diacylglycerol kinase zeta transgenic mice	Mus musculus

Organism

Organism	UniProt	Comment	Textmining
Mus musculus	-	-	-

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Release 2023.1 (January 2023)